Churg-Strauss syndrome risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
There are no established risk factors for [ | There are no established risk factors for [[eosinophilic granulomatosis with polyangiitis]]. However, certain environmental agents including various [[Allergen|allergens]], [[Infection|infections]], [[Desensitization (medicine)|desensitization]], [[vaccination]], and [[genetics]] may act as triggering agents. Those triggers may be responsible for the [[Inflammation|inflammatory response]] with [[Eosinophil granulocyte|eosinophils]] and [[Lymphocyte|lymphocytes]] and [[Macrophage|macrophages]]. | ||
==Risk Factors== | ==Risk Factors== | ||
* | *Various environmental agents including various [[Allergen|allergens]], [[Infection|infections]], [[Desensitization (medicine)|desensitization]], [[vaccination]], and [[genetics]] may act as triggering agents. These triggers may be responsible for the [[Inflammation|inflammatory response]] with [[Eosinophil granulocyte|eosinophils]] and [[Lymphocyte|lymphocytes]] leading to [[vasculitis]] and [[necrosis]]. | ||
==Common Risk Factors== | ==Common Risk Factors== | ||
Common risk factors in the development of eosinophilic granulomatosis with polyangiitis may be various allergens, infections, genetic, and desensitization to drugs and vaccinations. | Common [[Risk factor|risk factors]] in the development of [[eosinophilic granulomatosis with polyangiitis]] may be various [[Allergen|allergens]], [[Infection|infections]], [[Genetics|genetic factors]], and desensitization to [[:Category:Drugs|drugs]] and [[Vaccination|vaccinations.]] | ||
*Genetic determinants: | *Genetic determinants:<ref name="pmid17763415">{{cite journal |vauthors=Vaglio A, Martorana D, Maggiore U, Grasselli C, Zanetti A, Pesci A, Garini G, Manganelli P, Bottero P, Tumiati B, Sinico RA, Savi M, Buzio C, Neri TM |title=HLA-DRB4 as a genetic risk factor for Churg-Strauss syndrome |journal=Arthritis Rheum. |volume=56 |issue=9 |pages=3159–66 |date=September 2007 |pmid=17763415 |doi=10.1002/art.22834 |url=}}</ref><ref name="pmid18512809">{{cite journal |vauthors=Wieczorek S, Hellmich B, Arning L, Moosig F, Lamprecht P, Gross WL, Epplen JT |title=Functionally relevant variations of the interleukin-10 gene associated with antineutrophil cytoplasmic antibody-negative Churg-Strauss syndrome, but not with Wegener's granulomatosis |journal=Arthritis Rheum. |volume=58 |issue=6 |pages=1839–48 |date=June 2008 |pmid=18512809 |doi=10.1002/art.23496 |url=}}</ref> | ||
**HLA-DRB1*04 AND *07 | **[[Human leukocyte antigen|HLA]]-DRB1*04 AND *07 | ||
**HLA-DRB4 | **[[HLA-DRB4]] | ||
Interleukin 10 gene single nucleotide polymorphisms | **[[Interleukin 10]] gene [[Single nucleotide polymorphism|single nucleotide polymorphisms]] | ||
*Allergic agents | *[[Allergy|Allergic agents]] | ||
*Infections | *[[Infection|Infections]] | ||
*Vaccination | *[[Vaccination]] | ||
*Exposure to silica | *Exposure to [[Silicon dioxide|silica]]<ref name="pmid23820041">{{cite journal |vauthors=Gómez-Puerta JA, Gedmintas L, Costenbader KH |title=The association between silica exposure and development of ANCA-associated vasculitis: systematic review and meta-analysis |journal=Autoimmun Rev |volume=12 |issue=12 |pages=1129–35 |date=October 2013 |pmid=23820041 |pmc=4086751 |doi=10.1016/j.autrev.2013.06.016 |url=}}</ref> | ||
