Celiac disease risk factors: Difference between revisions
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===Risk modifiers=== | |||
There are various theories as to what determines whether a genetically susceptible individual will go on to develop coeliac disease. Major theories include infection by [[rotavirus]]<ref>{{cite journal |author=Stene L, Honeyman M, Hoffenberg E, Haas J, Sokol R, Emery L, Taki I, Norris J, Erlich H, Eisenbarth G, Rewers M |title=Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: a longitudinal study |journal=Am J Gastroenterol |volume=101 |issue=10 |pages=2333–40 |year=2006 |pmid=17032199}}</ref> or human intestinal [[adenovirus]].<ref>{{cite journal | author = Kagnoff M, Paterson Y, Kumar P, Kasarda D, Carbone F, Unsworth D, Austin R | title = Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease | journal = Gut | volume = 28 | issue = 8 | pages = 995–1001 | year = 1987 | id = PMID 2822550}}</ref> Some research has suggested that smoking is protective against adult onset coeliac disease.<ref>{{cite journal | author = Suman S, Williams E, Thomas P, Surgenor S, Snook J | title = Is the risk of adult coeliac disease causally related to cigarette exposure? | journal = Eur J Gastroenterol Hepatol | volume = 15 | issue = 9 | pages = 995–1000 | year = 2003 | id = PMID 12923372}}</ref> | |||
A 2005 prospective and observational study found that timing of the exposure to gluten in childhood was an important risk modifier. People exposed to wheat, barley, or rye before the [[Gut flora|gut barrier]] has fully developed (three months after birth) had five times the risk of developing coeliac disease over those exposed at 4 to 6 months. Those exposed later had a slightly increased risk relative to those exposed at 4 to 6 months.<ref name="Norris">{{cite journal|author= Norris JM, Barriga K, Hoffenberg EJ, Taki I, Miao D, Haas JE, Emery LM, Sokol RJ, Erlich HA, Eisenbarth GS, Rewers M.|title=Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease | journal=JAMA | year=2005| volume=293 | issue=19| pages=2343–2351 | id=PMID 15900004}}</ref> However a 2006 study with similar numbers found just the reverse, that early introduction of grains was protective.<ref>{{cite journal |author=Poole J, Barriga K, Leung D, Hoffman M, Eisenbarth G, Rewers M, Norris J |title=Timing of initial exposure to cereal grains and the risk of wheat allergy |journal=Pediatrics |volume=117 |issue=6 |pages=2175–82 |year=2006 |pmid=16740862}}</ref> Breastfeeding may also reduce risk. A [[meta-analysis]] indicates that prolonging [[breastfeeding]] until the introduction of gluten-containing grains into the diet was associated with a 52% reduced risk of developing coeliac disease in infancy; whether this persists into adulthood is not clear.<ref>{{cite journal |author=Akobeng A, Ramanan A, Buchan I, Heller R |title=Effect of breast feeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies |journal=Arch Dis Child |volume=91 |issue=1 |pages=39–43 |year=2006 |pmid=16287899}}</ref> | |||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]Seyedmahdi Pahlavani, M.D. [3]
Overview
Common risk factors in the development of celiac disease include family history, HLA genes, other autoimmune diseases, infections, and certain drugs.
Risk Factors
Common risk factors in the development of celiac disease may be environmental, genetic, infections and certain drugs.[1]
Common Risk Factors
- Common risk factors in the development of Celiac disease include:[2][3][4][5][6][7][8] [9][10] [11][12][13][14]
- Family history
- HLA DQ2 and DQ8 genes
- Other autoimmune diseases
- Type 1 diabetes mellitus
- IgA deficiency
- IgA nephropathy
- Insulin dependent diabetes mellitus (IDDM)
- Sjogren’s syndrome
- Juvenile idiopathic arthritis
- Juvenile rheumatoid arthritis
- Interferon-alpha
- Rotavirus
- Rod shaped bacteria
Less Common Risk Factors
- Less common risk factors in the development of celiac disease include:[15]
- Infant feeding practices
- Introduction of large amounts of gluten diet
- Exclusive gluten diet
- No breastfeeding
- Infant feeding practices
Risk modifiers
There are various theories as to what determines whether a genetically susceptible individual will go on to develop coeliac disease. Major theories include infection by rotavirus[16] or human intestinal adenovirus.[17] Some research has suggested that smoking is protective against adult onset coeliac disease.[18]
A 2005 prospective and observational study found that timing of the exposure to gluten in childhood was an important risk modifier. People exposed to wheat, barley, or rye before the gut barrier has fully developed (three months after birth) had five times the risk of developing coeliac disease over those exposed at 4 to 6 months. Those exposed later had a slightly increased risk relative to those exposed at 4 to 6 months.[19] However a 2006 study with similar numbers found just the reverse, that early introduction of grains was protective.[20] Breastfeeding may also reduce risk. A meta-analysis indicates that prolonging breastfeeding until the introduction of gluten-containing grains into the diet was associated with a 52% reduced risk of developing coeliac disease in infancy; whether this persists into adulthood is not clear.[21]
References
- ↑ Di Sabatino A, Corazza GR (2009). "Coeliac disease". Lancet. 373 (9673): 1480–93. doi:10.1016/S0140-6736(09)60254-3. PMID 19394538.
