Seperti hampir semua anak kecil di dunia, daku pernah bertanya-tanya, dari manakah datangnya seorang anak? Dan daku pernah mempunyai konsep yang amat sangat indah. Menurut pikiran daku yang waktu itu belum mengenal istilah pembuahan ataupun proses-proses kenikmatan yang mendahuluinya, anak dihasilkan dari pengharapan.
Like almost every child in this world, I was also questioning (wondering) where the babies come from. And I have a beautiful theory — from my innocent thought, which for sure at that time still don't know what the fertilization process is, or the pleasure activity preceding before it — a child comes from hope.
Saat sepasang suami-istri menikah, maka diberkatilah mereka. Mereka akan saling mengasihi dan berdoa bersama akan datangnya seorang anak. Oleh karena itu, tidak jarang kita akan mendengar perkataan, "Mereka masih menunggu datangnya seorang anak dalam kehidupan mereka." Bah, kenapa pakai kata-kata seperti itu? Kesannya terlalu saru. Sampai-sampai muncullah pemikiran bahwa seorang anak tiba-tiba 'diselipkan' begitu saja ke rahim seorang istri. Belakangan aku baru tahu kalau seorang anak itu bukan ditunggu kedatangannya, tapi 'diusahakan'.
When a man and a woman are blessed to become husband and wife, they shall love each other, and then pray together for a coming of a child. Because of that, we are often hear a lot of people say that the couple's hope of getting a child hasn't been granted yet — or they are still hoping (waiting) for a child to enter their life. Walae, why do we use those expression? It seems so ambiguous and made me think that a child can just be slipped into a woman's womb. Finally, I knew that a a child is not for us to wait but it is for us to work out... :)
Yah mungkin juga aku bisa berpikir seperti itu karena dulu belum tahu ada kasus yang istilahhnya 'hamil di luar nikah', 'kecelakaan' ataupun unwanted child. (Lah kalau memang anak didatangkan dengan doa, tentunya atas persetujuan Tuhan dong. Dengan kata lain yang bisa hamil itu cuma istri-istri dari pasangan yang diberkati di tempat ibadah secara agama dan direstui oleh seluruh sanak keluarga). Waktu itu juga sepertinya gelar MBA (Married By Accident) belum begitu populer.
Perhaps it was caused by my naive thinking, I didn't recognize a case of woman got pregnant out of wedlock, "accident" or even "unwanted child." If a child comes from a granted pray so it must comes from GOD's approval. Thus, all wives that are expecting baby is only the blessed ones from all churches, temples, mosque, etc. and must also blessed by the entire family — as at the time, when I was a kid — no such things as MBA (Married By Accident) or that phrase was not (too) popular.
Tapi aku pernah mendengar sebuah berita di televisi yang mengubah konsep 'anak datang dari doa'. Kalau tidak salah ingat, berita tersebut tentang seorang guru yang amat sangat genit dan sangat 'dekat dan akrab' dengan muridnya. (dekat dalam arti, Sangat... dekat sekali dalam makna denotasi)
My concept — a child comes form hope — suddenly changed when I was watching a local news on the TV. If I remembered correctly, it was about a flirty high school teacher, famous to be close to his student — close in the meaning 'too close' in a denotation meaning.
Nah kira-kira laporan yang dibacakan oleh narator (atau apalah namanya yang baca berita pas dikasih gambar) itu berbunyi, "Tersangka terkenal suka memegang-megang siswi. Ada yang pipinya dielus, bahkan ada yang hamil." Sudah bisa ditebak ada yang ada di pikiran daku waktu itu?
The news anchor (the person who read the story when you can see the illustration picture) was telling that the teacher loves to touch the girls. He loves to touch the cheek of the girls and even one of them gets pregnant... Can you guess how wild my imagination is when I heard that news?
"Oh... ternyata mengelus pipi bisa berefek samping hamil!!!" Pikiran daku tidak berhenti di sana, lalu aku mengambil satu kesimpulan teori: "Sentuhan seorang lelaki bisa meresap ke dalam kulit dan akhirnya tiba di perut? Membesar, membesar, dan akhirnya menjadi seorang bayi?" Bahaya bener... Pantesan orang-orang tua selalu bilang, "Ati-ati, jangan tidur sama lelaki!!" Wah, berarti pas tidur seranjang, sebelah-sebelahan, tiba-tiba tengah malam nanti ada 'sesuatu' yang tiba-tiba merayap keluar dari si jantan dan menyusup ke perut betina? Dan DUING!!! Mengembanglah perut sang betina. Tapi, belakangan (saat daku kira-kira udah SMA) tante daku malah bilang, "Tidur sama cowok itu gak papa. Asal bener tidur bareng ya. Kalau gak tidur, nah, itulah yang bahaya!" Hm... ada benarnya juga sih.
"Oh... so you can get pregnant if a man touch your cheek!!!" And my imagination didn't stop at that point. I concluded that a touch of a man can really go through into your skin and then turn up on your tummy. After that, it's getting bigger and bigger, and finally became a baby!! Wow... it's so dangerous... no wonder parents always says to their daughter, "Be careful, don't sleep with a man!!!" Wa... does it mean that if a man and a woman sleep side by side, then something will crawl slowly in the midnight from a man and will slip to a woman's tummy? And then, DUNG!!! The woman's tummy blows up. But, when I was in senior high school, my auntie said, "It's OK to sleep side by side with a man as long as you REALLY sleep!!! If you don't sleep... thus... IT IS DANGEROUS!!!". Hmm, it's quite true.
Oh iya, ngomong-ngomong. Kalau dilihat di komik ataupun di film kartun, ada yang menceritakan bahwa bayi itu didatangkan oleh burung besar! (entah jenis apa dan dari mana) Wah... kalau dipikir-pikir, aneh juga ya cerita ini, kira-kira masih ada anak kecil yang percaya gak ya? Soalnya menurut fakta, banyak hewan termasuk burung tentunya, terancam punah karena ekspansi wilayah yang dilakukan manusia ke habitat mereka di alam. Lalu di mana letak logikanya kalau pembawa kelahiran itu sendiri terancam punah sementara manusia malah semakin banyak? Yah, mungkin memang seharusnya cerita film kartun tidak boleh dianggap serius.
By the way, comics or cartoons are often tell us that a big bird (a type of crane?) will bring the babies... This story, according to me, is quite funny... do you think that many children still believe that? It's funny for me since, as you know, that a lot of animal, including birds are already in the rare category... almost gone because of human's expansion to their environment in the nature. So, where is the logical thinking, if the carrier itself are almost gone but human are getting more and more? Yeah, maybe that's way we may not consider cartoon movies so seriously.
Mari kita ke tahap selanjutnya, hal lahir melahirkan. Hm.. kayanya daku mengerti istilah 'caesar' terlebih dahulu daripada lahir alami. Kenapa bisa begitu? Gampang saja alasannya.
Let's move on to the next level... I think I understood Caesar operation as a delivery method earlier than the natural one... How could it be so? It was a very simple reason...
Setelah bayi tumbuh besar di dalam perut, ia perlu segera dikeluarkan sebelom perut ibunya meledak. Nah cara paling cepat adalah membuka perut ibu, mengeluarkan bayi, lalu kita tutup kembali. Hampir persis sama seperti cara kerja resleting. Bagaimana prosesnya secara lebih mendetail? Ah peduli amat sama tetek bengek proses 'caesar' itu. Toh dokter pasti punya obat bius kan? Tinggal suntik sana suntik sini, siaplah perut ibu dibelek tanpa rasa sakit.
My thinking was... after a baby grows in mum's tummy, he/she should be out of it before his/her mum's tummy explodes, so the easiest way is to open mum's tummy and then, close it up again. It almost looks like if we close up our zipper... How are the details of the process? Shall we care? No need, right? There are doctors to give the mummies a sleeping shots... shoot here... shoot there and mummy's tummy is ready to be opened without any pain.
Pada waktu masih SD, seorang teman menceritakan teorinya yang lebih ajaib lagi. Katanya, sebenarnya saat ibu hamil, isi perutnya adalah cairan. Lalu bagaimana cara melahirkan? Dengan penuh keyakinan dia berkata, "Melalui cara yang sama kaya kencing." "Heh? Kenapa bisa begitu? Kalau yang keluar cuma cairan, bayinya mana? Apa harus dibekukan sampai pada suhu 0°C? Pake cetakan kue?" "Denger dulu dong. Setelah semua cairan dikeluarkan, kempeslah perut si mama. Tugas dokter adalah memastikan agar cairan tersebut tertampung seluruhnya dengan baik. Jangan sampai ada yang tumpah! Nanti bisa-bisa bayinya cacat. Setelah ditampung, biarkan beberapa lama, lalu dengan sendirinya air kencing itu akan berubah menjadi seorang bayi!!!"
Another theory is come from my primary school's friend... and it is more imaginary than mine. He said that the pregnant mummy contains of a kind of liquid. If so, then how to deliver the baby? With full confidence, he said, "Using the same way like we go to urinate." "Huh? How come it is like that? If it's only liquid, so where is the baby? Do we have to freeze it in 0ºC and use a cake molder to shape the baby?" "Hey!!! Please hear it first!!! After all the liquid is out, of course mummy's tummy is smaller... then the doctor is supposed to make sure that he get all the liquid and there is no even one drop goes wasted, so the baby will be a healthy and complete baby. After that, the doctor shall keep the liquid for awhile... and then... abracadabra... By itself, the liquid turns to a baby!!!"
Heh? Kok gaya penjelasannya bahkan kaya di resep-resep masakan? (setelah matang, biarkan beberapa lama, lalu makanan siap dihidangkan). Mungkin juga teman daku itu berpikir kalau setelah cairan itu ditampung, lalu dimasukkan ke dalam inkubator. Jadi guna inkubator seperti guna oven pada pembuatan roti. Masukkan cairan, lalu cairan tersebut akan mengembang, sebagian menjadi daging, tulang, sebagian besar masih berupa cairan, yaitu darah. Mungkin teman daku itu terinspirasi untuk membandingkan antara inkubator ( yang bentuknya kotak) yang di rumah sakit dan oven (kotak juga!) yang ada di dapur.
The way she told me the theory sounded like told me about food recipes — after it's cooked, leave it for a while, then it's ready to be eaten... It might cross my friend's mind that after the doctor collects all the liquid, he will put it in an incubator. So the function of incubator is the same as the function of an oven when you make a bread. Put the liquid, let it blows up, a part of it will become flesh, bones, and the rest is still a liquid, i.e. blood. Maybe he was inspired by the form of an incubator in the hospital, which is square and the form of an oven (that's also square) in his mummy's kitchen.
http://www.kejut.com/lahir
Rabu, 26 November 2008
Rabu, 19 November 2008
Asthma
Asthma is a chronic disease involving the respiratory system in which the airways occasionally constrict, become inflamed, and are lined with excessive amounts of mucus, often in response to one or more triggers.[1] These episodes may be triggered by such things as exposure to an environmental stimulant such as an allergen, environmental tobacco smoke, cold or warm air, perfume, pet dander, moist air, exercise or exertion, or emotional stress. In children, the most common triggers are viral illnesses such as those that cause the common cold.[2] This airway narrowing causes symptoms such as wheezing, shortness of breath, chest tightness, and coughing. The airway constriction responds to bronchodilators. Between episodes, most patients feel well but can have mild symptoms and they may remain short of breath after exercise for longer periods of time than the unaffected individual. The symptoms of asthma, which can range from mild to life threatening, can usually be controlled with a combination of drugs and environmental changes.
Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.[3]
Signs and symptoms
In some individuals asthma is characterized by chronic respiratory impairment. In others it is an intermittent illness marked by episodic symptoms that may result from a number of triggering events, including upper respiratory infection, stress, airborne allergens, air pollutants (such as smoke or traffic fumes), or exercise. Some or all of the following symptoms may be present in those with asthma: dyspnea, wheezing, stridor, coughing, a tightness and itching of the chest or an inability for physical exertion. Some asthmatics who have severe shortness of breath and tightening of the lungs never wheeze or have stridor and their symptoms may be confused with a COPD-type disease.
An acute exacerbation of asthma is commonly referred to as an asthma attack. The clinical hallmarks of an attack are shortness of breath (dyspnea) and either wheezing or stridor.[4] Although the former is "often regarded as the sine qua non of asthma",[4] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard. When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in both respiratory phases).
Signs of an asthmatic episode include wheezing, prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. During a serious asthma attack, the accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used, shown as in-drawing of tissues between the ribs and above the sternum and clavicles.
During very severe attacks, an asthma sufferer can turn blue from lack of oxygen, and can experience chest pain or even loss of consciousness. Just before loss of consciousness, there is a chance that the patient will feel numbness in the limbs and palms may start to sweat. The person's feet may become icy cold. Severe asthma attacks, which may not be responsive to standard treatments (status asthmaticus), are life-threatening and may lead to respiratory arrest and death. Despite the severity of symptoms during an asthmatic episode, between attacks an asthmatic may show few or even no signs of the disease.[5]
[edit] Cause
Asthma is caused by a complex interaction of environmental and genetic factors that researchers do not yet fully understand.[6] These factors can also influence how severe a person’s asthma is and how well they respond to medication.[7] As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all of them have been replicated. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may affect asthma only when combined.
[edit] Environmental
Many environmental risk factors have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association.
Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[8] Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[8][9]
Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).[10]
Psychological stress, on the part of a child's caregiver, has been associated with asthma and is an area of active research. Stress can modify behaviors that affect asthma, like smoking, but research suggests that stress has other effects as well. There is growing evidence that stress may influence asthma and other diseases by influencing the immune system.[8]
Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.[8][11][12] Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[13]
The hygiene hypothesis is an hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, c-sections, and cleaning products.[13][10][14] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.
[edit] Genetic
Over 100 genes have been associated with asthma in at least one genetic association study.[15] However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[15]
* GSTM1
* IL10
* CTLA-4
* SPINK5
* LTC4S
* LTA
* GRPA
* NOD1
* CC16
* GSTP1
* STAT6
* NOS1
* CCL5
* TBXA2R
* TGFB1
* IL4
* IL13
* CD14
* ADRB2 (β-2 adrenergic receptor)
* HLA-DRB1
* HLA-DQB1
* TNF
* FCER1B
* IL4R
* ADAM33
Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[15] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma. For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.[16]
[edit] Gene-environment Interactions
Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.[6]
The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person’s genotype at CD14 C-159T and level of endotoxin exposure.[17]
CD14-endotoxin interaction based on CD14 SNP C-159T[17] Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk
[edit] Pathophysiology
In asthma, constriction of the airways occurs due to bronchoconstriction and bronchial inflammation. Bronchoconstriction is the narrowing of the airways in the lungs due to the tightening of surrounding smooth muscle. Bronchial inflammation also causes narrowing due to edema and swelling caused by an immune response to allergens.
[edit] Bronchoconstriction
Inflamed airways and bronchoconstriction in asthma. Airways narrowed as a result of the inflammatory response cause wheezing.
During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways.[18]
The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli (see below). (It is usually classified as type I hypersensitivity.)[19][20] In response to exposure to these triggers, the bronchi (large airways) contract into spasm (an "asthma attack"). Inflammation soon follows, leading to a further narrowing of the airways and excessive mucus production, which leads to coughing and other breathing difficulties.
The normal caliber of the bronchus is maintained by a balanced functioning of these systems, which both operate reflexively. The parasympathetic reflex loop consists of afferent nerve endings which originate under the inner lining of the bronchus. Whenever these afferent nerve endings are stimulated (for example, by dust, cold air or fumes) impulses travel to the brain-stem vagal center, then down the vagal afferent pathway to again reach the bronchus. Acetylcholine is released from the afferent nerve endings. This acetylcholine results in the excessive formation of cyclic Guanine Mono phosphate (cGMP). This initiates bronchoconstriction.
[edit] Bronchial inflammation
The mechanisms behind allergic asthma—i.e., asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both asthmatics and non-asthmatics, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen-presenting cells, or APCs. APCs then "present" pieces of the allergen to other immune system cells. In most people, these other immune cells (TH0 cells) "check" and usually ignore the allergen molecules. In asthmatics, however, these cells transform into a different type of cell (TH2), for reasons that are not well understood. The resultant TH2 cells activate an important arm of the immune system, known as the humoral immune system. The humoral immune system produces antibodies against the inhaled allergen. Later, when an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response. Inflammation results: chemicals are produced that cause the airways to constrict and release more mucus, and the cell-mediated arm of the immune system is activated. The inflammatory response is responsible for the clinical manifestations of an asthma attack.
[edit] Stimuli
* Allergens from nature, typically inhaled, which include waste from common household pests, such as the house dust mite and cockroach, grass pollen, mold spores, and pet epithelial cells;[citation needed]
* Indoor air pollution from volatile organic compounds, including perfumes and perfumed products. Examples include soap, dishwashing liquid, laundry detergent, fabric softener, paper tissues, paper towels, toilet paper, shampoo, hairspray, hair gel, cosmetics, facial cream, sun cream, deodorant, cologne, shaving cream, aftershave lotion, air freshener and candles, and products such as oil-based paint.[citation needed]
* Medications, including aspirin,[21] β-adrenergic antagonists (beta blockers), and penicillin.[citation needed]
* Food allergies such as milk, peanuts, and eggs. However, asthma is rarely the only symptom, and not all people with food or other allergies have asthma.[citation needed]
* Use of fossil fuel related allergenic air pollution, such as ozone, smog, summer smog, nitrogen dioxide, and sulfur dioxide, which is thought to be one of the major reasons for the high prevalence of asthma in urban areas.[citation needed]
* Various industrial compounds and other chemicals, notably sulfites; chlorinated swimming pools generate chloramines—monochloramine (NH2Cl), dichloramine (NHCl2) and trichloramine (NCl3)—in the air around them, which are known to induce asthma.[22]
* Early childhood infections, especially viral upper respiratory tract infections. However, persons of any age can have asthma triggered by colds and other respiratory infections even though their normal stimuli might be from another category (e.g. pollen) and absent at the time of infection. In many cases, significant asthma may not even occur until the respiratory infection is in its waning stage, and the person is seemingly improving. Eighty percent of asthma attacks in adults and 60% in children are caused by respiratory viruses.[citation needed]
* Exercise or intense use of respiratory system. The effects of which differ somewhat from those of the other triggers, since they are brief.
