Allergy causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Allergy causation can categorized as host or environmental factors. Biological factors are strongly familial related. Environmental factors very largely on the type of living environment. Allergies are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations.
Causes
Allergy causation can be placed in two general categories, namely host and environmental factors. Host factors include heredity, sex, race and age, with heredity being by far the most important. There are recent increases in the incidence of allergic disorders, however, that cannot be explained by genetic factors alone. The four main candidate environmental factors are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.[1]
Genetic Basis
Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins.[2] Allergic parents are more likely to have allergic children,[3] and their allergies are likely to be stronger than those from non-allergic parents. However some allergies are not consistent along genealogies; parents who are allergic to peanuts, may have children who are allergic to ragweed, or siblings that are allergic to different things. It seems that the likelihood of developing allergies is inherited and due to some irregularity in the way the immune system works, but the specific allergen, which causes the development of an allergy, is not.[3]
The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk.[4] Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.[4] The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.[5] Overall, boys have a higher risk of developing allergy than girls,[3] although for some diseases, namely asthma in young adults, females are more likely to be affected.[6] Sex differences tend to decrease in adulthood.[3] Ethnicity may play a role in some allergies, however racial factors have been difficult to separate from environmental influences and changes due to migration.[3] Interestingly, with regards to asthma, it has been suggested that different genetic loci are responsible for asthma in people of Caucasian, Hispanic, Asian, and African origins.[7]
Environmental Factors
International differences have been associated with the number of individuals within a population that suffer from allergy. Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations, although these differences are becoming less defined.[8]
Exposure to allergens, especially in early life, is an important risk factor for allergy. Alterations in exposure to microorganisms is the most plausible explanation, at present, for the increase in atopic allergy.[1] Since children that live in large families or overcrowded households, or attend day care, have a reduced incidence of allergic disease, a relationship has been proposed between exposures to bacteria and viruses during childhood, and protection against the development of allergy, which has been called – the "hygiene hypothesis".[8] Exposure to endotoxin and other components of bacteria may reduce atopic diseases.[9] Endotoxin exposure reduces release of inflammatory cytokines such as TNF-α, IFNγ, interleukin-10, and interleukin-12 from white blood cells (leukocytes) that circulate in the blood.[10] Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought to be involved in these processes.[11]
Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine chlorination and purification of drinking water supplies.[12] Recent research has shown that some common parasites, such as intestinal worms (e.g. hookworms), secrete chemicals into the gut wall (and hence the bloodstream) that suppress the immune system and prevent the body from attacking the parasite.[13] This gives rise to a new slant on the hygiene hypothesis theory — that co-evolution of man and parasites has led to an immune system that only functions correctly in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive.[14] In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants.[15] However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms.[8] Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.[16] It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work.[16] For more information on this topic, see Helminthic therapy.
Drug side effect
- Agalsidase beta
- Barium Sulfate
- Ceftazidime
- Cidofovir
- Dalfampridine
- Dexpanthenol
- Dipivefrine
- Efavirenz
- Filgastrim
- Gallium Citrate Ga 67
- Hydrocodone bitartrate and acetaminophen
- Hydroxocobalamin
- Idelalisib
- laronidase
- Natamycin
- Tiagabine
References
- ↑ 1.0 1.1 Janeway, Charles (2001). Immunobiology; Fifth Edition. New York and London: Garland Science. pp. e–book. ISBN 0-8153-4101-6. Unknown parameter
|coauthors=ignored (help). - ↑ Galli SJ (2000). "Allergy". Curr. Biol. 10 (3): R93–5. PMID 10679332.
- ↑ 3.0 3.1 3.2 3.3 3.4 De Swert LF (1999). "Risk factors for allergy". Eur. J. Pediatr. 158 (2): 89–94. PMID 10048601.
- ↑ 4.0 4.1 Croner S (1992). "Prediction and detection of allergy development: influence of genetic and environmental factors". J. Pediatr. 121 (5 Pt 2): S58–63. PMID 1447635.
- ↑ Jarvis D, Burney P (1997) Epidemiology of atopy and atopic disease In: Kay AB (ed) Allergy and allergic diseases, vol 2. Blackwell Science London, pp 1208–1224
- ↑ Anderson HR, Pottier AC, Strachan DP (1992). "Asthma from birth to age 23: incidence and relation to prior and concurrent atopic disease". Thorax. 47 (7): 537–42. PMID 1412098.
- ↑ Barnes KC, Grant AV, Hansel NN, Gao P, Dunston GM (2007). "African Americans with asthma: genetic insights". Proc Am Thorac Soc. 4 (1): 58–68. doi:10.1513/pats.200607-146JG. PMID 17202293.
- ↑ 8.0 8.1 8.2 Cooper PJ (2004). "Intestinal worms and human allergy". Parasite Immunol. 26 (11–12): 455–67. doi:10.1111/j.0141-9838.2004.00728.x. PMID 15771681.
- ↑ von Mutius E (2002). "Environmental factors influencing the development and progression of pediatric asthma". J. Allergy Clin. Immunol. 109 (6 Suppl): S525–32. PMID 12063508.
- ↑ Braun-Fahrländer C, Riedler J, Herz U; et al. (2002). "Environmental exposure to endotoxin and its relation to asthma in school-age children". N. Engl. J. Med. 347 (12): 869–77. doi:10.1056/NEJMoa020057. PMID 12239255.
- ↑ Garn H, Renz H (2007). "Epidemiological and immunological evidence for the hygiene hypothesis". Immunobiology. 212 (6): 441–52. doi:10.1016/j.imbio.2007.03.006. PMID 17544829.
- ↑ Macpherson CN, Gottstein B, Geerts S (2000). "Parasitic food-borne and water-borne zoonoses". Rev. - Off. Int. Epizoot. 19 (1): 240–58. PMID 11189719.
- ↑ Carvalho EM, Bastos LS, Araújo MI (2006). "Worms and allergy". Parasite Immunol. 28 (10): 525–34. doi:10.1111/j.1365-3024.2006.00894.x. PMID 16965288.
- ↑ Yazdanbakhsh M, Kremsner PG, van Ree R (2002). "Allergy, parasites, and the hygiene hypothesis". Science. 296 (5567): 490–4. doi:10.1126/science.296.5567.490. PMID 11964470.
- ↑ Emanuelsson C, Spangfort MD (2007). "Allergens as eukaryotic proteins lacking bacterial homologues". Mol. Immunol. 44 (12): 3256–60. doi:10.1016/j.molimm.2007.01.019. PMID 17382394.
- ↑ 16.0 16.1 Falcone FH, Pritchard DI (2005). "Parasite role reversal: worms on trial". Trends Parasitol. 21 (4): 157–60. doi:10.1016/j.pt.2005.02.002. PMID 15780835.