Polymyositis and dermatomyositis pathophysiology: Difference between revisions
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{{CMG}}; {{AE}} {{SSH}} | {{CMG}}; {{AE}} {{SSH}} | ||
==Overview== | ==Overview== | ||
The exact pathogenesis of polymyositis and dermatomyositis is not fully understood. | The exact pathogenesis of polymyositis and dermatomyositis is not fully understood. However, it is understood that polymyositis and dermatomyositis are the result of autoimmune attack but triggering factors are not well-known. | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
The exact pathogenesis of polymyositis and dermatomyositis is not fully understood. However, it is understood that polymyositis and dermatomyositis are the result of autoimmune attack but triggering factors | The exact pathogenesis of polymyositis and dermatomyositis is not fully understood. However, it is understood that polymyositis and dermatomyositis are the result of autoimmune attack but triggering factors are not well-known. | ||
==== Polymyositis ==== | ==== Polymyositis ==== | ||
*Polymyositis is caused by [[inflammation]] and [[degeneration]] of the [[Muscle|muscles]]. | *Polymyositis is caused by [[inflammation]] and [[degeneration]] of the [[Muscle|muscles]]. | ||
*In polymyositis, CD8-positive cytotoxic T cells invade muscle fibres that express MHC class I antigens which may leads to fibre necrosis via the perforin pathway. | *In polymyositis, CD8-positive cytotoxic T cells invade muscle fibres that express MHC class I antigens which may leads to fibre necrosis via the perforin pathway. | ||
*Hypoxia may reduce creatine phosphate and adenosine triphosphate (ATP) levels in muscle and lead to fatigue and muscle weakness. | |||
*Interleukin (IL) 21, tumor growth factor-b (TGF-b), and high-mobility group protein 1 (HMG-1) induce muscle fatigue by decreasing Ca release. | |||
==== Dermatomyositis ==== | ==== Dermatomyositis ==== | ||
*Dermatomyositis is caused by skin [[inflammation]].<ref name="pmid25182203">{{cite journal |vauthors=Bodoki L, Nagy-Vincze M, Griger Z, Betteridge Z, Szöllősi L, Dankó K |title=Four dermatomyositis-specific autoantibodies-anti-TIF1γ, anti-NXP2, anti-SAE and anti-MDA5-in adult and juvenile patients with idiopathic inflammatory myopathies in a Hungarian cohort |journal=Autoimmun Rev |volume=13 |issue=12 |pages=1211–9 |date=December 2014 |pmid=25182203 |doi=10.1016/j.autrev.2014.08.011 |url=}}</ref><ref name="pmid26429706">{{cite journal |vauthors=Tiniakou E, Mammen AL |title=Idiopathic Inflammatory Myopathies and Malignancy: a Comprehensive Review |journal=Clin Rev Allergy Immunol |volume=52 |issue=1 |pages=20–33 |date=February 2017 |pmid=26429706 |doi=10.1007/s12016-015-8511-x |url=}}</ref><ref name="BohanPeter1975">{{cite journal|last1=Bohan|first1=Anthony|last2=Peter|first2=James B.|title=Polymyositis and Dermatomyositis|journal=New England Journal of Medicine|volume=292|issue=8|year=1975|pages=403–407|issn=0028-4793|doi=10.1056/NEJM197502202920807}}</ref><ref name="pmid29579414">{{cite journal |vauthors=Adler BL, Christopher-Stine L |title=Triggers of inflammatory myopathy: insights into pathogenesis |journal=Discov Med |volume=25 |issue=136 |pages=75–83 |date=February 2018 |pmid=29579414 |doi= |url=}}</ref> | *Dermatomyositis is caused by skin [[inflammation]].<ref name="pmid25182203">{{cite journal |vauthors=Bodoki L, Nagy-Vincze M, Griger Z, Betteridge Z, Szöllősi L, Dankó K |title=Four dermatomyositis-specific autoantibodies-anti-TIF1γ, anti-NXP2, anti-SAE and anti-MDA5-in adult and juvenile patients with idiopathic inflammatory myopathies in a Hungarian cohort |journal=Autoimmun Rev |volume=13 |issue=12 |pages=1211–9 |date=December 2014 |pmid=25182203 |doi=10.1016/j.autrev.2014.08.011 |url=}}</ref><ref name="pmid26429706">{{cite journal |vauthors=Tiniakou E, Mammen AL |title=Idiopathic Inflammatory Myopathies and Malignancy: a Comprehensive Review |journal=Clin Rev Allergy Immunol |volume=52 |issue=1 |pages=20–33 |date=February 2017 |pmid=26429706 |doi=10.1007/s12016-015-8511-x |url=}}</ref><ref name="BohanPeter1975">{{cite journal|last1=Bohan|first1=Anthony|last2=Peter|first2=James B.|title=Polymyositis and Dermatomyositis|journal=New England Journal of Medicine|volume=292|issue=8|year=1975|pages=403–407|issn=0028-4793|doi=10.1056/NEJM197502202920807}}</ref><ref name="pmid29579414">{{cite journal |vauthors=Adler BL, Christopher-Stine L |title=Triggers of inflammatory myopathy: insights into pathogenesis |journal=Discov Med |volume=25 |issue=136 |pages=75–83 |date=February 2018 |pmid=29579414 |doi= |url=}}</ref> | ||
