Dermatomyositis pathophysiology: Difference between revisions
(Created page with "__NOTOC__ {{Dermatomyositis}} {{CMG}} ==Overview== ==Pathophysiology== The diagnosis of dermatomyositis can be confirmed by muscle biopsy, EMG, and blood tests. It should...") |
Kiran Singh (talk | contribs) |
||
| (4 intermediate revisions by 2 users not shown) | |||
| Line 4: | Line 4: | ||
==Overview== | ==Overview== | ||
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: | |||
* A mixed [[B-cell|B-]] and [[T-cell]] perivascular inflammatory infiltrate | * A mixed [[B-cell|B-]] and [[T-cell]] perivascular inflammatory infiltrate | ||
* Perifascicular muscle fiber atrophy | * Perifascicular muscle fiber atrophy | ||
| Line 14: | Line 15: | ||
===Mechanism=== | ===Mechanism=== | ||
The mechanism is conjectured to be [[Complement system|complement]]-mediated damage of microscopic vessels with muscle atrophy and lymphocytic inflammation secondary to tissue [[ischemia]].<ref>{{cite journal | last=Benveniste | first=O | coauthors=Squier W, Boyer O et al. | title=Pathogenesis of primary inflammatory myopathies | journal=Presse Médicale | volume=33 | issue=20 | pages=1444–1450 | month=November | year=2004 | pmid=15611679 | doi=10.1016/S0755-4982(04)98952-X }}</ref> | The mechanism is conjectured to be [[Complement system|complement]]-mediated damage of microscopic vessels with muscle atrophy and lymphocytic inflammation secondary to tissue [[ischemia]].<ref>{{cite journal | last=Benveniste | first=O | coauthors=Squier W, Boyer O et al. | title=Pathogenesis of primary inflammatory myopathies | journal=Presse Médicale | volume=33 | issue=20 | pages=1444–1450 | month=November | year=2004 | pmid=15611679 | doi=10.1016/S0755-4982(04)98952-X }}</ref> | ||
===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.<ref>Benveniste O, Squier W, Boyer O, Hilton-Jones D, Herson S. ''Presse Med''. '''2004''' Nov 20;33(20):1444-50. PMID: 15611679</ref> <ref>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.</ref> | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
| Line 23: | Line 30: | ||
[[Category:Autoimmune diseases]] | [[Category:Autoimmune diseases]] | ||
[[Category:Rheumatology]] | [[Category:Rheumatology]] | ||
Latest revision as of 18:44, 3 June 2015
|
Dermatomyositis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Dermatomyositis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Dermatomyositis pathophysiology |
|
Risk calculators and risk factors for Dermatomyositis pathophysiology |
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.