Microscopic polyangiitis overview: Difference between revisions
| Line 3: | Line 3: | ||
{{CMG}} ; {{AE}} {{VKG}} | {{CMG}} ; {{AE}} {{VKG}} | ||
==Overview== | ==Overview== | ||
The early case reports of [[Microscopic polyangiitis]] provide a historical context and foundation for better understanding of the current concepts of these [[Disease|diseases]] Microscopic polyangiitis.[[Microscopic polyangiitis]] was first introduced by Dr. Friedrich Wohlwill, a German [[neuropathologist]], who described two patients with [[Transmural care|transmural]] periarteritis with [[glomerulonephritis]] in 1923.Historically, most forms of [[vasculitis]] like microscopic polyangiitis described subsequently classified on the basis of features similar to or distinct from [[polyarteritis]]. | The early case reports of [[Microscopic polyangiitis]] provide a historical context and foundation for better understanding of the current concepts of these [[Disease|diseases]] Microscopic polyangiitis.[[Microscopic polyangiitis]] was first introduced by Dr. Friedrich Wohlwill, a German [[neuropathologist]], who described two patients with [[Transmural care|transmural]] periarteritis with [[glomerulonephritis]] in 1923.Historically, most forms of [[vasculitis]] like microscopic polyangiitis described subsequently classified on the basis of features similar to or distinct from [[polyarteritis]].According to The International Chapel Hill Consensus Conference (CHCC) criteria based on Antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV) into [[granulomatosis with polyangiitis]] (GPA), [[microscopic polyangiitis]] (MPA), including renal-limited vasculitis (RLV), and [[eosinophilic granulomatosis with polyangiitis]] (EGPA, [[Churg-Strauss syndrome|Churg-Strauss]]).The [[pathogenesis]] of [[Microscopic polyangiitis]] is currently not fully understood. However, certain [[Hypothesis|hypothesizes]] have been made to determine possible factors that may trigger the disease such as environmental factors and [[Anti-neutrophil cytoplasmic antibody|anti-neutrophil cytoplasmic antibodies.]] [[Capillary|Capillaries]] and [[venules]] are involved in the [[pathogenesis]] of [[microscopic polyangiitis]].The paucity of [[immunoglobulin]] deposition is shown in [[Immunohistochemical staining|Immunohistochemical]] staining. | ||
Revision as of 13:48, 30 April 2018
|
Microscopic polyangiitis Microchapters |
|
Differentiating Microscopic polyangiitis from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Microscopic polyangiitis overview On the Web |
|
American Roentgen Ray Society Images of Microscopic polyangiitis overview |
|
Risk calculators and risk factors for Microscopic polyangiitis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]
Overview
The early case reports of Microscopic polyangiitis provide a historical context and foundation for better understanding of the current concepts of these diseases Microscopic polyangiitis.Microscopic polyangiitis was first introduced by Dr. Friedrich Wohlwill, a German neuropathologist, who described two patients with transmural periarteritis with glomerulonephritis in 1923.Historically, most forms of vasculitis like microscopic polyangiitis described subsequently classified on the basis of features similar to or distinct from polyarteritis.According to The International Chapel Hill Consensus Conference (CHCC) criteria based on Antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV) into granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), including renal-limited vasculitis (RLV), and eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss).The pathogenesis of Microscopic polyangiitis is currently not fully understood. However, certain hypothesizes have been made to determine possible factors that may trigger the disease such as environmental factors and anti-neutrophil cytoplasmic antibodies. Capillaries and venules are involved in the pathogenesis of microscopic polyangiitis.The paucity of immunoglobulin deposition is shown in Immunohistochemical staining.