*In dermatomyositis, activation and deposition of complements may lead to lysis of endomysial capillaries and muscle ischemia.<ref name="DalakasHohlfeld2003">{{cite journal|last1=Dalakas|first1=Marinos C|last2=Hohlfeld|first2=Reinhard|title=Polymyositis and dermatomyositis|journal=The Lancet|volume=362|issue=9388|year=2003|pages=971–982|issn=01406736|doi=10.1016/S0140-6736(03)14368-1}}</ref> | *In dermatomyositis, activation and deposition of complements may lead to lysis of endomysial capillaries and muscle ischemia.<ref name="DalakasHohlfeld2003">{{cite journal|last1=Dalakas|first1=Marinos C|last2=Hohlfeld|first2=Reinhard|title=Polymyositis and dermatomyositis|journal=The Lancet|volume=362|issue=9388|year=2003|pages=971–982|issn=01406736|doi=10.1016/S0140-6736(03)14368-1}}</ref> | ||
==Genetics== | ==Genetics== | ||
*Genes might be associated with development of polymyositis and dermatomyositis, especially in familial cases, which include:<ref name="DalakasHohlfeld20032">{{cite journal|last1=Dalakas|first1=Marinos C|last2=Hohlfeld|first2=Reinhard|title=Polymyositis and dermatomyositis|journal=The Lancet|volume=362|issue=9388|year=2003|pages=971–982|issn=01406736|doi=10.1016/S0140-6736(03)14368-1}}</ref> | *Genes might be associated with development of polymyositis and dermatomyositis, especially in familial cases, which include:<ref name="DalakasHohlfeld20032">{{cite journal|last1=Dalakas|first1=Marinos C|last2=Hohlfeld|first2=Reinhard|title=Polymyositis and dermatomyositis|journal=The Lancet|volume=362|issue=9388|year=2003|pages=971–982|issn=01406736|doi=10.1016/S0140-6736(03)14368-1}}</ref> |
Revision as of 20:27, 18 April 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]
Overview
The exact pathogenesis of polymyositis and dermatomyositis is not fully understood. However, it is understood that polymyositis and dermatomyositis are the result of autoimmune attack but triggering factors are not well-known.
Pathophysiology
Pathogenesis
The exact pathogenesis of polymyositis and dermatomyositis is not fully understood. However, it is understood that polymyositis and dermatomyositis are the result of autoimmune attack but triggering factors are not well-known.
Polymyositis
- Polymyositis is caused by inflammation and degeneration of the muscles.
- In polymyositis, CD8-positive cytotoxic T cells invade muscle fibres that express MHC class I antigens which may leads to fibre necrosis via the perforin pathway.
- Hypoxia may reduce creatine phosphate and adenosine triphosphate (ATP) levels in muscle and lead to fatigue and muscle weakness.
- Interleukin (IL) 21, tumor growth factor-b (TGF-b), and high-mobility group protein 1 (HMG-1) induce muscle fatigue by decreasing Ca release.
Dermatomyositis
- Dermatomyositis is caused by skin inflammation.[1][2][3][4]
- In dermatomyositis, activation and deposition of complements may lead to lysis of endomysial capillaries and muscle ischemia.[5]
Genetics
- Genes might be associated with development of polymyositis and dermatomyositis, especially in familial cases, which include:[6]
- HLA DRB1*0301 alleles for polymyositis and inclusion-body myositis
- HLA DQA1*0501 for juvenile dermatomyositis,
- Tumour necrosis factor 308A polymorphism for photosensitivity in dermatomyositis
Associated Conditions
Different conditions associated with polymyositis and dermatomyositis include:
- Interstitial lung disease
- Conduction abnormalities and arrhythmia
- Myocardial infarction
- Other connective tissue diseases like
- Malignancies are as follows:
Association | Polymyositis | Dermatomyositis |
---|---|---|
Malignancy | 5-7 fold more risks than the general population |
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
- ↑ Bodoki L, Nagy-Vincze M, Griger Z, Betteridge Z, Szöllősi L, Dankó K (December 2014). "Four dermatomyositis-specific autoantibodies-anti-TIF1γ, anti-NXP2, anti-SAE and anti-MDA5-in adult and juvenile patients with idiopathic inflammatory myopathies in a Hungarian cohort". Autoimmun Rev. 13 (12): 1211–9. doi:10.1016/j.autrev.2014.08.011. PMID 25182203.
- ↑ Tiniakou E, Mammen AL (February 2017). "Idiopathic Inflammatory Myopathies and Malignancy: a Comprehensive Review". Clin Rev Allergy Immunol. 52 (1): 20–33. doi:10.1007/s12016-015-8511-x. PMID 26429706.
- ↑ Bohan, Anthony; Peter, James B. (1975). "Polymyositis and Dermatomyositis". New England Journal of Medicine. 292 (8): 403–407. doi:10.1056/NEJM197502202920807. ISSN 0028-4793.
- ↑ Adler BL, Christopher-Stine L (February 2018). "Triggers of inflammatory myopathy: insights into pathogenesis". Discov Med. 25 (136): 75–83. PMID 29579414.
- ↑ Dalakas, Marinos C; Hohlfeld, Reinhard (2003). "Polymyositis and dermatomyositis". The Lancet. 362 (9388): 971–982. doi:10.1016/S0140-6736(03)14368-1. ISSN 0140-6736.
- ↑ Dalakas, Marinos C; Hohlfeld, Reinhard (2003). "Polymyositis and dermatomyositis". The Lancet. 362 (9388): 971–982. doi:10.1016/S0140-6736(03)14368-1. ISSN 0140-6736.