* Hormonal changes in adolescent girls and adult women associated with their menstrual cycle can lead to a worsening of asthma. Some women also experience a worsening of their asthma during pregnancy whereas others find no significant changes, and in other women their asthma improves during their pregnancy.[citation needed]
* Emotional stress which is poorly understood as a trigger. Emotional stress can affect breathing temporarily, however unlike something such as heart problems, it is unclear if it has any long-term effect.[citation needed]
* Cold weather can make it harder for asthmatics to breathe.[23] Whether high altitude helps or worsens asthma is debatable and may vary from person to person.[24]
[edit] Pathogenesis
The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis: the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.
In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma.[25] Szentivanyi's Beta Adrenergic Theory is a citation classic[26] and has been cited more times than any other article in the history of the Journal of Allergy.
In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors.[27] Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergy.[28]
The Beta-Adrenergic Theory has been cited in the scholarship of such noted investigators as Richard F. Lockey (former President of the American Academy of Allergy, Asthma, and Immunology),[29] Charles Reed (Chief of Allergy at Mayo Medical School),[30] and Craig Venter (Human Genome Project).[31]
John P. McGovern, President of the American Association of Allergy nominated Szentivanyi for The 1968 Nobel Prize in Medicine in recognition of The Beta Adrenergic Theory.
In 2006, Researchers at Harvard Medical School found evidence that asthma is caused by over-proliferation of a special type of natural "killer" cell.[32]
[edit] Asthma and sleep apnea
It is recognized with increasing frequency, that patients who have both obstructive sleep apnea (OSA) and bronchial asthma, often improve tremendously when the sleep apnea is diagnosed and treated.[33] CPAP is not effective in patients with nocturnal asthma only.[34]
[edit] Asthma and gastro-esophageal reflux disease
If gastro-esophageal reflux disease (GERD) is present, the patient may have repetitive episodes of acid aspiration. GERD may be common in difficult-to-control asthma, but according to one study, treating it does not seem to affect the asthma.[35]
[edit] Diagnosis
Asthma is defined simply as reversible airway obstruction. Reversibility occurs either spontaneously or with treatment. The basic measurement is peak flow rates and the following diagnostic criteria are used by the British Thoracic Society:[36]
* ≥20% difference on at least three days in a week for at least two weeks;
* ≥20% improvement of peak flow following treatment, for example:
o 10 minutes of inhaled β-agonist (e.g., salbutamol);
o six week of inhaled corticosteroid (e.g., beclometasone);
o 14 days of 30mg prednisolone.
* ≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).
In many cases, a physician can diagnose asthma on the basis of typical findings in a patient's clinical history and examination. Asthma is strongly suspected if a patient suffers from eczema or other allergic conditions—suggesting a general atopic constitution—or has a family history of asthma. While measurement of airway function is possible for adults, most new cases are diagnosed in children who are unable to perform such tests. Diagnosis in children is based on a careful compilation and analysis of the patient's medical history and subsequent improvement with an inhaled bronchodilator medication. In adults, diagnosis can be made with a peak flow meter (which tests airway restriction), looking at both the diurnal variation and any reversibility following inhaled bronchodilator medication.
Testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young asthmatics who may experience only exercise-induced asthma. If the diagnosis is in doubt, a more formal lung function test may be conducted. Once a diagnosis of asthma is made, a patient can use peak flow meter testing to monitor the severity of the disease.
Monitoring asthma with a peak flow meter on an ongoing basis assists with self monitoring of asthma. Peak flow readings can be charted on graph paper charts together with a record of symptoms or use peak flow charting software.[37] This allows patients to track their peak flow readings and pass information back to their doctor or nurse.[38]
In the Emergency Department doctors may use a capnography which measures the amount of exhaled carbon dioxide,[39] along with pulse oximetry which shows the amount of oxygen dissolved in the blood, to determine the severity of an asthma attack as well as the response to treatment.
More recently, exhaled nitric oxide has been studied as a breath test indicative of airway inflammation in asthma.
[edit] Differential diagnosis
This article does not cite any references or sources.
Please help improve this article by adding citations to reliable sources. Unverifiable material may be challenged and removed. (November 2008)
Before diagnosing someone as asthmatic, alternative possibilities should be considered. A clinician taking a history should check whether the patient is using any known bronchoconstrictors (substances that cause narrowing of the airways, e.g., certain anti-inflammatory agents or beta-blockers).
Chronic obstructive pulmonary disease, which closely resembles asthma, is correlated with more exposure to cigarette smoke, an older patient, less symptom reversibility after bronchodilator administration (as measured by spirometry), and decreased likelihood of family history of atopy.
Pulmonary aspiration, whether direct due to dysphagia (swallowing disorder) or indirect (due to acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also indicate aspiration pneumonia. Direct aspiration (dysphagia) can be diagnosed by performing a Modified Barium Swallow test and treated with feeding therapy by a qualified speech therapist. If the aspiration is indirect (from acid reflux) then treatment directed at this is indicated.
A majority of children who are asthma sufferers have an identifiable allergy trigger. Specifically, in a 2004 study, 71% had positive test results for more than 1 allergen, and 42% had positive test results for more than 3 allergens.[40]
The majority of these triggers can often be identified from the history; for instance, asthmatics with hay fever or pollen allergy will have seasonal symptoms, those with allergies to pets may experience an abatement of symptoms when away from home, and those with occupational asthma may improve during leave from work. Allergy tests can help identify avoidable symptom triggers.
After a pulmonary function test has been carried out, radiological tests, such as a chest X-ray or CT scan, may be required to exclude the possibility of other lung diseases. In some people, asthma may be triggered by gastroesophageal reflux disease, which can be treated with suitable antacids. Very occasionally, specialized tests after inhalation of methacholine — or, even less commonly, histamine — may be performed.
Asthma is categorized by the United States National Heart, Lung, and Blood Institute as falling into one of four categories: intermittent, mild persistent, moderate persistent and severe persistent. The diagnosis of "severe persistent asthma" occurs when symptoms are continual with frequent exacerbations and frequent night-time symptoms, result in limited physical activity and when lung function as measured by PEV or FEV1 tests is less than 60% predicted with PEF variability greater than 30%.
[edit] Prevention
This article does not cite any references or sources.
Please help improve this article by adding citations to reliable sources. Unverifiable material may be challenged and removed. (November 2008)
Current treatment protocols recommend prevention medications such as an inhaled corticosteroid, which helps to suppress inflammation and reduces the swelling of the lining of the airways, in anyone who has frequent (greater than twice a week) need of relievers or who has severe symptoms. If symptoms persist, additional preventive drugs are added until the asthma is controlled. With the proper use of prevention drugs, asthmatics can avoid the complications that result from overuse of relief medications.
Asthmatics sometimes stop taking their preventive medication when they feel fine and have no problems breathing. This often results in further attacks, and no long-term improvement.
Preventive agents include the following.
* Inhaled glucocorticoids are the most widely used prevention medications and normally come as inhaler devices (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone).
Long-term use of corticosteroids can have many side effects including a redistribution of fat, increased appetite, blood glucose problems and weight gain. In particular high doses of steroids may cause osteoporosis. For this reasons inhaled steroids are generally used for prevention, as their smaller doses are targeted to the lungs, unlike the higher doses of oral preparations. Nevertheless, patients on high doses of inhaled steroids may still require prophylactic treatment to prevent osteoporosis.
Deposition of steroids in the mouth may cause a hoarse voice or oral thrush (due to decreased immunity). This may be minimised by rinsing the mouth with water after inhaler use, as well as by using a spacer which increases the amount of drug that reaches the lungs.
* Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton) provide anti-inflammatory effect similar to inhaled corticosteroids.
* Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil).
* Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium), which have a mixed reliever and preventer effect. These are often used to reduce bronchospasm when inhaled steroids do not produce sufficient relief.
* Methylxanthines (theophylline and aminophylline), which are sometimes considered if sufficient control cannot be achieved with inhaled glucocorticoids (or leukotriene modifiers) and long-acting β-agonists alone.
* Antihistamines, often used to treat allergic effects that may underlie the chronic inflammation.
* Hyposensitization, (also known as immunodesensitisation therapy) may be recommended in some cases where allergy is the suspected cause or trigger of asthma. Depending on the allergen, it can be given orally or by injection.
* Omalizumab, an IgE blocker; this can help patients with severe allergic asthma that does not respond to other drugs. However, it is expensive and must be injected.
* Methotrexate is occasionally used in some difficult-to-treat patients.
* If chronic acid indigestion (GERD) contributes to a patient's asthma, it should also be treated, because it may prolong the respiratory problem.
[edit] Trigger avoidance
As is common with respiratory disease, smoking is believed to adversely affect asthmatics in several ways, including an increased severity of symptoms, a more rapid decline of lung function, and decreased response to preventive medications.[41] Automobile emissions are considered an even more significant cause and aggravating factor.[42] Asthmatics who smoke or who live near traffic [1] typically require additional medications to help control their disease. Furthermore, exposure of both non-smokers and smokers to wood smoke, gas stove fumes and second-hand smoke is detrimental, resulting in more severe asthma, more emergency room visits, and more asthma-related hospital admissions.[43] Smoking cessation and avoidance of second-hand smoke is strongly encouraged in asthmatics.[44]
For those in whom exercise can trigger an asthma attack (exercise-induced asthma), higher levels of ventilation and cold, dry air tend to exacerbate attacks. For this reason, activities in which a patient breathes large amounts of cold air, such as skiing and running, tend to be worse for asthmatics, whereas swimming in an indoor, heated pool, with warm, humid air, or a shower is less likely to provoke a response.[4]
[edit] Air Filters
If an asthmatic lives with a smoker, use of air filter or room air cleaner is likely to be helpful. Secondhand smoke can worsen the symptoms. The same is true for those with hay fever (allergic rhino sinusitis) or COPD (emphysema or chronic bronchitis). Room air cleaners remove small particles that are in the air near the air cleaner. However, room air cleaners do not remove small allergen particles that are caused by local disturbances, such as the microscopic house dust mite feces that surround a pillow when your head hits it or you turn over in bed. There are several types of air filters available.[45]
* Mechanical air filters use a fan to force air through a special screen that traps particles such as smoke, pollens, and other airborne allergens. The high-efficiency particulate air (HEPA) filter is the best-known air filter. HEPA (which is a type of filter, not a brand name) was developed during World War II to prevent radioactive particles from escaping from laboratories.
* Electronic air filters use electrical charges to attract and deposit allergens and irritants. If the device contains collecting plates, the particles are captured within the system; otherwise, they stick to room surfaces and have to be cleared away.
* Hybrid air filters contain elements of both mechanical and electrostatic filters.
* Gas phase air filters use activated carbon granules to remove odors (volatile organic compounds or VOCs) and non-particulate pollution such as cooking gas, gases emitted from paint or building materials (such as formaldehyde), and perfume.
* Germicidal air cleaners use ultraviolet (UV) lights to kill bacteria, viruses, and molds that pass through the area with the UV light. Such UV lights can be included with other air cleaner devices, which use a fan.
* Ozone generators are devices that intentionally produce high concentrations of ozone to clean the air in a room. They are often used to decontaminate rooms after smoke exposure following a fire.
[edit] Treatment
This article does not cite any references or sources.
Please help improve this article by adding citations to reliable sources. Unverifiable material may be challenged and removed. (November 2008)
The most effective treatment for asthma is identifying triggers, such as pets or aspirin, and limiting or eliminating exposure to them. If trigger avoidance is insufficient, medical treatment is available. Desensitization is currently the only known "cure" to the disease.[46] Other forms of treatment include relief medication, prevention medication, long-acting β2-agonists, and emergency treatment.
[edit] Medical
The specific medical treatment recommended to patients with asthma depends on the severity of their illness and the frequency of their symptoms. Specific treatments for asthma are broadly classified as relievers, preventers and emergency treatment. The Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma (EPR-2)[44] of the U.S. National Asthma Education and Prevention Program, and the British Guideline on the Management of Asthma[47] are broadly used and supported by many doctors. On August 29, 2007 the final Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma was officially released. Bronchodilators are recommended for short-term relief in all patients. For those who experience occasional attacks, no other medication is needed. For those with mild persistent disease (more than two attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene modifier, a mast-cell stabilizer, or theophylline may be administered. For those who suffer daily attacks, a higher dose of glucocorticoid in conjunction with a long-acting inhaled β-2 agonist may be prescribed; alternatively, a leukotriene modifier or theophylline may substitute for the β-2 agonist. In severe asthmatics, oral glucocorticoids may be added to these treatments during severe attacks.
[edit] Pharmaceutical
Symptomatic control of episodes of wheezing and shortness of breath is generally achieved with fast-acting bronchodilators. These are typically provided in pocket-sized, metered-dose inhalers (MDIs). In young sufferers, who may have difficulty with the coordination necessary to use inhalers, or those with a poor ability to hold their breath for 10 seconds after inhaler use (generally the elderly), an asthma spacer (see top image) is used. The spacer is a plastic cylinder that mixes the medication with air in a simple tube, making it easier for patients to receive a full dose of the drug and allows for the active agent to be dispersed into smaller, more fully inhaled bits.
A nebulizer which provides a larger, continuous dose can also be used. Nebulizers work by vaporizing a dose of medication in a saline solution into a steady stream of foggy vapour, which the patient inhales continuously until the full dosage is administered. There is no clear evidence, however, that they are more effective than inhalers used with a spacer. Nebulizers may be helpful to some patients experiencing a severe attack. Such patients may not be able to inhale deeply, so regular inhalers may not deliver medication deeply into the lungs, even on repeated attempts. Since a nebulizer delivers the medication continuously, it is thought that the first few inhalations may relax the airways enough to allow the following inhalations to draw in more medication.
Relievers include:
* Short-acting, selective beta2-adrenoceptor agonists, such as salbutamol (albuterol USAN), levalbuterol, terbutaline and bitolterol.
Tremors, the major side effect, have been greatly reduced by inhaled delivery, which allows the drug to target the lungs specifically; oral and injected medications are delivered throughout the body. There may also be cardiac side effects at higher doses (due to Beta-1 agonist activity), such as elevated heart rate or blood pressure. Patients must be cautioned against using these medicines too frequently, as with such use their efficacy may decline, producing desensitization resulting in an exacerbation of symptoms which may lead to refractory asthma and death.
* Older, less selective adrenergic agonists, such as inhaled epinephrine and ephedrine tablets, have also been used. Cardiac side effects occur with these agents at either similar or lesser rates to albuterol.[48] [49] When used solely as a relief medication, inhaled epinephrine has been shown to be an effective agent to terminate an acute asthmatic exacerbation.[48] In emergencies, these drugs were sometimes administered by injection. Their use via injection has declined due to related adverse effects.
* Anticholinergic medications, such as ipratropium bromide may be used instead. They have no cardiac side effects and thus can be used in patients with heart disease; however, they take up to an hour to achieve their full effect and are not as powerful as the β2-adrenoreceptor agonists.
* Inhaled glucocorticoids are usually considered preventive medications while oral glucocorticoids are often used to supplement treatment of a severe attack. A randomized controlled trial has demonstrated the benefit of 250 microg beclomethasone when taken as an as-needed combination inhaler with 100 microg of albuterol.[50]
[edit] Long-acting β2-agonists
A typical inhaler, of Serevent (salmeterol), a long-acting bronchodilator.
Long-acting bronchodilators (LABD) are similar in structure to short-acting selective beta2-adrenoceptor agonists, but have much longer side chains resulting in a 12-hour effect, and are used to give a smoothed symptomatic relief (used morning and night). While patients report improved symptom control, these drugs do not replace the need for routine preventers, and their slow onset means the short-acting dilators may still be required. In November 2005, the American FDA released a health advisory alerting the public to findings that show the use of long-acting β2-agonists could lead to a worsening of symptoms, and in some cases death.[51]
Currently available long-acting beta2-adrenoceptor agonists include salmeterol, formoterol, bambuterol, and sustained-release oral albuterol. Combinations of inhaled steroids and long-acting bronchodilators are becoming more widespread; the most common combination currently in use is fluticasone/salmeterol (Advair in the United States, and Seretide in the United Kingdom). Another combination is budesonide/formoterol which is commercially known as Symbicort.