- ↑ Forsberg G, Fahlgren A, Hörstedt P, Hammarström S, Hernell O, Hammarström ML (2004). "Presence of bacteria and innate immunity of intestinal epithelium in childhood celiac disease". Am. J. Gastroenterol. 99 (5): 894–904. doi:10.1111/j.1572-0241.2004.04157.x. PMID 15128357.
- ↑ Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K (2003). "Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study". Arch. Intern. Med. 163 (3): 286–92. PMID 12578508.
- ↑ Murray JA (2005). "Celiac disease in patients with an affected member, type 1 diabetes, iron-deficiency, or osteoporosis?". Gastroenterology. 128 (4 Suppl 1): S52–6. PMID 15825127.
- ↑ "Gliadin immune reactivity is associated with overt and latent enteropathy in relatives of celiac patients - ScienceDirect".
- ↑ Nisticò L, Fagnani C, Coto I, Percopo S, Cotichini R, Limongelli MG, Paparo F, D'Alfonso S, Giordano M, Sferlazzas C, Magazzù G, Momigliano-Richiardi P, Greco L, Stazi MA (2006). "Concordance, disease progression, and heritability of coeliac disease in Italian twins". Gut. 55 (6): 803–8. doi:10.1136/gut.2005.083964. PMC 1856233. PMID 16354797.
- ↑ Sollid LM, Markussen G, Ek J, Gjerde H, Vartdal F, Thorsby E (1989). "Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer". J. Exp. Med. 169 (1): 345–50. PMC 2189170. PMID 2909659.
- ↑ "Co-occurrence of celiac disease and other autoimmune diseases in celiacs and their first-degree relatives - ScienceDirect".
- ↑ Cataldo F, Marino V, Bottaro G, Greco P, Ventura A (1997). "Celiac disease and selective immunoglobulin A deficiency". J. Pediatr. 131 (2): 306–8. PMID 9290622.
- ↑ "www.omicsonline.org".
- ↑ Cammarota G, Cuoco L, Cianci R, Pandolfi F, Gasbarrini G (2000). "Onset of coeliac disease during treatment with interferon for chronic hepatitis C". Lancet. 356 (9240): 1494–5. doi:10.1016/S0140-6736(00)02880-4. PMID 11081540.
- ↑ Stene LC, Honeyman MC, Hoffenberg EJ, Haas JE, Sokol RJ, Emery L, Taki I, Norris JM, Erlich HA, Eisenbarth GS, Rewers M (2006). "Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: a longitudinal study". Am. J. Gastroenterol. 101 (10): 2333–40. doi:10.1111/j.1572-0241.2006.00741.x. PMID 17032199.
- ↑ Zanoni G, Navone R, Lunardi C, Tridente G, Bason C, Sivori S, Beri R, Dolcino M, Valletta E, Corrocher R, Puccetti A (2006). "In celiac disease, a subset of autoantibodies against transglutaminase binds toll-like receptor 4 and induces activation of monocytes". PLoS Med. 3 (9): e358. doi:10.1371/journal.pmed.0030358. PMC 1569884. PMID 16984219.
- ↑ Molberg Ø, Solheim Flaete N, Jensen T, Lundin KE, Arentz-Hansen H, Anderson OD, Kjersti Uhlen A, Sollid LM (2003). "Intestinal T-cell responses to high-molecular-weight glutenins in celiac disease". Gastroenterology. 125 (2): 337–44. PMID 12891534.
- ↑ Ivarsson A, Hernell O, Stenlund H, Persson LA (2002). "Breast-feeding protects against celiac disease". Am. J. Clin. Nutr. 75 (5): 914–21. PMID 11976167.
- ↑ Stene L, Honeyman M, Hoffenberg E, Haas J, Sokol R, Emery L, Taki I, Norris J, Erlich H, Eisenbarth G, Rewers M (2006). "Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: a longitudinal study". Am J Gastroenterol. 101 (10): 2333–40. PMID 17032199.
- ↑ Kagnoff M, Paterson Y, Kumar P, Kasarda D, Carbone F, Unsworth D, Austin R (1987). "Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease". Gut. 28 (8): 995–1001. PMID 2822550.
- ↑ Suman S, Williams E, Thomas P, Surgenor S, Snook J (2003). "Is the risk of adult coeliac disease causally related to cigarette exposure?". Eur J Gastroenterol Hepatol. 15 (9): 995–1000. PMID 12923372.
- ↑ Norris JM, Barriga K, Hoffenberg EJ, Taki I, Miao D, Haas JE, Emery LM, Sokol RJ, Erlich HA, Eisenbarth GS, Rewers M. (2005). "Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease". JAMA. 293 (19): 2343–2351. PMID 15900004.
- ↑ Poole J, Barriga K, Leung D, Hoffman M, Eisenbarth G, Rewers M, Norris J (2006). "Timing of initial exposure to cereal grains and the risk of wheat allergy". Pediatrics. 117 (6): 2175–82. PMID 16740862.
- ↑ Akobeng A, Ramanan A, Buchan I, Heller R (2006). "Effect of breast feeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies". Arch Dis Child. 91 (1): 39–43. PMID 16287899.