Behçet's disease pathophysiology: Difference between revisions

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*The exact pathogenesis of [disease name] is not fully understood.
*The exact pathogenesis of [disease name] is not fully understood.
OR
OR
*It is understood that behcet disease is the result of [[vasculitis]]. It involves all sizes of blood vessels ( small, medium, and large). Arteries and venis are both involved in behcet disease.  
*It is understood that behcet disease is the result of [[vasculitis]]. It involves all sizes of blood vessels ( small, medium, and large). Arteries and venis are both involved in behcet disease. Major mechanisms in pathogenesis of behcet disease include:
**Polygenic 
**
*
*
*s with other autoimmune diseases, the disorder may represent aberrant immune activity triggered by exposure to an agent, perhaps infectious, in patients with a genetic predisposition to develop the disease. Major disease mechanisms in Behçet syndrome include the following 
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*[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.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
Line 52: Line 57:
==Genetics==
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*Genes involved in the pathogenesis of behcet disease include [gene1], [gene2], and [gene3].
*Genes involved in the pathogenesis of behcet disease include human leukocyte antigens, particularly HLA-B51. <ref name="pmid19790126">{{cite journal |vauthors=de Menthon M, Lavalley MP, Maldini C, Guillevin L, Mahr A |title=HLA-B51/B5 and the risk of Behçet's disease: a systematic review and meta-analysis of case-control genetic association studies |journal=Arthritis Rheum. |volume=61 |issue=10 |pages=1287–96 |date=October 2009 |pmid=19790126 |pmc=3867978 |doi=10.1002/art.24642 |url=}}</ref>
*The development of [disease name] is the result of multiple genetic mutations.
*Familial cases of behcet disease have higher rates of HLA-B51 in compare to sporadic cases.<ref name="pmid1341477">{{cite journal |vauthors=Akpolat T, Koç Y, Yeniay I, Akpek G, Güllü I, Kansu E, Kiraz S, Ersoy F, Batman F, Kansu T |title=Familial Behçet's disease |journal=Eur J Med |volume=1 |issue=7 |pages=391–5 |date=November 1992 |pmid=1341477 |doi= |url=}}</ref>
*Genetic anticipation: earlier age of onset of disease in children of pateints with behcet disease.<ref name="pmid9536823">{{cite journal |vauthors=Fresko I, Soy M, Hamuryudan V, Yurdakul S, Yavuz S, Tümer Z, Yazici H |title=Genetic anticipation in Behçet's syndrome |journal=Ann. Rheum. Dis. |volume=57 |issue=1 |pages=45–8 |date=January 1998 |pmid=9536823 |pmc=1752455 |doi= |url=}}</ref>
*. Affected children of patients with Behçet syndrome may have an earlier age of onset, a property termed genetic anticipation
*HLA-B51 rates are higher in familial than in sporadic cases
*The development of behcet disease is the result of multiple genetic mutations.


==Associated Conditions==
==Associated Conditions==
Line 59: Line 68:
==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
<figure-inline>[[File:Behcet's syndrome 11.jpeg|502x502px]]</figure-inline>
<figure-inline><figure-inline>[[File:Behcet's syndrome 11.jpeg|502x502px]]</figure-inline></figure-inline>


==Microscopic Pathology==
==Microscopic Pathology==

Revision as of 15:14, 22 March 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [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 behcet disease is the result of vasculitis. It involves all sizes of blood vessels ( small, medium, and large). Arteries and venis are both involved in behcet disease. Major mechanisms in pathogenesis of behcet disease include:
    • Polygenic
  • s with other autoimmune diseases, the disorder may represent aberrant immune activity triggered by exposure to an agent, perhaps infectious, in patients with a genetic predisposition to develop the disease. Major disease mechanisms in Behçet syndrome include the following 
  • [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

  • [Disease name] is transmitted in [mode of genetic transmission] pattern.
  • Genes involved in the pathogenesis of behcet disease include human leukocyte antigens, particularly HLA-B51. [1]
  • Familial cases of behcet disease have higher rates of HLA-B51 in compare to sporadic cases.[2]
  • Genetic anticipation: earlier age of onset of disease in children of pateints with behcet disease.[3]
  • . Affected children of patients with Behçet syndrome may have an earlier age of onset, a property termed genetic anticipation
  • HLA-B51 rates are higher in familial than in sporadic cases
  • The development of behcet disease is the result of multiple genetic mutations.

Associated Conditions

Gross Pathology

  • On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

<figure-inline><figure-inline></figure-inline></figure-inline>

Microscopic Pathology

  • On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].


References

  1. de Menthon M, Lavalley MP, Maldini C, Guillevin L, Mahr A (October 2009). "HLA-B51/B5 and the risk of Behçet's disease: a systematic review and meta-analysis of case-control genetic association studies". Arthritis Rheum. 61 (10): 1287–96. doi:10.1002/art.24642. PMC 3867978. PMID 19790126.
  2. Akpolat T, Koç Y, Yeniay I, Akpek G, Güllü I, Kansu E, Kiraz S, Ersoy F, Batman F, Kansu T (November 1992). "Familial Behçet's disease". Eur J Med. 1 (7): 391–5. PMID 1341477.
  3. Fresko I, Soy M, Hamuryudan V, Yurdakul S, Yavuz S, Tümer Z, Yazici H (January 1998). "Genetic anticipation in Behçet's syndrome". Ann. Rheum. Dis. 57 (1): 45–8. PMC 1752455. PMID 9536823.

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