A recent meta-analysis of the roles of long-acting beta-agonists may indicate a danger to asthma patients. The study, published in the Annals of Internal Medicine in 2006, found that long-acting beta-agonists increased the risk for asthma hospitalizations and asthma deaths 2- to 4-fold, compared with placebo.[52] "These agents can improve symptoms through bronchodilation at the same time as increasing underlying inflammation and bronchial hyper-responsiveness, thus worsening asthma control without any warning of increased symptoms," said Shelley Salpeter in a press release after the publication of the study. The release goes on to say that "Three common asthma inhalers containing the drugs salmeterol or formoterol may be causing four out of five US asthma-related deaths per year and should be taken off the market".[53] This assertion is viewed by many asthma specialists as being inaccurate. Dr. Hal Nelson, in a recent letter to the Annals of Internal Medicine, points out the following:
"Salpeter and colleagues also assert that salmeterol may be responsible for 4000 of the 5000 asthma-related deaths that occur in the United States annually. However, when salmeterol was introduced in 1994, more than 5000 asthma-related deaths occurred per year. Since the peak of asthma deaths in 1996, salmeterol sales have increased about 5-fold, while overall asthma mortality rates have decreased by about 25%, despite a continued increase in asthma diagnoses. In fact, according to the most recent data from the National Center for Health Statistics, U.S. asthma mortality rates peaked in 1996 (with 5667 deaths) and have decreased steadily since. The last available data, from 2004, indicate that 3780 deaths occurred. Thus, the suggestion that a vast majority of asthma deaths could be attributable to LABA use is inconsistent with the facts."
Dr. Shelley Salpeter, in a letter to the Annals of Internal Medicine, responds to the comments of Dr. Nelson, as follows:
"It is true that the asthma death rate increased after salmeterol was introduced, then peaked and is now starting to decline despite continued use of the long-acting beta-agonists. This trend in death rates can best be explained by examining the ratio of beta-agonist use to inhaled corticosteroids... In the recent past, inhaled corticosteroid use has increased steadily while long-acting beta-agonist use has begun to stabilize and short-acting beta-agonist use has declined... Using this estimate, we can imagine that if long-acting beta-agonists were withdrawn from the market while maintaining high inhaled corticosteroid use, the death rate in the United States could be reduced significantly..."
[edit] Emergency
When an asthma attack is unresponsive to a patient's usual medication, other treatments are available to the physician or hospital:[54]
* Oxygen to alleviate the hypoxia (but not the asthma itself) that results from extreme asthma attacks.
* Nebulized salbutamol or terbutaline (short-acting beta-2-agonists), often combined with ipratropium (an anticholinergic).
* Systemic steroids, oral or intravenous (prednisone, prednisolone, methylprednisolone, dexamethasone, or hydrocortisone). Some research has looked into an alternative inhaled route.[55]
* Other bronchodilators that are occasionally effective when the usual drugs fail:
o Intravenous salbutamol
o Nonspecific beta-agonists, injected or inhaled (epinephrine, isoetharine, isoproterenol, metaproterenol)
o Anticholinergics, IV or nebulized, with systemic effects (glycopyrrolate, atropine, ipratropium)
o Methylxanthines (theophylline, aminophylline)
o Inhalation anesthetics that have a bronchodilatory effect (isoflurane, halothane, enflurane)
o The dissociative anaesthetic ketamine, often used in endotracheal tube induction
o Magnesium sulfate, intravenous
* Intubation and mechanical ventilation, for patients in or approaching respiratory arrest.
* Heliox, a mixture of helium and oxygen, may be used in a hospital setting. It has a more laminar flow than ambient air and moves more easily through constricted airways.
[edit] Non-medical treatments
Many asthmatics, like those who suffer from other chronic disorders, use alternative treatments; surveys show that roughly 50% of asthma patients use some form of unconventional therapy.[56][57] There is little data to support the effectiveness of most of these therapies. A Cochrane systematic review of acupuncture for asthma found no evidence of efficacy.[58] A similar review of air ionisers found no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.[59] Another systematic study reviewed a range of dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others. Overall these methods had no effect on asthma symptoms .[60] A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvres, found there is insufficient evidence to support or refute their use in treating asthma;[61] these manoeuvers include various osteopathic and chiropractic techniques to "increase movement in the rib cage and the spine to try and improve the working of the lungs and circulation"; chest tapping, shaking, vibration, and the use of "postures to help shift and cough up phlegm." One meta-analysis finds that homeopathy may have a potentially mild benefit in reducing the intensity of symptoms.[62] However, the number of patients involved in the analysis was small, and subsequent studies have not supported this finding.[63] Several small trials have suggested some benefit from various yoga practices, ranging from integrated yoga programs,[64] yogasanas, Pranayama, meditation, and kriyas, to sahaja yoga,[65] a form of 'new religious' meditation.
[edit] Treatment controversies
In November 2007 The New York Times reported a review of more than 500 studies finding that independently backed studies on inhaled corticosteroids are up to four times more likely to find adverse effects than studies paid for by drug companies.[66][67]
[edit] Prognosis
The prognosis for asthmatics is good; especially for children with mild disease. For asthmatics diagnosed during childhood, 54% will no longer carry the diagnosis after a decade. The extent of permanent lung damage in asthmatics is unclear. Airway remodelling is observed, but it is unknown whether these represent harmful or beneficial changes.[18] Although conclusions from studies are mixed, most studies show that early treatment with glucocorticoids prevents or ameliorates decline in lung function as measured by several parameters.[68] For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities. The mortality rate for asthma is low, with around 6000 deaths per year in a population of some 10 million patients in the United States.[4] Better control of the condition may help prevent some of these deaths.
[edit] Epidemiology
The prevalence of childhood asthma has increased since 1980, especially in younger children.
The highest levels of asthma in the world according to the Global INitiative for Asthma (GINA) report of February 2004[69] occurred for about 30% of children in the United Kingdom, New Zealand and Australia, or 20% of children in Peru, New Zealand and Australia according to the method of interview, and for about 25% of adults in Great Britain, Australia and Canada. The United States also ranks highly. More than 6% of children in the United States have been diagnosed with asthma, a 75% increase in recent decades. The rate soars to 40% among some populations of urban children.[citation needed]
Current research suggests that the prevalence of childhood asthma has been increasing. According to the Centers for Disease Control and Prevention's National Health Interview Surveys, some 9% of US children below 18 years of age had asthma in 2001, compared with just 3.6% in 1980 (see figure). The World Health Organization (WHO) reports that some 8% of the Swiss population suffers from asthma today, compared with just 2% some 25–30 years ago.[70] Although asthma is more common in affluent countries, it is by no means a problem restricted to the affluent; the WHO estimate that there are between 15 and 20 million asthmatics in India. In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole. Globally, asthma is responsible for around 180,000 deaths annually.[70]
[edit] Population disparities
Asthma prevalence, morbidity, mortality, and drug response vary greatly across populations. There is an almost 30-fold difference in asthma prevalence between some of the countries included in the International Study of Asthma and Allergy in Childhood [2], with a trend toward more developed and westernized countries having higher asthma prevalence. Westernization can’t explain the entire difference in asthma prevalence between countries, however, and the disparities may also be affected by differences in genetic, social and environmental risk factors.[8] There are also worldwide disparities in asthma mortality, which is most common in low to middle income countries.[71]
Asthma prevalence in the US is higher than in most other countries in the world, but varies drastically between diverse US populations.[8] In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos and Native Hawaiians, and lowest in Mexicans and Koreans.[72][73][74] Mortality rates follow similar trends, and response to albuterol is lower in Puerto Ricans than in African Americans or Mexicans.[75][76] As with worldwide asthma disparities, differences in asthma prevalence, mortality, and drug response in the US may be explained by differences in genetic, social and environmental risk factors.
Asthma prevalence also differs between populations of the same ethnicity who are born and live in different places.[77] US-born Mexican populations, for example, have higher asthma rates than non-US born Mexican populations that are living in the US.[78] This probably reflects differences in social and environmental risk factors associated with acculturation to the US.[citation needed]
Asthma prevalence and asthma deaths also differ by gender. Males are more likely to be diagnosed with asthma as children, but asthma is more likely to persist into adulthood in females. Sixty five percent more adult women than men will die from asthma. This difference may be attributable to hormonal differences, among other things. In support of this, girls who reach puberty before age 12 were found to have a later diagnosis of asthma more than twice as much as girls who reach puberty after age 12. Asthma is also the number one cause of missed days from school.
[edit] Socioeconomic factors
The incidence of asthma is highest among low-income populations (asthma deaths are most common in low to middle income countries [3]), which in the western world are disproportionately ethnic minorities[79] and are more likely to live near industrial areas. Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters, which is more likely in such neighborhoods.
Asthma incidence and quality of treatment varies among different racial groups, though this may be due to correlations with income (and thus affordability of health care) and geography. For example, Black Americans are less likely to receive outpatient treatment for asthma despite having a higher prevalence of the disease. They are much more likely to have emergency room visits or hospitalization for asthma, and are three times as likely to die from an asthma attack compared to whites. The prevalence of "severe persistent" asthma is also greater in low-income communities compared with communities with better access to treatment.[80][81]
[edit] Asthma and athletics
Asthma appears to be more prevalent in athletes than in the general population. One survey of participants in the 1996 Summer Olympic Games, in Atlanta, Georgia, U.S., showed that 15% had been diagnosed with asthma, and that 10% were on asthma medication.[82] These statistics have been questioned on at least two bases. Athletes with mild asthma may be more likely to be diagnosed with the condition than non-athletes, because even subtle symptoms may interfere with their performance and lead to pursuit of a diagnosis. It has also been suggested that some professional athletes who do not suffer from asthma claim to do so in order to obtain special permits to use certain performance-enhancing drugs.[citation needed]
There appears to be a relatively high incidence of asthma in sports such as cycling, mountain biking, and long-distance running, and a relatively lower incidence in weightlifting and diving. It is unclear how much of these disparities are from the effects of training in the sport, and from self-selection of sports that may appear to minimize the triggering of asthma.[82][83]
In addition, there exists a variant of asthma called exercise-induced asthma that shares many features with allergic asthma. It may occur either independently, or concurrent with the latter. Exercise studies may be helpful in diagnosing and assessing this condition.
[edit] History
Asthma was long considered a psychosomatic disease, and
... during the 1930s–50s, was even known as one of the 'holy seven' psychosomatic illnesses. At that time, psychoanalytic theories described the aetiology of asthma as psychological, with treatment often primarily involving psychoanalysis and other 'talking cures'. As the asthmatic wheeze was interpreted as the child's suppressed cry for his or her mother, psychoanalysts viewed the treatment of depression as especially important for individuals with asthma.[84]
[edit] See also
Wikimedia Commons has media related to:
Asthma
* Asthma and Allergy Foundation of America
* Atopy
* Global Initiative for Asthma (GINA)
* Hopkins syndrome
* Hygiene hypothesis
* Immune system
* Occupational asthma
* Reactive airway disease
* World Asthma Day
* Vocal cord dysfunction
[edit] References
1. ^ "Asthma: What Causes Asthma". Asthma and Allergy Foundation of America. Retrieved on 2008-01-03.
2. ^ Zhao J, Takamura M, Yamaoka A, Odajima Y, Iikura Y (February 2002). "Altered eosinophil levels as a result of viral infection in asthma exacerbation in childhood". Pediatr Allergy Immunol 13 (1): 47–50. doi:10.1034/j.1399-3038.2002.00051.x. PMID 12000498.
3. ^ Lilly CM (2005). "Diversity of asthma: evolving concepts of pathophysiology and lessons from genetics". J. Allergy Clin. Immunol. 115 (4 Suppl): S526–31. doi:10.1016/j.jaci.2005.01.028. PMID 15806035.
4. ^ a b c d McFadden ER, Jr (2004). "Asthma", Harrison's Principles of Internal Medicine (Kasper DL, Fauci AS, Longo DL, et al (eds)), 16th ed., New York: McGraw-Hill, 1508–16.
5. ^ Longmore, Murray et al (2007). Oxford Handbook of Clinical Medicine, 7th ed., Oxford University Press. ISBN 978-0198568377.
6. ^ a b Martinez FD (2007). "Genes, environments, development and asthma: a reappraisal". Eur Respir J 29 (1): 179–84. doi:10.1183/09031936.00087906. PMID 17197483.
7. ^ Choudhry S, Seibold MA, Borrell LN "et al." (2007). "Dissecting complex diseases in complex populations: asthma in latino americans". Proc Am Thorac Soc 4 (3): 226–33. doi:10.1513/pats.200701-029AW. PMID 17607004.
8. ^ a b c d e f Gold DR,Wright R (2005). "Population disparities in asthma". Annu Rev Public Health 26: 89–113. doi:10.1146/annurev.publhealth.26.021304.144528. PMID 15760282.
9. ^ "California Children's Health Study".
10. ^ a b Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell, CR (2007). "A meta-analysis of the association between Caesarean section and childhood asthma". Clin. And Exper. Allergy online ahead of print: 629. doi:10.1111/j.1365-2222.2007.02780.x.
11. ^ Harju TH, Leinonen M, Nokso-Koivisto J, et al (2006). "Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma". Thorax 61 (7): 579–84. doi:10.1136/thx.2005.056291. PMID 16517571.
12. ^ Richeldi L, Ferrara G, Fabbri LM, Lasserson TJ, Gibson PG (2005). "Macrolides for chronic asthma". Cochrane Database Syst Rev (4): CD002997. doi:10.1002/14651858.CD002997.pub3. PMID 16235309.
13. ^ a b Marra F, Lynd L, Coombes M "et al." (2006). "Does antibiotic exposure during infancy lead to development of asthma?: a systematic review and metaanalysis". Chest 129 (3): 610–8. doi:10.1378/chest.129.3.610. PMID 16537858.
14. ^ Jeremy Laurance. "Asthma blamed on cleaning sprays and air fresheners".
15. ^ a b c Ober C,Hoffjan S (2006). "Asthma genetics 2006: the long and winding road to gene discovery". Genes Immun 7 (2): 95–100. doi:10.1038/sj.gene.6364284. PMID 16395390.
16. ^ Bouzigon E, Corda E, Aschard H, et al (October 2008). "Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma". The New England journal of medicine. doi:10.1056/NEJMoa0806604. PMID 18923164.
17. ^ a b Martinez FD (2007). "CD14, endotoxin, and asthma risk: actions and interactions". Proc Am Thorac Soc 4 (3): 221–5. doi:10.1513/pats.200702-035AW. PMID 17607003.
18. ^ a b Maddox L, Schwartz DA (2002). "The pathophysiology of asthma". Annu. Rev. Med. 53: 477–98. doi:10.1146/annurev.med.53.082901.103921. PMID 11818486.
19. ^ "Lecture 14: Hypersensitivity". Retrieved on 2008-09-18.
20. ^ "Allergy & Asthma Disease Management Center: Ask the Expert". Retrieved on 2008-09-18.
21. ^ Jenkins C, Costello J, Hodge L (2004). "Systematic review of prevalence of aspirin induced asthma and its implications for clinical practice". BMJ 328 (7437): 434. doi:10.1136/bmj.328.7437.434. PMID 14976098.
22. ^ Nemery B, Hoet PH, Nowak D (2002). "Indoor swimming pools, water chlorination and respiratory health". Eur. Respir. J. 19 (5): 790–3. doi:10.1183/09031936.02.00308602. PMID 12030714.
23. ^ about.com article
24. ^ Asthma and Altitude
25. ^ Szentivanyi, Andor (1968). The Beta Adrenergic Theory of the Atopic Abnormality in Asthma.
26. ^ Lockey, Richard, In lasting tribute: Andor Szentivanyi, MD. J. Allergy and Clinical Immunology, January, 2006
27. ^ Szentivanyi A., Ali K., Calderon EG., Brooks SM., Coffey RG., Lockey RF. (1993). "The in vitro effect of Imunnoglobulin E {IgE} on cyclic AMP concentrations in A549 human pulmonary epithelial cells with or without beta adrenergic stimulation". J. Allergy Clin Immunol. 91: 379. - Part of Abstracts from:
"50th Anniversary of the American Academy of Allergy and Immunology. 49th Annual Meeting. Chicago, Illinois, March 12-17, 1993. Abstracts". J. Allergy Clin. Immunol. 91 (1 Pt 2): 141–379. 1993. PMID 8421135.
28. ^ (2001) in Kowalak JP, Hughes AS et al (eds): Professional Guide To Diseases, 7th ed., Springhouse.
29. ^ Lockey, Richard F. (2006-04-28). "Anaphylaxis: Synopsis". Allergic Diseases Resource Center. World Allergy Organization. Retrieved on September 23, 2006.[dead link]
30. ^ Ouellette JJ, Reed CE (1967). "The effect of partial beta adrenergic blockade on the bronchial response of hay fever subjects to ragweed aerosol". J Allergy 39 (3): 160–6. doi:10.1016/0021-8707(67)90033-0. PMID 5227155.
31. ^ Fraser CM, Venter JC (1980). "The synthesis of beta-adrenergic receptors in cultured human lung cells: induction by glucocorticoids". Biochem. Biophys. Res. Commun. 94 (1): 390–7. doi:10.1016/S0006-291X(80)80233-6. PMID 6248064.
32. ^ Cromie, William J. (2006-03-16). "Researchers uncover cause of asthma", Harvard University Gazette, Harvard News Office. Retrieved on 23 September 2006.
33. ^ University of Michigan Health System (May 25, 2005). "Breathing disorders during sleep are common among asthmatics, may help predict severe asthma". Press release. Retrieved on 2006-09-23.
34. ^ Basner, Robert C. (2006-07-25). "Asthma and OSA". ASAA Resources > Publications. American Sleep Apnea Association. Retrieved on September 23, 2006.
