Sandbox:Chandra: Difference between revisions
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==Genetics== | ==Genetics== | ||
* | *HLA-DRB1*7, and HLA-DRB4 are associated with the development of eosinophilic granulomatosis with polyangiitis. HLA-DRB4 is correlated with increasing risk of development of vascular manifestations of the churg-strauss syndrome.<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> | ||
* | *Single-nucleotide polymorphisms in the Interleukin-10 gene (IL10.2 haplotype) have been associated with eosinophilic granulomatosis with polyangitis.<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> | ||
==Associated Conditions== | ==Associated Conditions== |
Revision as of 20:03, 27 March 2018
Churg-Strauss syndrome Microchapters |
Diagnosis |
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Treatment |
Case Studies |
Sandbox:Chandra On the Web |
American Roentgen Ray Society Images of Sandbox:Chandra |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- The exact pathogenesis of [disease name] is not fully understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- HLA-DRB1*7, and HLA-DRB4 are associated with the development of eosinophilic granulomatosis with polyangiitis. HLA-DRB4 is correlated with increasing risk of development of vascular manifestations of the churg-strauss syndrome.[1]
- Single-nucleotide polymorphisms in the Interleukin-10 gene (IL10.2 haplotype) have been associated with eosinophilic granulomatosis with polyangitis.[2]
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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.