Dermatomyositis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
The underlying mechanism of dermatomyositis is conjectured to be [[Complement system|complement]]-mediated damage of microscopic vessels with muscle atrophy and lymphocytic inflammation secondary to tissue [[ischemia]]. On microscopy, both [[B-cell | The underlying mechanism of dermatomyositis is conjectured to be [[Complement system|complement]]-mediated damage of the microscopic vessels with [[muscle atrophy]] and lymphocytic inflammation secondary to tissue [[ischemia]]. On microscopy, both [[B-cell]] and [[T-cell]] infiltrate are seen. | ||
==Pathophysiology== | ==Pathophysiology== | ||
On the muscle biopsy, there are two classic microscopic findings of dermatomyositis. They are: | On the muscle biopsy, there are two classic microscopic findings of dermatomyositis. They are: | ||
Revision as of 18:06, 5 November 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The underlying mechanism of dermatomyositis is conjectured to be complement-mediated damage of the microscopic vessels with muscle atrophy and lymphocytic inflammation secondary to tissue ischemia. On microscopy, both B-cell and T-cell infiltrate are seen.
Pathophysiology
On the muscle biopsy, there are two classic microscopic findings of dermatomyositis. They are:
Dermatomyositis is associated with autoantibodies, especially anti-Jo1 antibody.[1]
Mechanism
The mechanism is conjectured to be complement-mediated damage of microscopic vessels with muscle atrophy and lymphocytic inflammation secondary to tissue ischemia.[2]
Microscopic findings
Cross sections of muscle reveal muscle fascicles with small, shrunken polygonal muscle fibers on the periphery of a fascicle surrounding central muscle fibers of normal, uniform size.
Aggregates of mature lymphocytes with small, dark nuclei and scant cytoplasm are seen surrounding vessels. Other inflammatory cells are distinctly uncommon. Immunohistochemistry can be used to demonstrate that both B- and T-cells are present in approximately equal numbers.[3] [4]
References
- ↑ Ghirardello, A (2006). "Clinical implications of autoantibody screening in patients with autoimmune myositis". Autoimmunity. 39 (3): 217–221. doi:10.1080/08916930600622645. PMID 16769655. Unknown parameter
|coauthors=ignored (help); Unknown parameter|month=ignored (help) - ↑ Benveniste, O (2004). "Pathogenesis of primary inflammatory myopathies". Presse Médicale. 33 (20): 1444–1450. doi:10.1016/S0755-4982(04)98952-X. PMID 15611679. Unknown parameter
|coauthors=ignored (help); Unknown parameter|month=ignored (help) - ↑ Benveniste O, Squier W, Boyer O, Hilton-Jones D, Herson S. Presse Med. 2004 Nov 20;33(20):1444-50. PMID: 15611679
- ↑ Nirmalananthan N, Holton JL, Hanna MG. Is it really myositis? A consideration of the differential diagnosis. Curr Opin Rheumatol. 2004 Nov;16(6):684-91.