35. ^ Leggett JJ, Johnston BT, Mills M, Gamble J, Heaney LG (2005). "Prevalence of gastroesophageal reflux in difficult asthma: relationship to asthma outcome". Chest 127 (4): 1227–31. doi:10.1378/chest.127.4.1227. PMID 15821199, http://www.chestjournal.org/cgi/content/full/127/4/1227.
36. ^ Pinnock H, Shah R (2007). "Asthma". BMJ 334 (7598): 847–50. doi:10.1136/bmj.39140.634896.BE. PMID 17446617.
37. ^ "Peak flow charting software".
38. ^ "'Be in control' pack" (PDF). Asthma UK. Retrieved on 2007-11-19.
39. ^ Corbo J, Bijur P, Lahn M, Gallagher EJ (2005). "Concordance between capnography and arterial blood gas measurements of carbon dioxide in acute asthma". Annals of emergency medicine 46 (4): 323–7. doi:10.1016/j.annemergmed.2004.12.005. PMID 16187465.
40. ^ Vargas PA, Simpson PM, Gary Wheeler J, et al (2004). "Characteristics of children with asthma who are enrolled in a Head Start program". J. Allergy Clin. Immunol. 114 (3): 499–504. doi:10.1016/j.jaci.2004.05.025. PMID 15356547.
41. ^ Thomson NC, Spears M (2005). "The influence of smoking on the treatment response in patients with asthma". Curr Opin Allergy Clin Immunol 5 (1): 57–63. PMID 15643345.
42. ^ EWG || Auto Asthma Index
43. ^ Eisner MD, Yelin EH, Katz PP, Earnest G, Blanc PD (2002). "Exposure to indoor combustion and adult asthma outcomes: environmental tobacco smoke, gas stoves, and woodsmoke". Thorax 57 (11): 973–8. doi:10.1136/thorax.57.11.973. PMID 12403881.
44. ^ a b National Asthma Education and Prevention Program. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97–4051. Bethesda, MD, 1997. (PDF)
45. ^ Asthma and Air Filters Asthma and Air Filters[dead link]
46. ^ Abramson MJ, Puy RM, Weiner JM (1995). "Is allergen immunotherapy effective in asthma? A meta-analysis of randomized controlled trials". Am. J. Respir. Crit. Care Med. 151 (4): 969–74. PMID 7697274.
47. ^ "British Guideline on the Management of Asthma" (PDF). Scottish Intercollegiate Guidelines Network (2008). Retrieved on 2008-08-04.
48. ^ a b Hendeles L, Marshik PL, Ahrens R, Kifle Y, Shuster J (2005). "Response to nonprescription epinephrine inhaler during nocturnal asthma". Ann. Allergy Asthma Immunol. 95 (6): 530–4. PMID 16400891.
49. ^ Rodrigo GJ, Nannini LJ (2006). "Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials". Am J Emerg Med 24 (2): 217–22. doi:10.1016/j.ajem.2005.10.008. PMID 16490653.
50. ^ Papi A, Canonica GW, Maestrelli P, et al (2007). "Rescue use of beclomethasone and albuterol in a single inhaler for mild asthma". N. Engl. J. Med. 356 (20): 2040–52. doi:10.1056/NEJMoa063861. PMID 17507703.
51. ^ "Serevent Diskus, Advair Diskus, and Foradil Information (Long Acting Beta Agonists) - Drug information". FDA (2006-03-03).
52. ^ Salpeter S, Buckley N, Ormiston T, Salpeter E (2006). "Meta-analysis: effect of long-acting beta-agonists on severe asthma exacerbations and asthma-related deaths". Ann Intern Med 144 (12): 904–12. PMID 16754916.
53. ^ Ramanujan, Krishna (2006-06-09). "Common asthma inhalers cause up to 80 percent of asthma-related deaths, Cornell and Stanford researchers assert". Cornell Chronicle Online. Cornell News Service. Retrieved on 2006-09-23.
54. ^ Rodrigo GJ, Rodrigo C, Hall JB (2004). "Acute asthma in adults: a review". Chest 125 (3): 1081–102. doi:10.1378/chest.125.3.1081. PMID 15006973.
55. ^ Rodrigo G (2005). "Comparison of inhaled fluticasone with intravenous hydrocortisone in the treatment of adult acute asthma". Am J Respir Crit Care Med 171 (11): 1231–6. doi:10.1164/rccm.200410-1415OC. PMID 15764724.
56. ^ Blanc PD, Trupin L, Earnest G, Katz PP, Yelin EH, Eisner MD (2001). "Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis : data from a population-based survey". Chest 120 (5): 1461–7. doi:10.1378/chest.120.5.1461. PMID 11713120.
57. ^ Shenfield G, Lim E, Allen H (2002). "Survey of the use of complementary medicines and therapies in children with asthma". J Paediatr Child Health 38 (3): 252–7. doi:10.1046/j.1440-1754.2002.00770.x. PMID 12047692.
58. ^ McCarney RW, Brinkhaus B, Lasserson TJ, Linde K (2004). "Acupuncture for chronic asthma". Cochrane Database Syst Rev (1): CD000008. doi:10.1002/14651858.CD000008.pub2. PMID 14973944.
59. ^ Blackhall K, Appleton S, Cates CJ (2003). "Ionisers for chronic asthma". Cochrane Database Syst Rev (3): CD002986. doi:10.1002/14651858.CD002986. PMID 12917939.
60. ^ PC Gøtzsche, HK Johansen (2008). "House dust mite control measures for asthma". Cochrane Database Syst Rev (2): CD001187. doi:10.1002/14651858.CD001187.pub3.
61. ^ Hondras MA, Linde K, Jones AP (2005). "Manual therapy for asthma". Cochrane Database Syst Rev (2): CD001002. doi:10.1002/14651858.CD001002.pub2. PMID 15846609.
62. ^ Reilly D, Taylor MA, Beattie NG, et al (1994). "Is evidence for homoeopathy reproducible?". Lancet 344 (8937): 1601–6. doi:10.1016/S0140-6736(94)90407-3. PMID 7983994.
63. ^ White A, Slade P, Hunt C, Hart A, Ernst E (2003). "Individualised homeopathy as an adjunct in the treatment of childhood asthma: a randomised placebo controlled trial". Thorax 58 (4): 317–21. doi:10.1136/thorax.58.4.317. PMID 12668794.
64. ^ Nagendra HR, Nagarathna R (1986). "An integrated approach of yoga therapy for bronchial asthma: a 3-54-month prospective study". J Asthma 23 (3): 123–37. doi:10.3109/02770908609077486. PMID 3745111.
65. ^ Manocha R, Marks GB, Kenchington P, Peters D, Salome CM (2002). "Sahaja yoga in the management of moderate to severe asthma: a randomised controlled trial". Thorax 57 (2): 110–5. doi:10.1136/thorax.57.2.110. PMID 11828038.
66. ^ Nagourney E (2007-11-13). "For the Record: In Tests of Inhalers, Results May Depend on Who Pays", The New York Times. Retrieved on 2 December 2007.
67. ^ Nieto A, Mazon A, Pamies R, et al (2007). "Adverse effects of inhaled corticosteroids in funded and nonfunded studies". Arch. Intern. Med. 167 (19): 2047–53. doi:10.1001/archinte.167.19.2047. PMID 17954797.
68. ^ Beckett PA, Howarth PH (2003). "Pharmacotherapy and airway remodelling in asthma?". Thorax 58 (2): 163–74. doi:10.1136/thorax.58.2.163. PMID 12554904.
69. ^ Masoli, Matthew; Denise Fabian, Shaun Holt, Richard Beasley (2004). "Global Burden of Asthma(TM)" (PDF). Retrieved on 2008-08-08.
70. ^ a b World Health Organization. "Bronchial asthma: scope of the problem". Retrieved on 2005-08-23.
71. ^ World Health Organization. "WHO: Asthma". Retrieved on 2007-12-29.
72. ^ Lara M, Akinbami L, Flores G,Morgenstern H (2006). "Heterogeneity of childhood asthma among Hispanic children: Puerto Rican children bear a disproportionate burden". Pediatrics 117 (1): 43–53. doi:10.1542/peds.2004-1714. PMID 16396859.
73. ^ Davis AM, Kreutzer R, Lipsett M, King G,Shaikh N (2006). "Asthma prevalence in Hispanic and Asian American ethnic subgroups: results from the California Healthy Kids Survey". Pediatrics 118 (2): e363–70. doi:10.1542/peds.2005-2687. PMID 16882779.
74. ^ Johnson DB, Oyama N, LeMarchand L,Wilkens L (2004). "Native Hawaiians mortality, morbidity, and lifestyle: comparing data from 1982, 1990, and 2000". Pac Health Dialog 11 (2): 120–30. PMID 16281689.
75. ^ Naqvi M, Thyne S, Choudhry S "et al." (2007). "Ethnic-specific differences in bronchodilator responsiveness among african americans, puerto ricans, and mexicans with asthma". J Asthma 44 (8): 639–48. doi:10.1080/02770900701554441. PMID 17943575.
76. ^ Burchard EG, Avila PC, Nazario S "et al." (2004). "Lower bronchodilator responsiveness in Puerto Rican than in Mexican subjects with asthma". Am J Respir Crit Care Med 169 (3): 386–92. doi:10.1164/rccm.200309-1293OC. PMID 14617512.
77. ^ Gold DR,Acevedo-Garcia D (2005). "Immigration to the United States and acculturation as risk factors for asthma and allergy". J Allergy Clin Immunol 116 (1): 38–41. doi:10.1016/j.jaci.2005.04.033. PMID 15990770.
78. ^ Eldeirawi KM,Persky VW (2006). "Associations of acculturation and country of birth with asthma and wheezing in Mexican American youths". J Asthma 43 (4): 279–86. doi:10.1080/0277090060022869. PMID 16809241.
79. ^ "Patient/Public Education: Fast Facts - Asthma Demographics/Statistics". American Academy of Allergy Asthma & Immunology. Retrieved on 2006-05-02.
80. ^ National Heart, Lung, and Blood Institute (May 2004). Morbidity & Mortality: 2004 Chart Book On Cardiovascular, Lung, and Blood Diseases, National Institutes of Health.
81. ^ National Center for Health Statistics (7 April 2006). "Asthma Prevalence, Health Care Use and Mortality, 2002". Centers for Disease Control and Prevention.
82. ^ a b Weiler JM, Layton T, Hunt M (1998). "Asthma in United States Olympic athletes who participated in the 1996 Summer Games". J. Allergy Clin. Immunol. 102 (5): 722–6. doi:10.1016/S0091-6749(98)70010-7. PMID 9819287.
83. ^ Helenius I, Haahtela T (2000). "Allergy and asthma in elite summer sport athletes". J. Allergy Clin. Immunol. 106 (3): 444–52. doi:10.1067/mai.2000.107749. PMID 10984362.
84. ^ Opolski M, Wilson I (September 2005). "Asthma and depression: a pragmatic review of the literature and recommendations for future research". Clin Pract Epidemol Ment Health 1: 18. doi:10.1186/1745-0179-1-18. PMID 16185365.
http://en.wikipedia.org/wiki/Asthma
Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.[3]
Signs and symptoms
In some individuals asthma is characterized by chronic respiratory impairment. In others it is an intermittent illness marked by episodic symptoms that may result from a number of triggering events, including upper respiratory infection, stress, airborne allergens, air pollutants (such as smoke or traffic fumes), or exercise. Some or all of the following symptoms may be present in those with asthma: dyspnea, wheezing, stridor, coughing, a tightness and itching of the chest or an inability for physical exertion. Some asthmatics who have severe shortness of breath and tightening of the lungs never wheeze or have stridor and their symptoms may be confused with a COPD-type disease.
An acute exacerbation of asthma is commonly referred to as an asthma attack. The clinical hallmarks of an attack are shortness of breath (dyspnea) and either wheezing or stridor.[4] Although the former is "often regarded as the sine qua non of asthma",[4] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard. When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in both respiratory phases).
Signs of an asthmatic episode include wheezing, prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. During a serious asthma attack, the accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used, shown as in-drawing of tissues between the ribs and above the sternum and clavicles.
During very severe attacks, an asthma sufferer can turn blue from lack of oxygen, and can experience chest pain or even loss of consciousness. Just before loss of consciousness, there is a chance that the patient will feel numbness in the limbs and palms may start to sweat. The person's feet may become icy cold. Severe asthma attacks, which may not be responsive to standard treatments (status asthmaticus), are life-threatening and may lead to respiratory arrest and death. Despite the severity of symptoms during an asthmatic episode, between attacks an asthmatic may show few or even no signs of the disease.[5]
[edit] Cause
Asthma is caused by a complex interaction of environmental and genetic factors that researchers do not yet fully understand.[6] These factors can also influence how severe a person’s asthma is and how well they respond to medication.[7] As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all of them have been replicated. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may affect asthma only when combined.
[edit] Environmental
Many environmental risk factors have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association.
Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[8] Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[8][9]
Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).[10]
Psychological stress, on the part of a child's caregiver, has been associated with asthma and is an area of active research. Stress can modify behaviors that affect asthma, like smoking, but research suggests that stress has other effects as well. There is growing evidence that stress may influence asthma and other diseases by influencing the immune system.[8]
Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.[8][11][12] Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[13]
The hygiene hypothesis is an hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, c-sections, and cleaning products.[13][10][14] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.
[edit] Genetic
Over 100 genes have been associated with asthma in at least one genetic association study.[15] However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[15]
* GSTM1
* IL10
* CTLA-4
* SPINK5
* LTC4S
* LTA
* GRPA
* NOD1
* CC16
* GSTP1
* STAT6
* NOS1
* CCL5
* TBXA2R
* TGFB1
* IL4
* IL13
* CD14
* ADRB2 (β-2 adrenergic receptor)
* HLA-DRB1
* HLA-DQB1
* TNF
* FCER1B
* IL4R
* ADAM33
Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[15] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma. For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.[16]
[edit] Gene-environment Interactions
Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.[6]
The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person’s genotype at CD14 C-159T and level of endotoxin exposure.[17]
CD14-endotoxin interaction based on CD14 SNP C-159T[17] Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk
[edit] Pathophysiology
In asthma, constriction of the airways occurs due to bronchoconstriction and bronchial inflammation. Bronchoconstriction is the narrowing of the airways in the lungs due to the tightening of surrounding smooth muscle. Bronchial inflammation also causes narrowing due to edema and swelling caused by an immune response to allergens.
[edit] Bronchoconstriction
Inflamed airways and bronchoconstriction in asthma. Airways narrowed as a result of the inflammatory response cause wheezing.
During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways.[18]
The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli (see below). (It is usually classified as type I hypersensitivity.)[19][20] In response to exposure to these triggers, the bronchi (large airways) contract into spasm (an "asthma attack"). Inflammation soon follows, leading to a further narrowing of the airways and excessive mucus production, which leads to coughing and other breathing difficulties.
The normal caliber of the bronchus is maintained by a balanced functioning of these systems, which both operate reflexively. The parasympathetic reflex loop consists of afferent nerve endings which originate under the inner lining of the bronchus. Whenever these afferent nerve endings are stimulated (for example, by dust, cold air or fumes) impulses travel to the brain-stem vagal center, then down the vagal afferent pathway to again reach the bronchus. Acetylcholine is released from the afferent nerve endings. This acetylcholine results in the excessive formation of cyclic Guanine Mono phosphate (cGMP). This initiates bronchoconstriction.
[edit] Bronchial inflammation
The mechanisms behind allergic asthma—i.e., asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both asthmatics and non-asthmatics, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen-presenting cells, or APCs. APCs then "present" pieces of the allergen to other immune system cells. In most people, these other immune cells (TH0 cells) "check" and usually ignore the allergen molecules. In asthmatics, however, these cells transform into a different type of cell (TH2), for reasons that are not well understood. The resultant TH2 cells activate an important arm of the immune system, known as the humoral immune system. The humoral immune system produces antibodies against the inhaled allergen. Later, when an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response. Inflammation results: chemicals are produced that cause the airways to constrict and release more mucus, and the cell-mediated arm of the immune system is activated. The inflammatory response is responsible for the clinical manifestations of an asthma attack.
[edit] Stimuli
* Allergens from nature, typically inhaled, which include waste from common household pests, such as the house dust mite and cockroach, grass pollen, mold spores, and pet epithelial cells;[citation needed]
* Indoor air pollution from volatile organic compounds, including perfumes and perfumed products. Examples include soap, dishwashing liquid, laundry detergent, fabric softener, paper tissues, paper towels, toilet paper, shampoo, hairspray, hair gel, cosmetics, facial cream, sun cream, deodorant, cologne, shaving cream, aftershave lotion, air freshener and candles, and products such as oil-based paint.[citation needed]
* Medications, including aspirin,[21] β-adrenergic antagonists (beta blockers), and penicillin.[citation needed]
* Food allergies such as milk, peanuts, and eggs. However, asthma is rarely the only symptom, and not all people with food or other allergies have asthma.[citation needed]
* Use of fossil fuel related allergenic air pollution, such as ozone, smog, summer smog, nitrogen dioxide, and sulfur dioxide, which is thought to be one of the major reasons for the high prevalence of asthma in urban areas.[citation needed]
* Various industrial compounds and other chemicals, notably sulfites; chlorinated swimming pools generate chloramines—monochloramine (NH2Cl), dichloramine (NHCl2) and trichloramine (NCl3)—in the air around them, which are known to induce asthma.[22]
* Early childhood infections, especially viral upper respiratory tract infections. However, persons of any age can have asthma triggered by colds and other respiratory infections even though their normal stimuli might be from another category (e.g. pollen) and absent at the time of infection. In many cases, significant asthma may not even occur until the respiratory infection is in its waning stage, and the person is seemingly improving. Eighty percent of asthma attacks in adults and 60% in children are caused by respiratory viruses.[citation needed]
* Exercise or intense use of respiratory system. The effects of which differ somewhat from those of the other triggers, since they are brief.
