Polyarteritis nodosa pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Polyarteritis nodosa is a disease of unknown cause that affects arteries, the blood vessels that carry oxygenated blood to organs and tissues. It occurs when certain immune cells attack the affected arteries.Inflammation starts in the vessel intima and results in [[fibrinoid necrosis]] by destroying the internal and external elastic lamina. Aneurysms and thrombi may develop at the site of lesions. One hypothesis is that this condition is caused by antibodies against HBV, via a [[Hypersensitivity#Type_3_-_immune_complex | type IIII hypersensitivity reaction]]. [[Hepatitis C]] associated polyarteritis nodosa is the most common type among the hepatitis C associated vasculitis and has a severe clinical presentation.<ref name="pmid20981809">{{cite journal |author=Saadoun D, Terrier B, Semoun O, ''et al.'' |title=Hepatitis C virus-associated polyarteritis nodosa |journal=Arthritis Care Res (Hoboken) |volume=63 |issue=3 |pages=427–35 |year=2011 |month=March |pmid=20981809 |doi=10.1002/acr.20381 |url=}}</ref> | Polyarteritis nodosa is a disease of unknown cause that affects arteries, the blood vessels that carry oxygenated blood to organs and tissues. It occurs when certain immune cells attack the affected arteries.Inflammation starts in the vessel intima and results in [[fibrinoid necrosis]] by destroying the internal and external elastic lamina. Aneurysms and thrombi may develop at the site of lesions. One hypothesis is that this condition is caused by antibodies against HBV, via a [[Hypersensitivity#Type_3_-_immune_complex | type IIII hypersensitivity reaction]]. [[Hepatitis C]] associated polyarteritis nodosa is the most common type among the hepatitis C associated vasculitis and has a severe clinical presentation.<ref name="pmid20981809">{{cite journal |author=Saadoun D, Terrier B, Semoun O, ''et al.'' |title=Hepatitis C virus-associated polyarteritis nodosa |journal=Arthritis Care Res (Hoboken) |volume=63 |issue=3 |pages=427–35 |year=2011 |month=March |pmid=20981809 |doi=10.1002/acr.20381 |url=}}</ref> | ||
The pathogenesis of PAN remains unknown. However, the clinical responses to immunosuppressive therapy suggest that immunological mechanisms play an active pathogenic role. Due to inflammation of the medium to small sized vessels in PAN and the presence of impaired endothelial function, there could be direct endothelial cell activation and damage resulting from proinflammatory cytokines or antibodies (anti-endothelial cells antibodies). These anti-endothelial cells antibodies in turn stimulate greater production of cytokines and adhesion molecules potentiating the inflammation causing more damage to the vessels <ref name="pmid12525387">{{cite journal| author=Filer AD, Gardner-Medwin JM, Thambyrajah J, Raza K, Carruthers DM, Stevens RJ et al.| title=Diffuse endothelial dysfunction is common to ANCA associated systemic vasculitis and polyarteritis nodosa. | journal=Ann Rheum Dis | year= 2003 | volume= 62 | issue= 2 | pages= 162-7 | pmid=12525387 | doi= | pmc=1754444 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12525387 }} </ref>. | |||
==References== | ==References== | ||
Revision as of 14:39, 3 November 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: Olufunmilola Olubukola M.D.[3]Cafer Zorkun, M.D., Ph.D. [4]; Haritha Machavarapu, M.B.B.S.
Overview
Pathophysiology
Polyarteritis nodosa is a disease of unknown cause that affects arteries, the blood vessels that carry oxygenated blood to organs and tissues. It occurs when certain immune cells attack the affected arteries.Inflammation starts in the vessel intima and results in fibrinoid necrosis by destroying the internal and external elastic lamina. Aneurysms and thrombi may develop at the site of lesions. One hypothesis is that this condition is caused by antibodies against HBV, via a type IIII hypersensitivity reaction. Hepatitis C associated polyarteritis nodosa is the most common type among the hepatitis C associated vasculitis and has a severe clinical presentation.[1]
The pathogenesis of PAN remains unknown. However, the clinical responses to immunosuppressive therapy suggest that immunological mechanisms play an active pathogenic role. Due to inflammation of the medium to small sized vessels in PAN and the presence of impaired endothelial function, there could be direct endothelial cell activation and damage resulting from proinflammatory cytokines or antibodies (anti-endothelial cells antibodies). These anti-endothelial cells antibodies in turn stimulate greater production of cytokines and adhesion molecules potentiating the inflammation causing more damage to the vessels [2].
References
- ↑ Saadoun D, Terrier B, Semoun O; et al. (2011). "Hepatitis C virus-associated polyarteritis nodosa". Arthritis Care Res (Hoboken). 63 (3): 427–35. doi:10.1002/acr.20381. PMID 20981809. Unknown parameter
|month=ignored (help) - ↑ Filer AD, Gardner-Medwin JM, Thambyrajah J, Raza K, Carruthers DM, Stevens RJ; et al. (2003). "Diffuse endothelial dysfunction is common to ANCA associated systemic vasculitis and polyarteritis nodosa". Ann Rheum Dis. 62 (2): 162–7. PMC 1754444. PMID 12525387.