*Drugs: | *[[:Category:Drugs|Drugs]]:<ref name="pmid18549941">{{cite journal |vauthors=Puéchal X, Rivereau P, Vinchon F |title=Churg-Strauss syndrome associated with omalizumab |journal=Eur. J. Intern. Med. |volume=19 |issue=5 |pages=364–6 |date=July 2008 |pmid=18549941 |doi=10.1016/j.ejim.2007.09.001 |url=}}</ref><ref name="pmid8834352">{{cite journal |vauthors=Orriols R, Muñoz X, Ferrer J, Huget P, Morell F |title=Cocaine-induced Churg-Strauss vasculitis |journal=Eur. Respir. J. |volume=9 |issue=1 |pages=175–7 |date=January 1996 |pmid=8834352 |doi= |url=}}</ref> | ||
**Leukotriene receptor antagonists (eg, montelukast, zafirlukast) | **[[Leukotriene antagonist|Leukotriene receptor antagonists]]/ Leukotriene modifying agents (eg, [[montelukast]], [[zafirlukast]]) | ||
**Anti-IgE antibody (eg,omalizumab) | **Anti-IgE antibody (eg, [[omalizumab]]) | ||
**Cocaine | **[[Cocaine]] | ||
**Inhaled glucocorticoids | **Inhaled [[glucocorticoids]] | ||
**Mesalazine | **[[Mesalazine]] | ||
**Propylthiouracil | **[[Propylthiouracil]] | ||
**Methimazole | **[[Methimazole]] | ||
**[[Macrolide|Macrolides]] | |||
==References== | ==References== | ||
Latest revision as of 17:52, 12 April 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
There are no established risk factors for eosinophilic granulomatosis with polyangiitis. However, certain environmental agents including various allergens, infections, desensitization, vaccination, and genetics may act as triggering agents. Those triggers may be responsible for the inflammatory response with eosinophils and lymphocytes and macrophages.
Risk Factors
- Various environmental agents including various allergens, infections, desensitization, vaccination, and genetics may act as triggering agents. These triggers may be responsible for the inflammatory response with eosinophils and lymphocytes leading to vasculitis and necrosis.
Common Risk Factors
Common risk factors in the development of eosinophilic granulomatosis with polyangiitis may be various allergens, infections, genetic factors, and desensitization to drugs and vaccinations.
- Genetic determinants:[1][2]
- HLA-DRB1*04 AND *07
- HLA-DRB4
- Interleukin 10 gene single nucleotide polymorphisms
- Allergic agents
- Infections
- Vaccination
- Exposure to silica[3]
- Drugs:[4][5]
- Leukotriene receptor antagonists/ Leukotriene modifying agents (eg, montelukast, zafirlukast)
- Anti-IgE antibody (eg, omalizumab)
- Cocaine
- Inhaled glucocorticoids
- Mesalazine
- Propylthiouracil
- Methimazole
- Macrolides
References
- ↑ Vaglio A, Martorana D, Maggiore U, Grasselli C, Zanetti A, Pesci A, Garini G, Manganelli P, Bottero P, Tumiati B, Sinico RA, Savi M, Buzio C, Neri TM (September 2007). "HLA-DRB4 as a genetic risk factor for Churg-Strauss syndrome". Arthritis Rheum. 56 (9): 3159–66. doi:10.1002/art.22834. PMID 17763415.
- ↑ Wieczorek S, Hellmich B, Arning L, Moosig F, Lamprecht P, Gross WL, Epplen JT (June 2008). "Functionally relevant variations of the interleukin-10 gene associated with antineutrophil cytoplasmic antibody-negative Churg-Strauss syndrome, but not with Wegener's granulomatosis". Arthritis Rheum. 58 (6): 1839–48. doi:10.1002/art.23496. PMID 18512809.
- ↑ Gómez-Puerta JA, Gedmintas L, Costenbader KH (October 2013). "The association between silica exposure and development of ANCA-associated vasculitis: systematic review and meta-analysis". Autoimmun Rev. 12 (12): 1129–35. doi:10.1016/j.autrev.2013.06.016. PMC 4086751. PMID 23820041.
- ↑ Puéchal X, Rivereau P, Vinchon F (July 2008). "Churg-Strauss syndrome associated with omalizumab". Eur. J. Intern. Med. 19 (5): 364–6. doi:10.1016/j.ejim.2007.09.001. PMID 18549941.
- ↑ Orriols R, Muñoz X, Ferrer J, Huget P, Morell F (January 1996). "Cocaine-induced Churg-Strauss vasculitis". Eur. Respir. J. 9 (1): 175–7. PMID 8834352.