* Hormonal changes in adolescent girls and adult women associated with their menstrual cycle can lead to a worsening of asthma. Some women also experience a worsening of their asthma during pregnancy whereas others find no significant changes, and in other women their asthma improves during their pregnancy.[citation needed]
* Emotional stress which is poorly understood as a trigger. Emotional stress can affect breathing temporarily, however unlike something such as heart problems, it is unclear if it has any long-term effect.[citation needed]
* Cold weather can make it harder for asthmatics to breathe.[23] Whether high altitude helps or worsens asthma is debatable and may vary from person to person.[24]
[edit] Pathogenesis
The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis: the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.
In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma.[25] Szentivanyi's Beta Adrenergic Theory is a citation classic[26] and has been cited more times than any other article in the history of the Journal of Allergy.
In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors.[27] Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergy.[28]
The Beta-Adrenergic Theory has been cited in the scholarship of such noted investigators as Richard F. Lockey (former President of the American Academy of Allergy, Asthma, and Immunology),[29] Charles Reed (Chief of Allergy at Mayo Medical School),[30] and Craig Venter (Human Genome Project).[31]
John P. McGovern, President of the American Association of Allergy nominated Szentivanyi for The 1968 Nobel Prize in Medicine in recognition of The Beta Adrenergic Theory.
In 2006, Researchers at Harvard Medical School found evidence that asthma is caused by over-proliferation of a special type of natural "killer" cell.[32]
[edit] Asthma and sleep apnea
It is recognized with increasing frequency, that patients who have both obstructive sleep apnea (OSA) and bronchial asthma, often improve tremendously when the sleep apnea is diagnosed and treated.[33] CPAP is not effective in patients with nocturnal asthma only.[34]
[edit] Asthma and gastro-esophageal reflux disease
If gastro-esophageal reflux disease (GERD) is present, the patient may have repetitive episodes of acid aspiration. GERD may be common in difficult-to-control asthma, but according to one study, treating it does not seem to affect the asthma.[35]
[edit] Diagnosis
Asthma is defined simply as reversible airway obstruction. Reversibility occurs either spontaneously or with treatment. The basic measurement is peak flow rates and the following diagnostic criteria are used by the British Thoracic Society:[36]
* ≥20% difference on at least three days in a week for at least two weeks;
* ≥20% improvement of peak flow following treatment, for example:
o 10 minutes of inhaled β-agonist (e.g., salbutamol);
o six week of inhaled corticosteroid (e.g., beclometasone);
o 14 days of 30mg prednisolone.
* ≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).
In many cases, a physician can diagnose asthma on the basis of typical findings in a patient's clinical history and examination. Asthma is strongly suspected if a patient suffers from eczema or other allergic conditions—suggesting a general atopic constitution—or has a family history of asthma. While measurement of airway function is possible for adults, most new cases are diagnosed in children who are unable to perform such tests. Diagnosis in children is based on a careful compilation and analysis of the patient's medical history and subsequent improvement with an inhaled bronchodilator medication. In adults, diagnosis can be made with a peak flow meter (which tests airway restriction), looking at both the diurnal variation and any reversibility following inhaled bronchodilator medication.
Testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young asthmatics who may experience only exercise-induced asthma. If the diagnosis is in doubt, a more formal lung function test may be conducted. Once a diagnosis of asthma is made, a patient can use peak flow meter testing to monitor the severity of the disease.
Monitoring asthma with a peak flow meter on an ongoing basis assists with self monitoring of asthma. Peak flow readings can be charted on graph paper charts together with a record of symptoms or use peak flow charting software.[37] This allows patients to track their peak flow readings and pass information back to their doctor or nurse.[38]
In the Emergency Department doctors may use a capnography which measures the amount of exhaled carbon dioxide,[39] along with pulse oximetry which shows the amount of oxygen dissolved in the blood, to determine the severity of an asthma attack as well as the response to treatment.
More recently, exhaled nitric oxide has been studied as a breath test indicative of airway inflammation in asthma.
[edit] Differential diagnosis
This article does not cite any references or sources.
Please help improve this article by adding citations to reliable sources. Unverifiable material may be challenged and removed. (November 2008)
Before diagnosing someone as asthmatic, alternative possibilities should be considered. A clinician taking a history should check whether the patient is using any known bronchoconstrictors (substances that cause narrowing of the airways, e.g., certain anti-inflammatory agents or beta-blockers).
Chronic obstructive pulmonary disease, which closely resembles asthma, is correlated with more exposure to cigarette smoke, an older patient, less symptom reversibility after bronchodilator administration (as measured by spirometry), and decreased likelihood of family history of atopy.
Pulmonary aspiration, whether direct due to dysphagia (swallowing disorder) or indirect (due to acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also indicate aspiration pneumonia. Direct aspiration (dysphagia) can be diagnosed by performing a Modified Barium Swallow test and treated with feeding therapy by a qualified speech therapist. If the aspiration is indirect (from acid reflux) then treatment directed at this is indicated.
A majority of children who are asthma sufferers have an identifiable allergy trigger. Specifically, in a 2004 study, 71% had positive test results for more than 1 allergen, and 42% had positive test results for more than 3 allergens.[40]
The majority of these triggers can often be identified from the history; for instance, asthmatics with hay fever or pollen allergy will have seasonal symptoms, those with allergies to pets may experience an abatement of symptoms when away from home, and those with occupational asthma may improve during leave from work. Allergy tests can help identify avoidable symptom triggers.
After a pulmonary function test has been carried out, radiological tests, such as a chest X-ray or CT scan, may be required to exclude the possibility of other lung diseases. In some people, asthma may be triggered by gastroesophageal reflux disease, which can be treated with suitable antacids. Very occasionally, specialized tests after inhalation of methacholine — or, even less commonly, histamine — may be performed.
Asthma is categorized by the United States National Heart, Lung, and Blood Institute as falling into one of four categories: intermittent, mild persistent, moderate persistent and severe persistent. The diagnosis of "severe persistent asthma" occurs when symptoms are continual with frequent exacerbations and frequent night-time symptoms, result in limited physical activity and when lung function as measured by PEV or FEV1 tests is less than 60% predicted with PEF variability greater than 30%.
[edit] Prevention
This article does not cite any references or sources.
Please help improve this article by adding citations to reliable sources. Unverifiable material may be challenged and removed. (November 2008)
Current treatment protocols recommend prevention medications such as an inhaled corticosteroid, which helps to suppress inflammation and reduces the swelling of the lining of the airways, in anyone who has frequent (greater than twice a week) need of relievers or who has severe symptoms. If symptoms persist, additional preventive drugs are added until the asthma is controlled. With the proper use of prevention drugs, asthmatics can avoid the complications that result from overuse of relief medications.
Asthmatics sometimes stop taking their preventive medication when they feel fine and have no problems breathing. This often results in further attacks, and no long-term improvement.
Preventive agents include the following.
* Inhaled glucocorticoids are the most widely used prevention medications and normally come as inhaler devices (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone).
Long-term use of corticosteroids can have many side effects including a redistribution of fat, increased appetite, blood glucose problems and weight gain. In particular high doses of steroids may cause osteoporosis. For this reasons inhaled steroids are generally used for prevention, as their smaller doses are targeted to the lungs, unlike the higher doses of oral preparations. Nevertheless, patients on high doses of inhaled steroids may still require prophylactic treatment to prevent osteoporosis.
Deposition of steroids in the mouth may cause a hoarse voice or oral thrush (due to decreased immunity). This may be minimised by rinsing the mouth with water after inhaler use, as well as by using a spacer which increases the amount of drug that reaches the lungs.
* Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton) provide anti-inflammatory effect similar to inhaled corticosteroids.
* Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil).
* Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium), which have a mixed reliever and preventer effect. These are often used to reduce bronchospasm when inhaled steroids do not produce sufficient relief.
* Methylxanthines (theophylline and aminophylline), which are sometimes considered if sufficient control cannot be achieved with inhaled glucocorticoids (or leukotriene modifiers) and long-acting β-agonists alone.
* Antihistamines, often used to treat allergic effects that may underlie the chronic inflammation.
* Hyposensitization, (also known as immunodesensitisation therapy) may be recommended in some cases where allergy is the suspected cause or trigger of asthma. Depending on the allergen, it can be given orally or by injection.
* Omalizumab, an IgE blocker; this can help patients with severe allergic asthma that does not respond to other drugs. However, it is expensive and must be injected.
* Methotrexate is occasionally used in some difficult-to-treat patients.
* If chronic acid indigestion (GERD) contributes to a patient's asthma, it should also be treated, because it may prolong the respiratory problem.
[edit] Trigger avoidance
As is common with respiratory disease, smoking is believed to adversely affect asthmatics in several ways, including an increased severity of symptoms, a more rapid decline of lung function, and decreased response to preventive medications.[41] Automobile emissions are considered an even more significant cause and aggravating factor.[42] Asthmatics who smoke or who live near traffic [1] typically require additional medications to help control their disease. Furthermore, exposure of both non-smokers and smokers to wood smoke, gas stove fumes and second-hand smoke is detrimental, resulting in more severe asthma, more emergency room visits, and more asthma-related hospital admissions.[43] Smoking cessation and avoidance of second-hand smoke is strongly encouraged in asthmatics.[44]
For those in whom exercise can trigger an asthma attack (exercise-induced asthma), higher levels of ventilation and cold, dry air tend to exacerbate attacks. For this reason, activities in which a patient breathes large amounts of cold air, such as skiing and running, tend to be worse for asthmatics, whereas swimming in an indoor, heated pool, with warm, humid air, or a shower is less likely to provoke a response.[4]
[edit] Air Filters
If an asthmatic lives with a smoker, use of air filter or room air cleaner is likely to be helpful. Secondhand smoke can worsen the symptoms. The same is true for those with hay fever (allergic rhino sinusitis) or COPD (emphysema or chronic bronchitis). Room air cleaners remove small particles that are in the air near the air cleaner. However, room air cleaners do not remove small allergen particles that are caused by local disturbances, such as the microscopic house dust mite feces that surround a pillow when your head hits it or you turn over in bed. There are several types of air filters available.[45]
* Mechanical air filters use a fan to force air through a special screen that traps particles such as smoke, pollens, and other airborne allergens. The high-efficiency particulate air (HEPA) filter is the best-known air filter. HEPA (which is a type of filter, not a brand name) was developed during World War II to prevent radioactive particles from escaping from laboratories.
* Electronic air filters use electrical charges to attract and deposit allergens and irritants. If the device contains collecting plates, the particles are captured within the system; otherwise, they stick to room surfaces and have to be cleared away.
* Hybrid air filters contain elements of both mechanical and electrostatic filters.
* Gas phase air filters use activated carbon granules to remove odors (volatile organic compounds or VOCs) and non-particulate pollution such as cooking gas, gases emitted from paint or building materials (such as formaldehyde), and perfume.
* Germicidal air cleaners use ultraviolet (UV) lights to kill bacteria, viruses, and molds that pass through the area with the UV light. Such UV lights can be included with other air cleaner devices, which use a fan.
* Ozone generators are devices that intentionally produce high concentrations of ozone to clean the air in a room. They are often used to decontaminate rooms after smoke exposure following a fire.
[edit] Treatment
This article does not cite any references or sources.
Please help improve this article by adding citations to reliable sources. Unverifiable material may be challenged and removed. (November 2008)
The most effective treatment for asthma is identifying triggers, such as pets or aspirin, and limiting or eliminating exposure to them. If trigger avoidance is insufficient, medical treatment is available. Desensitization is currently the only known "cure" to the disease.[46] Other forms of treatment include relief medication, prevention medication, long-acting β2-agonists, and emergency treatment.
[edit] Medical
The specific medical treatment recommended to patients with asthma depends on the severity of their illness and the frequency of their symptoms. Specific treatments for asthma are broadly classified as relievers, preventers and emergency treatment. The Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma (EPR-2)[44] of the U.S. National Asthma Education and Prevention Program, and the British Guideline on the Management of Asthma[47] are broadly used and supported by many doctors. On August 29, 2007 the final Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma was officially released. Bronchodilators are recommended for short-term relief in all patients. For those who experience occasional attacks, no other medication is needed. For those with mild persistent disease (more than two attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene modifier, a mast-cell stabilizer, or theophylline may be administered. For those who suffer daily attacks, a higher dose of glucocorticoid in conjunction with a long-acting inhaled β-2 agonist may be prescribed; alternatively, a leukotriene modifier or theophylline may substitute for the β-2 agonist. In severe asthmatics, oral glucocorticoids may be added to these treatments during severe attacks.
[edit] Pharmaceutical
Symptomatic control of episodes of wheezing and shortness of breath is generally achieved with fast-acting bronchodilators. These are typically provided in pocket-sized, metered-dose inhalers (MDIs). In young sufferers, who may have difficulty with the coordination necessary to use inhalers, or those with a poor ability to hold their breath for 10 seconds after inhaler use (generally the elderly), an asthma spacer (see top image) is used. The spacer is a plastic cylinder that mixes the medication with air in a simple tube, making it easier for patients to receive a full dose of the drug and allows for the active agent to be dispersed into smaller, more fully inhaled bits.
A nebulizer which provides a larger, continuous dose can also be used. Nebulizers work by vaporizing a dose of medication in a saline solution into a steady stream of foggy vapour, which the patient inhales continuously until the full dosage is administered. There is no clear evidence, however, that they are more effective than inhalers used with a spacer. Nebulizers may be helpful to some patients experiencing a severe attack. Such patients may not be able to inhale deeply, so regular inhalers may not deliver medication deeply into the lungs, even on repeated attempts. Since a nebulizer delivers the medication continuously, it is thought that the first few inhalations may relax the airways enough to allow the following inhalations to draw in more medication.
Relievers include:
* Short-acting, selective beta2-adrenoceptor agonists, such as salbutamol (albuterol USAN), levalbuterol, terbutaline and bitolterol.
Tremors, the major side effect, have been greatly reduced by inhaled delivery, which allows the drug to target the lungs specifically; oral and injected medications are delivered throughout the body. There may also be cardiac side effects at higher doses (due to Beta-1 agonist activity), such as elevated heart rate or blood pressure. Patients must be cautioned against using these medicines too frequently, as with such use their efficacy may decline, producing desensitization resulting in an exacerbation of symptoms which may lead to refractory asthma and death.
* Older, less selective adrenergic agonists, such as inhaled epinephrine and ephedrine tablets, have also been used. Cardiac side effects occur with these agents at either similar or lesser rates to albuterol.[48] [49] When used solely as a relief medication, inhaled epinephrine has been shown to be an effective agent to terminate an acute asthmatic exacerbation.[48] In emergencies, these drugs were sometimes administered by injection. Their use via injection has declined due to related adverse effects.
* Anticholinergic medications, such as ipratropium bromide may be used instead. They have no cardiac side effects and thus can be used in patients with heart disease; however, they take up to an hour to achieve their full effect and are not as powerful as the β2-adrenoreceptor agonists.
* Inhaled glucocorticoids are usually considered preventive medications while oral glucocorticoids are often used to supplement treatment of a severe attack. A randomized controlled trial has demonstrated the benefit of 250 microg beclomethasone when taken as an as-needed combination inhaler with 100 microg of albuterol.[50]
[edit] Long-acting β2-agonists
A typical inhaler, of Serevent (salmeterol), a long-acting bronchodilator.
Long-acting bronchodilators (LABD) are similar in structure to short-acting selective beta2-adrenoceptor agonists, but have much longer side chains resulting in a 12-hour effect, and are used to give a smoothed symptomatic relief (used morning and night). While patients report improved symptom control, these drugs do not replace the need for routine preventers, and their slow onset means the short-acting dilators may still be required. In November 2005, the American FDA released a health advisory alerting the public to findings that show the use of long-acting β2-agonists could lead to a worsening of symptoms, and in some cases death.[51]
Currently available long-acting beta2-adrenoceptor agonists include salmeterol, formoterol, bambuterol, and sustained-release oral albuterol. Combinations of inhaled steroids and long-acting bronchodilators are becoming more widespread; the most common combination currently in use is fluticasone/salmeterol (Advair in the United States, and Seretide in the United Kingdom). Another combination is budesonide/formoterol which is commercially known as Symbicort.
A recent meta-analysis of the roles of long-acting beta-agonists may indicate a danger to asthma patients. The study, published in the Annals of Internal Medicine in 2006, found that long-acting beta-agonists increased the risk for asthma hospitalizations and asthma deaths 2- to 4-fold, compared with placebo.[52] "These agents can improve symptoms through bronchodilation at the same time as increasing underlying inflammation and bronchial hyper-responsiveness, thus worsening asthma control without any warning of increased symptoms," said Shelley Salpeter in a press release after the publication of the study. The release goes on to say that "Three common asthma inhalers containing the drugs salmeterol or formoterol may be causing four out of five US asthma-related deaths per year and should be taken off the market".[53] This assertion is viewed by many asthma specialists as being inaccurate. Dr. Hal Nelson, in a recent letter to the Annals of Internal Medicine, points out the following:
"Salpeter and colleagues also assert that salmeterol may be responsible for 4000 of the 5000 asthma-related deaths that occur in the United States annually. However, when salmeterol was introduced in 1994, more than 5000 asthma-related deaths occurred per year. Since the peak of asthma deaths in 1996, salmeterol sales have increased about 5-fold, while overall asthma mortality rates have decreased by about 25%, despite a continued increase in asthma diagnoses. In fact, according to the most recent data from the National Center for Health Statistics, U.S. asthma mortality rates peaked in 1996 (with 5667 deaths) and have decreased steadily since. The last available data, from 2004, indicate that 3780 deaths occurred. Thus, the suggestion that a vast majority of asthma deaths could be attributable to LABA use is inconsistent with the facts."
Dr. Shelley Salpeter, in a letter to the Annals of Internal Medicine, responds to the comments of Dr. Nelson, as follows:
"It is true that the asthma death rate increased after salmeterol was introduced, then peaked and is now starting to decline despite continued use of the long-acting beta-agonists. This trend in death rates can best be explained by examining the ratio of beta-agonist use to inhaled corticosteroids... In the recent past, inhaled corticosteroid use has increased steadily while long-acting beta-agonist use has begun to stabilize and short-acting beta-agonist use has declined... Using this estimate, we can imagine that if long-acting beta-agonists were withdrawn from the market while maintaining high inhaled corticosteroid use, the death rate in the United States could be reduced significantly..."
[edit] Emergency
When an asthma attack is unresponsive to a patient's usual medication, other treatments are available to the physician or hospital:[54]
* Oxygen to alleviate the hypoxia (but not the asthma itself) that results from extreme asthma attacks.
* Nebulized salbutamol or terbutaline (short-acting beta-2-agonists), often combined with ipratropium (an anticholinergic).
* Systemic steroids, oral or intravenous (prednisone, prednisolone, methylprednisolone, dexamethasone, or hydrocortisone). Some research has looked into an alternative inhaled route.[55]
* Other bronchodilators that are occasionally effective when the usual drugs fail:
o Intravenous salbutamol
o Nonspecific beta-agonists, injected or inhaled (epinephrine, isoetharine, isoproterenol, metaproterenol)
o Anticholinergics, IV or nebulized, with systemic effects (glycopyrrolate, atropine, ipratropium)
o Methylxanthines (theophylline, aminophylline)
o Inhalation anesthetics that have a bronchodilatory effect (isoflurane, halothane, enflurane)
o The dissociative anaesthetic ketamine, often used in endotracheal tube induction
o Magnesium sulfate, intravenous
* Intubation and mechanical ventilation, for patients in or approaching respiratory arrest.
* Heliox, a mixture of helium and oxygen, may be used in a hospital setting. It has a more laminar flow than ambient air and moves more easily through constricted airways.
[edit] Non-medical treatments
Many asthmatics, like those who suffer from other chronic disorders, use alternative treatments; surveys show that roughly 50% of asthma patients use some form of unconventional therapy.[56][57] There is little data to support the effectiveness of most of these therapies. A Cochrane systematic review of acupuncture for asthma found no evidence of efficacy.[58] A similar review of air ionisers found no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.[59] Another systematic study reviewed a range of dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others. Overall these methods had no effect on asthma symptoms .[60] A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvres, found there is insufficient evidence to support or refute their use in treating asthma;[61] these manoeuvers include various osteopathic and chiropractic techniques to "increase movement in the rib cage and the spine to try and improve the working of the lungs and circulation"; chest tapping, shaking, vibration, and the use of "postures to help shift and cough up phlegm." One meta-analysis finds that homeopathy may have a potentially mild benefit in reducing the intensity of symptoms.[62] However, the number of patients involved in the analysis was small, and subsequent studies have not supported this finding.[63] Several small trials have suggested some benefit from various yoga practices, ranging from integrated yoga programs,[64] yogasanas, Pranayama, meditation, and kriyas, to sahaja yoga,[65] a form of 'new religious' meditation.
[edit] Treatment controversies
In November 2007 The New York Times reported a review of more than 500 studies finding that independently backed studies on inhaled corticosteroids are up to four times more likely to find adverse effects than studies paid for by drug companies.[66][67]
[edit] Prognosis
The prognosis for asthmatics is good; especially for children with mild disease. For asthmatics diagnosed during childhood, 54% will no longer carry the diagnosis after a decade. The extent of permanent lung damage in asthmatics is unclear. Airway remodelling is observed, but it is unknown whether these represent harmful or beneficial changes.[18] Although conclusions from studies are mixed, most studies show that early treatment with glucocorticoids prevents or ameliorates decline in lung function as measured by several parameters.[68] For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities. The mortality rate for asthma is low, with around 6000 deaths per year in a population of some 10 million patients in the United States.[4] Better control of the condition may help prevent some of these deaths.
[edit] Epidemiology
The prevalence of childhood asthma has increased since 1980, especially in younger children.
The highest levels of asthma in the world according to the Global INitiative for Asthma (GINA) report of February 2004[69] occurred for about 30% of children in the United Kingdom, New Zealand and Australia, or 20% of children in Peru, New Zealand and Australia according to the method of interview, and for about 25% of adults in Great Britain, Australia and Canada. The United States also ranks highly. More than 6% of children in the United States have been diagnosed with asthma, a 75% increase in recent decades. The rate soars to 40% among some populations of urban children.[citation needed]
Current research suggests that the prevalence of childhood asthma has been increasing. According to the Centers for Disease Control and Prevention's National Health Interview Surveys, some 9% of US children below 18 years of age had asthma in 2001, compared with just 3.6% in 1980 (see figure). The World Health Organization (WHO) reports that some 8% of the Swiss population suffers from asthma today, compared with just 2% some 25–30 years ago.[70] Although asthma is more common in affluent countries, it is by no means a problem restricted to the affluent; the WHO estimate that there are between 15 and 20 million asthmatics in India. In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole. Globally, asthma is responsible for around 180,000 deaths annually.[70]
[edit] Population disparities
Asthma prevalence, morbidity, mortality, and drug response vary greatly across populations. There is an almost 30-fold difference in asthma prevalence between some of the countries included in the International Study of Asthma and Allergy in Childhood [2], with a trend toward more developed and westernized countries having higher asthma prevalence. Westernization can’t explain the entire difference in asthma prevalence between countries, however, and the disparities may also be affected by differences in genetic, social and environmental risk factors.[8] There are also worldwide disparities in asthma mortality, which is most common in low to middle income countries.[71]
Asthma prevalence in the US is higher than in most other countries in the world, but varies drastically between diverse US populations.[8] In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos and Native Hawaiians, and lowest in Mexicans and Koreans.[72][73][74] Mortality rates follow similar trends, and response to albuterol is lower in Puerto Ricans than in African Americans or Mexicans.[75][76] As with worldwide asthma disparities, differences in asthma prevalence, mortality, and drug response in the US may be explained by differences in genetic, social and environmental risk factors.
Asthma prevalence also differs between populations of the same ethnicity who are born and live in different places.[77] US-born Mexican populations, for example, have higher asthma rates than non-US born Mexican populations that are living in the US.[78] This probably reflects differences in social and environmental risk factors associated with acculturation to the US.[citation needed]
Asthma prevalence and asthma deaths also differ by gender. Males are more likely to be diagnosed with asthma as children, but asthma is more likely to persist into adulthood in females. Sixty five percent more adult women than men will die from asthma. This difference may be attributable to hormonal differences, among other things. In support of this, girls who reach puberty before age 12 were found to have a later diagnosis of asthma more than twice as much as girls who reach puberty after age 12. Asthma is also the number one cause of missed days from school.
[edit] Socioeconomic factors
The incidence of asthma is highest among low-income populations (asthma deaths are most common in low to middle income countries [3]), which in the western world are disproportionately ethnic minorities[79] and are more likely to live near industrial areas. Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters, which is more likely in such neighborhoods.
Asthma incidence and quality of treatment varies among different racial groups, though this may be due to correlations with income (and thus affordability of health care) and geography. For example, Black Americans are less likely to receive outpatient treatment for asthma despite having a higher prevalence of the disease. They are much more likely to have emergency room visits or hospitalization for asthma, and are three times as likely to die from an asthma attack compared to whites. The prevalence of "severe persistent" asthma is also greater in low-income communities compared with communities with better access to treatment.[80][81]
[edit] Asthma and athletics
Asthma appears to be more prevalent in athletes than in the general population. One survey of participants in the 1996 Summer Olympic Games, in Atlanta, Georgia, U.S., showed that 15% had been diagnosed with asthma, and that 10% were on asthma medication.[82] These statistics have been questioned on at least two bases. Athletes with mild asthma may be more likely to be diagnosed with the condition than non-athletes, because even subtle symptoms may interfere with their performance and lead to pursuit of a diagnosis. It has also been suggested that some professional athletes who do not suffer from asthma claim to do so in order to obtain special permits to use certain performance-enhancing drugs.[citation needed]
There appears to be a relatively high incidence of asthma in sports such as cycling, mountain biking, and long-distance running, and a relatively lower incidence in weightlifting and diving. It is unclear how much of these disparities are from the effects of training in the sport, and from self-selection of sports that may appear to minimize the triggering of asthma.[82][83]
In addition, there exists a variant of asthma called exercise-induced asthma that shares many features with allergic asthma. It may occur either independently, or concurrent with the latter. Exercise studies may be helpful in diagnosing and assessing this condition.
[edit] History
Asthma was long considered a psychosomatic disease, and
... during the 1930s–50s, was even known as one of the 'holy seven' psychosomatic illnesses. At that time, psychoanalytic theories described the aetiology of asthma as psychological, with treatment often primarily involving psychoanalysis and other 'talking cures'. As the asthmatic wheeze was interpreted as the child's suppressed cry for his or her mother, psychoanalysts viewed the treatment of depression as especially important for individuals with asthma.[84]
[edit] See also
Wikimedia Commons has media related to:
Asthma
* Asthma and Allergy Foundation of America
* Atopy
* Global Initiative for Asthma (GINA)
* Hopkins syndrome
* Hygiene hypothesis
* Immune system
* Occupational asthma
* Reactive airway disease
* World Asthma Day
* Vocal cord dysfunction
[edit] References
1. ^ "Asthma: What Causes Asthma". Asthma and Allergy Foundation of America. Retrieved on 2008-01-03.
2. ^ Zhao J, Takamura M, Yamaoka A, Odajima Y, Iikura Y (February 2002). "Altered eosinophil levels as a result of viral infection in asthma exacerbation in childhood". Pediatr Allergy Immunol 13 (1): 47–50. doi:10.1034/j.1399-3038.2002.00051.x. PMID 12000498.
3. ^ Lilly CM (2005). "Diversity of asthma: evolving concepts of pathophysiology and lessons from genetics". J. Allergy Clin. Immunol. 115 (4 Suppl): S526–31. doi:10.1016/j.jaci.2005.01.028. PMID 15806035.
4. ^ a b c d McFadden ER, Jr (2004). "Asthma", Harrison's Principles of Internal Medicine (Kasper DL, Fauci AS, Longo DL, et al (eds)), 16th ed., New York: McGraw-Hill, 1508–16.
5. ^ Longmore, Murray et al (2007). Oxford Handbook of Clinical Medicine, 7th ed., Oxford University Press. ISBN 978-0198568377.
6. ^ a b Martinez FD (2007). "Genes, environments, development and asthma: a reappraisal". Eur Respir J 29 (1): 179–84. doi:10.1183/09031936.00087906. PMID 17197483.
7. ^ Choudhry S, Seibold MA, Borrell LN "et al." (2007). "Dissecting complex diseases in complex populations: asthma in latino americans". Proc Am Thorac Soc 4 (3): 226–33. doi:10.1513/pats.200701-029AW. PMID 17607004.
8. ^ a b c d e f Gold DR,Wright R (2005). "Population disparities in asthma". Annu Rev Public Health 26: 89–113. doi:10.1146/annurev.publhealth.26.021304.144528. PMID 15760282.
9. ^ "California Children's Health Study".
10. ^ a b Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell, CR (2007). "A meta-analysis of the association between Caesarean section and childhood asthma". Clin. And Exper. Allergy online ahead of print: 629. doi:10.1111/j.1365-2222.2007.02780.x.
11. ^ Harju TH, Leinonen M, Nokso-Koivisto J, et al (2006). "Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma". Thorax 61 (7): 579–84. doi:10.1136/thx.2005.056291. PMID 16517571.
12. ^ Richeldi L, Ferrara G, Fabbri LM, Lasserson TJ, Gibson PG (2005). "Macrolides for chronic asthma". Cochrane Database Syst Rev (4): CD002997. doi:10.1002/14651858.CD002997.pub3. PMID 16235309.
13. ^ a b Marra F, Lynd L, Coombes M "et al." (2006). "Does antibiotic exposure during infancy lead to development of asthma?: a systematic review and metaanalysis". Chest 129 (3): 610–8. doi:10.1378/chest.129.3.610. PMID 16537858.
14. ^ Jeremy Laurance. "Asthma blamed on cleaning sprays and air fresheners".
15. ^ a b c Ober C,Hoffjan S (2006). "Asthma genetics 2006: the long and winding road to gene discovery". Genes Immun 7 (2): 95–100. doi:10.1038/sj.gene.6364284. PMID 16395390.
16. ^ Bouzigon E, Corda E, Aschard H, et al (October 2008). "Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma". The New England journal of medicine. doi:10.1056/NEJMoa0806604. PMID 18923164.
17. ^ a b Martinez FD (2007). "CD14, endotoxin, and asthma risk: actions and interactions". Proc Am Thorac Soc 4 (3): 221–5. doi:10.1513/pats.200702-035AW. PMID 17607003.
18. ^ a b Maddox L, Schwartz DA (2002). "The pathophysiology of asthma". Annu. Rev. Med. 53: 477–98. doi:10.1146/annurev.med.53.082901.103921. PMID 11818486.
19. ^ "Lecture 14: Hypersensitivity". Retrieved on 2008-09-18.
20. ^ "Allergy & Asthma Disease Management Center: Ask the Expert". Retrieved on 2008-09-18.
21. ^ Jenkins C, Costello J, Hodge L (2004). "Systematic review of prevalence of aspirin induced asthma and its implications for clinical practice". BMJ 328 (7437): 434. doi:10.1136/bmj.328.7437.434. PMID 14976098.
22. ^ Nemery B, Hoet PH, Nowak D (2002). "Indoor swimming pools, water chlorination and respiratory health". Eur. Respir. J. 19 (5): 790–3. doi:10.1183/09031936.02.00308602. PMID 12030714.
23. ^ about.com article
24. ^ Asthma and Altitude
25. ^ Szentivanyi, Andor (1968). The Beta Adrenergic Theory of the Atopic Abnormality in Asthma.
26. ^ Lockey, Richard, In lasting tribute: Andor Szentivanyi, MD. J. Allergy and Clinical Immunology, January, 2006
27. ^ Szentivanyi A., Ali K., Calderon EG., Brooks SM., Coffey RG., Lockey RF. (1993). "The in vitro effect of Imunnoglobulin E {IgE} on cyclic AMP concentrations in A549 human pulmonary epithelial cells with or without beta adrenergic stimulation". J. Allergy Clin Immunol. 91: 379. - Part of Abstracts from:
"50th Anniversary of the American Academy of Allergy and Immunology. 49th Annual Meeting. Chicago, Illinois, March 12-17, 1993. Abstracts". J. Allergy Clin. Immunol. 91 (1 Pt 2): 141–379. 1993. PMID 8421135.
28. ^ (2001) in Kowalak JP, Hughes AS et al (eds): Professional Guide To Diseases, 7th ed., Springhouse.
29. ^ Lockey, Richard F. (2006-04-28). "Anaphylaxis: Synopsis". Allergic Diseases Resource Center. World Allergy Organization. Retrieved on September 23, 2006.[dead link]
30. ^ Ouellette JJ, Reed CE (1967). "The effect of partial beta adrenergic blockade on the bronchial response of hay fever subjects to ragweed aerosol". J Allergy 39 (3): 160–6. doi:10.1016/0021-8707(67)90033-0. PMID 5227155.
31. ^ Fraser CM, Venter JC (1980). "The synthesis of beta-adrenergic receptors in cultured human lung cells: induction by glucocorticoids". Biochem. Biophys. Res. Commun. 94 (1): 390–7. doi:10.1016/S0006-291X(80)80233-6. PMID 6248064.
32. ^ Cromie, William J. (2006-03-16). "Researchers uncover cause of asthma", Harvard University Gazette, Harvard News Office. Retrieved on 23 September 2006.
33. ^ University of Michigan Health System (May 25, 2005). "Breathing disorders during sleep are common among asthmatics, may help predict severe asthma". Press release. Retrieved on 2006-09-23.
34. ^ Basner, Robert C. (2006-07-25). "Asthma and OSA". ASAA Resources > Publications. American Sleep Apnea Association. Retrieved on September 23, 2006.
35. ^ Leggett JJ, Johnston BT, Mills M, Gamble J, Heaney LG (2005). "Prevalence of gastroesophageal reflux in difficult asthma: relationship to asthma outcome". Chest 127 (4): 1227–31. doi:10.1378/chest.127.4.1227. PMID 15821199, http://www.chestjournal.org/cgi/content/full/127/4/1227.
36. ^ Pinnock H, Shah R (2007). "Asthma". BMJ 334 (7598): 847–50. doi:10.1136/bmj.39140.634896.BE. PMID 17446617.
37. ^ "Peak flow charting software".
38. ^ "'Be in control' pack" (PDF). Asthma UK. Retrieved on 2007-11-19.
39. ^ Corbo J, Bijur P, Lahn M, Gallagher EJ (2005). "Concordance between capnography and arterial blood gas measurements of carbon dioxide in acute asthma". Annals of emergency medicine 46 (4): 323–7. doi:10.1016/j.annemergmed.2004.12.005. PMID 16187465.
40. ^ Vargas PA, Simpson PM, Gary Wheeler J, et al (2004). "Characteristics of children with asthma who are enrolled in a Head Start program". J. Allergy Clin. Immunol. 114 (3): 499–504. doi:10.1016/j.jaci.2004.05.025. PMID 15356547.
41. ^ Thomson NC, Spears M (2005). "The influence of smoking on the treatment response in patients with asthma". Curr Opin Allergy Clin Immunol 5 (1): 57–63. PMID 15643345.
42. ^ EWG || Auto Asthma Index
43. ^ Eisner MD, Yelin EH, Katz PP, Earnest G, Blanc PD (2002). "Exposure to indoor combustion and adult asthma outcomes: environmental tobacco smoke, gas stoves, and woodsmoke". Thorax 57 (11): 973–8. doi:10.1136/thorax.57.11.973. PMID 12403881.
44. ^ a b National Asthma Education and Prevention Program. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97–4051. Bethesda, MD, 1997. (PDF)
45. ^ Asthma and Air Filters Asthma and Air Filters[dead link]
46. ^ Abramson MJ, Puy RM, Weiner JM (1995). "Is allergen immunotherapy effective in asthma? A meta-analysis of randomized controlled trials". Am. J. Respir. Crit. Care Med. 151 (4): 969–74. PMID 7697274.
47. ^ "British Guideline on the Management of Asthma" (PDF). Scottish Intercollegiate Guidelines Network (2008). Retrieved on 2008-08-04.
48. ^ a b Hendeles L, Marshik PL, Ahrens R, Kifle Y, Shuster J (2005). "Response to nonprescription epinephrine inhaler during nocturnal asthma". Ann. Allergy Asthma Immunol. 95 (6): 530–4. PMID 16400891.
49. ^ Rodrigo GJ, Nannini LJ (2006). "Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials". Am J Emerg Med 24 (2): 217–22. doi:10.1016/j.ajem.2005.10.008. PMID 16490653.
50. ^ Papi A, Canonica GW, Maestrelli P, et al (2007). "Rescue use of beclomethasone and albuterol in a single inhaler for mild asthma". N. Engl. J. Med. 356 (20): 2040–52. doi:10.1056/NEJMoa063861. PMID 17507703.
51. ^ "Serevent Diskus, Advair Diskus, and Foradil Information (Long Acting Beta Agonists) - Drug information". FDA (2006-03-03).
52. ^ Salpeter S, Buckley N, Ormiston T, Salpeter E (2006). "Meta-analysis: effect of long-acting beta-agonists on severe asthma exacerbations and asthma-related deaths". Ann Intern Med 144 (12): 904–12. PMID 16754916.
53. ^ Ramanujan, Krishna (2006-06-09). "Common asthma inhalers cause up to 80 percent of asthma-related deaths, Cornell and Stanford researchers assert". Cornell Chronicle Online. Cornell News Service. Retrieved on 2006-09-23.
54. ^ Rodrigo GJ, Rodrigo C, Hall JB (2004). "Acute asthma in adults: a review". Chest 125 (3): 1081–102. doi:10.1378/chest.125.3.1081. PMID 15006973.
55. ^ Rodrigo G (2005). "Comparison of inhaled fluticasone with intravenous hydrocortisone in the treatment of adult acute asthma". Am J Respir Crit Care Med 171 (11): 1231–6. doi:10.1164/rccm.200410-1415OC. PMID 15764724.
56. ^ Blanc PD, Trupin L, Earnest G, Katz PP, Yelin EH, Eisner MD (2001). "Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis : data from a population-based survey". Chest 120 (5): 1461–7. doi:10.1378/chest.120.5.1461. PMID 11713120.
57. ^ Shenfield G, Lim E, Allen H (2002). "Survey of the use of complementary medicines and therapies in children with asthma". J Paediatr Child Health 38 (3): 252–7. doi:10.1046/j.1440-1754.2002.00770.x. PMID 12047692.
58. ^ McCarney RW, Brinkhaus B, Lasserson TJ, Linde K (2004). "Acupuncture for chronic asthma". Cochrane Database Syst Rev (1): CD000008. doi:10.1002/14651858.CD000008.pub2. PMID 14973944.
59. ^ Blackhall K, Appleton S, Cates CJ (2003). "Ionisers for chronic asthma". Cochrane Database Syst Rev (3): CD002986. doi:10.1002/14651858.CD002986. PMID 12917939.
60. ^ PC Gøtzsche, HK Johansen (2008). "House dust mite control measures for asthma". Cochrane Database Syst Rev (2): CD001187. doi:10.1002/14651858.CD001187.pub3.
61. ^ Hondras MA, Linde K, Jones AP (2005). "Manual therapy for asthma". Cochrane Database Syst Rev (2): CD001002. doi:10.1002/14651858.CD001002.pub2. PMID 15846609.
62. ^ Reilly D, Taylor MA, Beattie NG, et al (1994). "Is evidence for homoeopathy reproducible?". Lancet 344 (8937): 1601–6. doi:10.1016/S0140-6736(94)90407-3. PMID 7983994.
63. ^ White A, Slade P, Hunt C, Hart A, Ernst E (2003). "Individualised homeopathy as an adjunct in the treatment of childhood asthma: a randomised placebo controlled trial". Thorax 58 (4): 317–21. doi:10.1136/thorax.58.4.317. PMID 12668794.
64. ^ Nagendra HR, Nagarathna R (1986). "An integrated approach of yoga therapy for bronchial asthma: a 3-54-month prospective study". J Asthma 23 (3): 123–37. doi:10.3109/02770908609077486. PMID 3745111.
65. ^ Manocha R, Marks GB, Kenchington P, Peters D, Salome CM (2002). "Sahaja yoga in the management of moderate to severe asthma: a randomised controlled trial". Thorax 57 (2): 110–5. doi:10.1136/thorax.57.2.110. PMID 11828038.
66. ^ Nagourney E (2007-11-13). "For the Record: In Tests of Inhalers, Results May Depend on Who Pays", The New York Times. Retrieved on 2 December 2007.
67. ^ Nieto A, Mazon A, Pamies R, et al (2007). "Adverse effects of inhaled corticosteroids in funded and nonfunded studies". Arch. Intern. Med. 167 (19): 2047–53. doi:10.1001/archinte.167.19.2047. PMID 17954797.
68. ^ Beckett PA, Howarth PH (2003). "Pharmacotherapy and airway remodelling in asthma?". Thorax 58 (2): 163–74. doi:10.1136/thorax.58.2.163. PMID 12554904.
69. ^ Masoli, Matthew; Denise Fabian, Shaun Holt, Richard Beasley (2004). "Global Burden of Asthma(TM)" (PDF). Retrieved on 2008-08-08.
70. ^ a b World Health Organization. "Bronchial asthma: scope of the problem". Retrieved on 2005-08-23.
71. ^ World Health Organization. "WHO: Asthma". Retrieved on 2007-12-29.
72. ^ Lara M, Akinbami L, Flores G,Morgenstern H (2006). "Heterogeneity of childhood asthma among Hispanic children: Puerto Rican children bear a disproportionate burden". Pediatrics 117 (1): 43–53. doi:10.1542/peds.2004-1714. PMID 16396859.
73. ^ Davis AM, Kreutzer R, Lipsett M, King G,Shaikh N (2006). "Asthma prevalence in Hispanic and Asian American ethnic subgroups: results from the California Healthy Kids Survey". Pediatrics 118 (2): e363–70. doi:10.1542/peds.2005-2687. PMID 16882779.
74. ^ Johnson DB, Oyama N, LeMarchand L,Wilkens L (2004). "Native Hawaiians mortality, morbidity, and lifestyle: comparing data from 1982, 1990, and 2000". Pac Health Dialog 11 (2): 120–30. PMID 16281689.
75. ^ Naqvi M, Thyne S, Choudhry S "et al." (2007). "Ethnic-specific differences in bronchodilator responsiveness among african americans, puerto ricans, and mexicans with asthma". J Asthma 44 (8): 639–48. doi:10.1080/02770900701554441. PMID 17943575.
76. ^ Burchard EG, Avila PC, Nazario S "et al." (2004). "Lower bronchodilator responsiveness in Puerto Rican than in Mexican subjects with asthma". Am J Respir Crit Care Med 169 (3): 386–92. doi:10.1164/rccm.200309-1293OC. PMID 14617512.
77. ^ Gold DR,Acevedo-Garcia D (2005). "Immigration to the United States and acculturation as risk factors for asthma and allergy". J Allergy Clin Immunol 116 (1): 38–41. doi:10.1016/j.jaci.2005.04.033. PMID 15990770.
78. ^ Eldeirawi KM,Persky VW (2006). "Associations of acculturation and country of birth with asthma and wheezing in Mexican American youths". J Asthma 43 (4): 279–86. doi:10.1080/0277090060022869. PMID 16809241.
79. ^ "Patient/Public Education: Fast Facts - Asthma Demographics/Statistics". American Academy of Allergy Asthma & Immunology. Retrieved on 2006-05-02.
80. ^ National Heart, Lung, and Blood Institute (May 2004). Morbidity & Mortality: 2004 Chart Book On Cardiovascular, Lung, and Blood Diseases, National Institutes of Health.
81. ^ National Center for Health Statistics (7 April 2006). "Asthma Prevalence, Health Care Use and Mortality, 2002". Centers for Disease Control and Prevention.
82. ^ a b Weiler JM, Layton T, Hunt M (1998). "Asthma in United States Olympic athletes who participated in the 1996 Summer Games". J. Allergy Clin. Immunol. 102 (5): 722–6. doi:10.1016/S0091-6749(98)70010-7. PMID 9819287.
83. ^ Helenius I, Haahtela T (2000). "Allergy and asthma in elite summer sport athletes". J. Allergy Clin. Immunol. 106 (3): 444–52. doi:10.1067/mai.2000.107749. PMID 10984362.
84. ^ Opolski M, Wilson I (September 2005). "Asthma and depression: a pragmatic review of the literature and recommendations for future research". Clin Pract Epidemol Ment Health 1: 18. doi:10.1186/1745-0179-1-18. PMID 16185365.
http://en.wikipedia.org/wiki/Asthma
Senin, 17 November 2008
Diabetes
Diabetes is a chronic (lifelong) disease marked by high levels of sugar in the blood.
Causes
Insulin is a hormone produced by the pancreas to control blood sugar. Diabetes can be caused by too little insulin, resistance to insulin, or both.
To understand diabetes, it is important to first understand the normal process by which food is broken down and used by the body for energy. Several things happen when food is digested:
* A sugar called glucose enters the bloodstream. Glucose is a source of fuel for the body.
* An organ called the pancreas makes insulin. The role of insulin is to move glucose from the bloodstream into muscle, fat, and liver cells, where it can be used as fuel.
People with diabetes have high blood sugar. This is because:
* Their pancreas does not make enough insulin
* Their muscle, fat, and liver cells do not respond to insulin normally
* Both of the above
There are three major types of diabetes:
* Type 1 diabetes is usually diagnosed in childhood. Many patients are diagnosed when they are older than age 20. In this disease, the body makes little or no insulin. Daily injections of insulin are needed. The exact cause is unknown. Genetics, viruses, and autoimmune problems may play a role.
* Type 2 diabetes is far more common than type 1. It makes up most of diabetes cases. It usually occurs in adulthood, but young people are increasingly being diagnosed with this disease. The pancreas does not make enough insulin to keep blood glucose levels normal, often because the body does not respond well to insulin. Many people with type 2 diabetes do not know they have it, although it is a serious condition. Type 2 diabetes is becoming more common due to increasing obesity and failure to exercise.
* Gestational diabetes is high blood glucose that develops at any time during pregnancy in a woman who does not have diabetes.
Diabetes affects more than 20 million Americans. Over 40 million Americans have prediabetes.
There are many risk factors for type 2 diabetes, including:
* Age over 45 years
* A parent, brother, or sister with diabetes
* Gestational diabetes or delivering a baby weighing more than 9 pounds
* Heart disease
* High blood cholesterol level
* Obesity
* Not getting enough exercise
* Polycystic ovary disease (in women)
* Previous impaired glucose tolerance
* Some ethnic groups (particularly African Americans, Native Americans, Asians, Pacific Islanders, and Hispanic Americans)
Back to TopSymptoms
High blood levels of glucose can cause several problems, including:
* Blurry vision
* Excessive thirst
* Fatigue
* Frequent urination
* Hunger
* Weight loss
However, because type 2 diabetes develops slowly, some people with high blood sugar experience no symptoms at all.
Symptoms of type 1 diabetes:
* Fatigue
* Increased thirst
* Increased urination
* Nausea
* Vomiting
* Weight loss in spite of increased appetite
Patients with type 1 diabetes usually develop symptoms over a short period of time. The condition is often diagnosed in an emergency setting.
Symptoms of type 2 diabetes:
* Blurred vision
* Fatigue
* Increased appetite
* Increased thirst
* Increased urination
Back to TopExams and Tests
A urine analysis may be used to look for glucose and ketones from the breakdown of fat. However, a urine test alone does not diagnose diabetes.
The following blood glucose tests are used to diagnose diabetes:
* Fasting blood glucose level -- diabetes is diagnosed if higher than 126 mg/dL on two occasions. Levels between 100 and 126 mg/dL are referred to as impaired fasting glucose or pre-diabetes. These levels are considered to be risk factors for type 2 diabetes and its complications.
* Oral glucose tolerance test -- diabetes is diagnosed if glucose level is higher than 200 mg/dL after 2 hours. (This test is used more for type 2 diabetes.)
* Random (non-fasting) blood glucose level -- diabetes is suspected if higher than 200 mg/dL and accompanied by the classic diabetes symptoms of increased thirst, urination, and fatigue. (This test must be confirmed with a fasting blood glucose test.)
You need your hemoglobin A1c (HbA1c) level checked every 3 - 6 months. The HbA1c is a measure of average blood glucose during the previous 2 - 3 months. It is a very helpful way to determine how well treatment is working.
Back to TopTreatment
The immediate goals are to treat diabetic ketoacidosis and high blood glucose levels. Because type 1 diabetes can start suddenly and have severe symptoms, people who are newly diagnosed may need to go to the hospital.
The long-term goals of treatment are to:
* Prolong life
* Reduce symptoms
* Prevent diabetes-related complications such as blindness, heart disease, kidney failure, and amputation of limbs
These goals are accomplished through:
* Careful self testing of blood glucose levels
* Education
* Exercise
* Foot care
* Meal planning and weight control
* Medication or insulin use
There is no cure for diabetes. Treatment involves medicines, diet, and exercise to control blood sugar and prevent symptoms.
LEARN THESE SKILLS
Basic diabetes management skills will help prevent the need for emergency care. These skills include:
* How to recognize and treat low blood sugar (hypoglycemia) and high blood sugar (hyperglycemia)
* What to eat and when
* How to take insulin or oral medication
* How to test and record blood glucose
* How to test urine for ketones (type 1 diabetes only)
* How to adjust insulin or food intake when changing exercise and eating habits
* How to handle sick days
* Where to buy diabetes supplies and how to store them
After you learn the basics of diabetes care, learn how the disease can cause long-term health problems and the best ways to prevent these problems. Review and update your knowledge, because new research and improved ways to treat diabetes are constantly being developed.
SELF-TESTING
If you have diabetes, your doctor may tell you to regularly check your blood sugar levels at home. There are a number of devices available, and they use only a drop of blood. Self-monitoring tells you how well diet, medication, and exercise are working together to control your diabetes. It can help your doctor prevent complications.
The American Diabetes Association recommends keeping blood sugar levels in the range of:
* 80 - 120 mg/dL before meals
* 100 - 140 mg/dL at bedtime
Your doctor may adjust this depending on your circumstances.
WHAT TO EAT
You should work closely with your health care provider to learn how much fat, protein, and carbohydrates you need in your diet. A registered dietician can help you plan your dietary needs.
People with type 1 diabetes should eat at about the same times each day and try to be consistent with the types of food they choose. This helps to prevent blood sugar from becoming extremely high or low.
People with type 2 diabetes should follow a well-balanced and low-fat diet.
See: Diabetes diet
HOW TO TAKE MEDICATION
Medications to treat diabetes include insulin and glucose-lowering pills called oral hypoglycemic drugs.
People with type 1 diabetes cannot make their own insulin. They need daily insulin injections. Insulin does not come in pill form. Injections are generally needed one to four times per day. Some people use an insulin pump. It is worn at all times and delivers a steady flow of insulin throughout the day. Other people may use a new type of inhaled insulin.
Unlike type 1 diabetes, type 2 diabetes may respond to treatment with exercise, diet, and medicines taken by mouth. There are several types of medicines used to lower blood glucose in type 2 diabetes.
Medications may be switched to insulin during pregnancy and while breastfeeding.
Gestational diabetes is treated with changes in diet.
EXERCISE
Regular exercise is especially important for people with diabetes. It helps with blood sugar control, weight loss, and high blood pressure. People with diabetes who exercise are less likely to experience a heart attack or stroke than those who do not exercise regularly.
Here are some exercise considerations:
* Always check with your doctor before starting a new exercise program.
* Ask your doctor or nurse if you have the right footwear.
* Choose an enjoyable physical activity that is appropriate for your current fitness level.
* Exercise every day, and at the same time of day, if possible.
* Monitor blood glucose levels before and after exercise.
* Carry food that contains a fast-acting carbohydrate in case you become hypoglycemic during or after exercise.
* Carry a diabetes identification card and a cell phone in case of emergency.
* Drink extra fluids that do not contain sugar before, during, and after exercise.
You may need to change your diet or medication dose if you change your exercise intensity or duration to keep blood sugar levels from going too high or low.
FOOT CARE
People with diabetes are more likely to have foot problems. Diabetes can damage blood vessels and nerves and decrease the body's ability to fight infection. You may not notice a foot injury until an infection develops. Death of skin and other tissue can occur.
If left untreated, the affected foot may need to be amputated. Diabetes is the most common condition leading to amputations.
To prevent injury to the feet, check and care for your feet every day.
http://health.nytimes.com/health/guides/disease/diabetes/overview.html
Causes
Insulin is a hormone produced by the pancreas to control blood sugar. Diabetes can be caused by too little insulin, resistance to insulin, or both.
To understand diabetes, it is important to first understand the normal process by which food is broken down and used by the body for energy. Several things happen when food is digested:
* A sugar called glucose enters the bloodstream. Glucose is a source of fuel for the body.
* An organ called the pancreas makes insulin. The role of insulin is to move glucose from the bloodstream into muscle, fat, and liver cells, where it can be used as fuel.
People with diabetes have high blood sugar. This is because:
* Their pancreas does not make enough insulin
* Their muscle, fat, and liver cells do not respond to insulin normally
* Both of the above
There are three major types of diabetes:
* Type 1 diabetes is usually diagnosed in childhood. Many patients are diagnosed when they are older than age 20. In this disease, the body makes little or no insulin. Daily injections of insulin are needed. The exact cause is unknown. Genetics, viruses, and autoimmune problems may play a role.
* Type 2 diabetes is far more common than type 1. It makes up most of diabetes cases. It usually occurs in adulthood, but young people are increasingly being diagnosed with this disease. The pancreas does not make enough insulin to keep blood glucose levels normal, often because the body does not respond well to insulin. Many people with type 2 diabetes do not know they have it, although it is a serious condition. Type 2 diabetes is becoming more common due to increasing obesity and failure to exercise.
* Gestational diabetes is high blood glucose that develops at any time during pregnancy in a woman who does not have diabetes.
Diabetes affects more than 20 million Americans. Over 40 million Americans have prediabetes.
There are many risk factors for type 2 diabetes, including:
* Age over 45 years
* A parent, brother, or sister with diabetes
* Gestational diabetes or delivering a baby weighing more than 9 pounds
* Heart disease
* High blood cholesterol level
* Obesity
* Not getting enough exercise
* Polycystic ovary disease (in women)
* Previous impaired glucose tolerance
* Some ethnic groups (particularly African Americans, Native Americans, Asians, Pacific Islanders, and Hispanic Americans)
Back to TopSymptoms
High blood levels of glucose can cause several problems, including:
* Blurry vision
* Excessive thirst
* Fatigue
* Frequent urination
* Hunger
* Weight loss
However, because type 2 diabetes develops slowly, some people with high blood sugar experience no symptoms at all.
Symptoms of type 1 diabetes:
* Fatigue
* Increased thirst
* Increased urination
* Nausea
* Vomiting
* Weight loss in spite of increased appetite
Patients with type 1 diabetes usually develop symptoms over a short period of time. The condition is often diagnosed in an emergency setting.
Symptoms of type 2 diabetes:
* Blurred vision
* Fatigue
* Increased appetite
* Increased thirst
* Increased urination
Back to TopExams and Tests
A urine analysis may be used to look for glucose and ketones from the breakdown of fat. However, a urine test alone does not diagnose diabetes.
The following blood glucose tests are used to diagnose diabetes:
* Fasting blood glucose level -- diabetes is diagnosed if higher than 126 mg/dL on two occasions. Levels between 100 and 126 mg/dL are referred to as impaired fasting glucose or pre-diabetes. These levels are considered to be risk factors for type 2 diabetes and its complications.
* Oral glucose tolerance test -- diabetes is diagnosed if glucose level is higher than 200 mg/dL after 2 hours. (This test is used more for type 2 diabetes.)
* Random (non-fasting) blood glucose level -- diabetes is suspected if higher than 200 mg/dL and accompanied by the classic diabetes symptoms of increased thirst, urination, and fatigue. (This test must be confirmed with a fasting blood glucose test.)
You need your hemoglobin A1c (HbA1c) level checked every 3 - 6 months. The HbA1c is a measure of average blood glucose during the previous 2 - 3 months. It is a very helpful way to determine how well treatment is working.
Back to TopTreatment
The immediate goals are to treat diabetic ketoacidosis and high blood glucose levels. Because type 1 diabetes can start suddenly and have severe symptoms, people who are newly diagnosed may need to go to the hospital.
The long-term goals of treatment are to:
* Prolong life
* Reduce symptoms
* Prevent diabetes-related complications such as blindness, heart disease, kidney failure, and amputation of limbs
These goals are accomplished through:
* Careful self testing of blood glucose levels
* Education
* Exercise
* Foot care
* Meal planning and weight control
* Medication or insulin use
There is no cure for diabetes. Treatment involves medicines, diet, and exercise to control blood sugar and prevent symptoms.
LEARN THESE SKILLS
Basic diabetes management skills will help prevent the need for emergency care. These skills include:
* How to recognize and treat low blood sugar (hypoglycemia) and high blood sugar (hyperglycemia)
* What to eat and when
* How to take insulin or oral medication
* How to test and record blood glucose
* How to test urine for ketones (type 1 diabetes only)
* How to adjust insulin or food intake when changing exercise and eating habits
* How to handle sick days
* Where to buy diabetes supplies and how to store them
After you learn the basics of diabetes care, learn how the disease can cause long-term health problems and the best ways to prevent these problems. Review and update your knowledge, because new research and improved ways to treat diabetes are constantly being developed.
SELF-TESTING
If you have diabetes, your doctor may tell you to regularly check your blood sugar levels at home. There are a number of devices available, and they use only a drop of blood. Self-monitoring tells you how well diet, medication, and exercise are working together to control your diabetes. It can help your doctor prevent complications.
The American Diabetes Association recommends keeping blood sugar levels in the range of:
* 80 - 120 mg/dL before meals
* 100 - 140 mg/dL at bedtime
Your doctor may adjust this depending on your circumstances.
WHAT TO EAT
You should work closely with your health care provider to learn how much fat, protein, and carbohydrates you need in your diet. A registered dietician can help you plan your dietary needs.
People with type 1 diabetes should eat at about the same times each day and try to be consistent with the types of food they choose. This helps to prevent blood sugar from becoming extremely high or low.
People with type 2 diabetes should follow a well-balanced and low-fat diet.
See: Diabetes diet
HOW TO TAKE MEDICATION
Medications to treat diabetes include insulin and glucose-lowering pills called oral hypoglycemic drugs.
People with type 1 diabetes cannot make their own insulin. They need daily insulin injections. Insulin does not come in pill form. Injections are generally needed one to four times per day. Some people use an insulin pump. It is worn at all times and delivers a steady flow of insulin throughout the day. Other people may use a new type of inhaled insulin.
Unlike type 1 diabetes, type 2 diabetes may respond to treatment with exercise, diet, and medicines taken by mouth. There are several types of medicines used to lower blood glucose in type 2 diabetes.
Medications may be switched to insulin during pregnancy and while breastfeeding.
Gestational diabetes is treated with changes in diet.
EXERCISE
Regular exercise is especially important for people with diabetes. It helps with blood sugar control, weight loss, and high blood pressure. People with diabetes who exercise are less likely to experience a heart attack or stroke than those who do not exercise regularly.
Here are some exercise considerations:
* Always check with your doctor before starting a new exercise program.
* Ask your doctor or nurse if you have the right footwear.
* Choose an enjoyable physical activity that is appropriate for your current fitness level.
* Exercise every day, and at the same time of day, if possible.
* Monitor blood glucose levels before and after exercise.
* Carry food that contains a fast-acting carbohydrate in case you become hypoglycemic during or after exercise.
* Carry a diabetes identification card and a cell phone in case of emergency.
* Drink extra fluids that do not contain sugar before, during, and after exercise.
You may need to change your diet or medication dose if you change your exercise intensity or duration to keep blood sugar levels from going too high or low.
FOOT CARE
People with diabetes are more likely to have foot problems. Diabetes can damage blood vessels and nerves and decrease the body's ability to fight infection. You may not notice a foot injury until an infection develops. Death of skin and other tissue can occur.
If left untreated, the affected foot may need to be amputated. Diabetes is the most common condition leading to amputations.
To prevent injury to the feet, check and care for your feet every day.
http://health.nytimes.com/health/guides/disease/diabetes/overview.html
Enzyme
Enzyme: A protein (or protein-based molecule) that speeds up a chemical reaction in a living organism. An enzyme acts as catalyst for specific chemical reactions, converting a specific set of reactants (called substrates) into specific products. Without enzymes, life as we know it would not exist.
Enzymes are nonetheless subject to error. In 1902 Sir Archibald Garrod was the first to attribute a disease to an enzyme defect, to what Garrod called an "inborn error of metabolism." Today, newborns are routinely screened for certain enzyme defects such as PKU (phenylketonuria) and galactosemia, an error in the handling (metabolism) of the sugar galactose.
http://www.medterms.com
Enzymes are nonetheless subject to error. In 1902 Sir Archibald Garrod was the first to attribute a disease to an enzyme defect, to what Garrod called an "inborn error of metabolism." Today, newborns are routinely screened for certain enzyme defects such as PKU (phenylketonuria) and galactosemia, an error in the handling (metabolism) of the sugar galactose.
http://www.medterms.com
Sabtu, 15 November 2008
Diet Golongan Darah AB
Golongan darah AB, adalah golongan darah terakhir, yang diketahui 1000 tahun SM. Dr. Peter J.D'Adamo mengatakan saat itu leluhur kita mulai mengubah gaya hidupnya ke arah modern. Jenis makanan yang disarankan adalah perpaduan antara makanan yang diperbolehkan dikonsumsi oleh para pemilik golongan darah A dan B.
Sebenarnya, jenis makanan golongan darah A dan B sangat bertolak belakang. Orang bergolongan darah B disarankan untuk mengonsumsi berbagai jenis makanan, sedangkan pemilik golongan darah A disarankan hanya mengonsumsi tumbuh-tumbuhan, alias berpola makan vegetarian. Untuk itu Dr. Peter J.D'Adamo menganjurkan agar pemilik golongan darah AB lebih banyak melakukan diet vegetarian tapi tetap mengkonsumsi produk susu pada saat tertentu. Terutama saat berolahraga.Golongan darah AB sendiri sebagai golongan darah yang masih cukup jarang dijumpai secara keseluruhan lebih stabil dari golongan darah A dan B karena dapat memiliki sebagian besar keuntungan dan intoleransi dari golongan darah A dan B. Golongan darah ini juga dinilai memiliki sistem daya tahan tubuh paling baik dibandingkan golongan darah lain, namun di sisi lain juga rentan terhadap penyakit-penyakit serius seperti penyakit jantung, saraf dan kanker.
Pada golongan darah AB juga dianjurkan olahraga yang berkaitan dengan relaksasi dan meditasi. Makanan-makanan yang dianjurkan untuk golongan darah ini antara lain adalah makanan laut, produk susu, beberapa jenis kacang-kacangan dan yang tidak dianjurkan adalah seperti daging merah, kacang merah dan jagung.
Berkaitan dengan nutrisi yang dibutuhkan ini, tubuh sebenarnya memerlukan makanan-makanan organik termasuk bahan nabati organik dengan kelengkapan gizi yang sesuai dengan golongan darah tertentu, dan ini menyangkut semua kebutuhan prebiotik dan probiotik serta enzim-enzim, vitamin, mineral serta asam amino esensial untuk mengoptimalkan fungsi tubuh.
Diet Golongan Darah O
Di dalam bukunya Dr. Peter J.D'Adamo mengatakan bahwa berdasarkan sejarah evolusi sekitar 50.000 hingga 25.000 tahun SM, leluhur manusia memiliki golongan darah yang sama, yakni O. Mereka adalah para pemburu sejati yang selalu mengkonsumsi daging hasil buruan. Untuk itulah Dr. Peter J.D'Adamo menyarankan agar pemilik golongan darah O lebih banyak mengonsumsi makanan berprotein tinggi, mengikuti diet rendah karbohidrat dengan banyak makan daging atau ikan tapi menghindari produk susu dan gandum.
Pemilik golongan darah O bebas mengonsumsi daging dan ikan yang dicampur minyak zaitun. Selain itu, bebas mengonsumsi telur, kacang, tetapi sebaiknya membatasi buah. Sementara makanan yang harus benar-benar dihindari adalah sereal, berbagai jenis pasta dan nasi. Untuk mendapatkan stamina tubuh yang maksimal Dr. Peter J.D'Adamo menganjurkan untuk melakukan olahraga erobik yang gerakannya mirip gerakan para pemburu.
Ciri khas golongan darah O
• Memiliki sistem kekebalan tubuh yang lebih tinggi dibandingkan tipe darah lain.
• Mudah beradaptasi dengan berbagai makanan pada lingkungan yang ditempati.
• Untuk mengatasi stres disarankan melakukan erobik.
• Dianjurkan untuk mengonsumsi makanan tinggi protein dan rendah karbohidrat, seperti daging, buah, ikan, sayuran.
Bila makanan yang dikonsumsi tidak sesuai, maka Anda berisiko terkena penyakit yang disebabkan oleh radang dan kerusakan organ seperti arthritis
Menu diet yang dianjurkan:
Sarapan : 2 potong roti bakar lapis mentega + Satu buah Pisang
Snack siang : Teh herbal
Makan Siang: Sepotong daging panggang + Salad bayam + Apel
Snack Sore : Sepotong kue
Makan Malam : Sepotong daging domba dan asparagus yang direbus + Kentang rebus + Buah + Teh herbal
Diet untuk Golongan Darah B
Ciri khas golongan darah B:
• Dianjurkan untuk melakukan diet dengan berbagai variasi makanan golongan darah, namun membatasi asupan daging.
• Disarankan mengonsumsi makanan dan minuman berbahan dasar susu untuk meningkatkan sistem kekebalan tubuh.
• Olahraga yang cocok dilakukan adalah renang, tenis, jalan kaki dan meditasi.
• Untuk mengatasi stres, sebaiknya mencari kegiatan rutin berupa hobi dan kreativitas.
Orang bergolongan darah B disarankan untuk mengonsumsi berbagai jenis makanan, sedangkan pemilik golongan darah A disarankan hanya mengonsumsi tumbuh-tumbuhan, alias berpola makan vegetarian. Untuk itu Dr. Peter J.D'Adamo menganjurkan agar pemilik golongan darah AB lebih banyak melakukan diet vegetarian tapi tetap mengkonsumsi produk susu pada saat tertentu. Terutama saat berolahraga.
Karakteristik pemilik golongan darah B adalah:
• Memiliki jalur pencernaan yang sensitif.
• Disarankan untuk mengkonsumsi makanan dalam jumlah sedikit, namun kekerapan makan lebih padat (lebih sering makan dengan porsi kecil)
Untuk lebih berenergi biasakan berolahraga di pagi hari.
Menu Diet yang dianjurkan
• Sarapan : Air putih dicampur jeruk nipis + Juice Anggur + Roti dua potong + Satu potong keju.
• Snack siang : Yogurt
• Makan Siang : Dada Ayam 4 irisan + Salad + 2 buah Plum + Teh Herbal
• Snack Sore : Cheesecake + Teh Herbal
Makan Malam : Omelet + Salad Buah + Kopi
http://dietsehatalami.com/
Diet Golongan Darah A
Dr. Peter J.D'Adamo dalam bukunya, Eat Right For Your Type menyebutkan pada 15.000 SM golongan darah A ditemukan. Pada masa itu, leluhur kita adalah pemburu yang mulai membentuk komunitas dan bertempat tinggal tetap.
Mereka mulai bercocok tanam dan mengonsumsi sayur-sayuran dan hanya makan daging dalam jumlah sangat sedikit. Untuk itulah Dr. Peter J.D'Adamo menyarankan agar pemilik golongan darah A menjalani diet vegetarian.
Ciri khas Golongan darah A
• Memiliki sistem pencernaan yang relatif sensitif.
• Harus menghindari makanan yang terbuat dari produk susu dan daging
• Dianjurkan menjadi vegetarian atau mengonsumsi makanan berkadar karbohidrat tinggi, namun rendah lemak.
• Meminimalisasi stres dengan meditasi, atau olahraga non kompetitif dan cukup istirahat
Menu diet yang dianjurkan
• Sarapan : Air putih dicampur jeruk nipis + Oatmel
• Snack Siang : Juice Anggur / Kopi
• Makan Siang : Salad + Roti Gandum satu potong + Teh Herbal
• Snack Sore : Kue Beras dua potong + Teh Hijau
( Bila perlu boleh makan Malam : Pasta tanpa daging + Brokoli + Yoghurt + Teh Herbal )
Langganan:
Postingan (Atom)
