Polymyalgia rheumatica pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The underlying pathophysiology of polymyalgia rheumatica (PMR) remains unknown. It has been hypothesized that genetic and environmental factors are implicated, particularly due to the seasonal and geographical differences in the prevalence of this disease.[1][2][3] It has also been hypothesized that PMR is associated with infections such as parainfluenza virus type 1, mycoplasma pneumoniae, chlamydia pneumoniae, and parvovirus B19. In addition, histological exam of synovial biopsies of affected individuals revealed mild synovitis with predominance of CD4 T cells and macrophages.
References
- ↑ Smeeth L, Cook C, Hall AJ (2006). "Incidence of diagnosed polymyalgia rheumatica and temporal arteritis in the United Kingdom, 1990-2001". Ann Rheum Dis. 65 (8): 1093–8. doi:10.1136/ard.2005.046912. PMC 1798240. PMID 16414971.
- ↑ Alvarez-Rodriguez L, Carrasco-Marin E, Lopez-Hoyos M, Mata C, Fernandez-Prieto L, Ruiz-Soto M; et al. (2009). "Interleukin-1RN gene polymorphisms in elderly patients with rheumatic inflammatory chronic conditions: Association of IL-1RN*2/2 genotype with polymyalgia rheumatica". Hum Immunol. 70 (1): 49–54. doi:10.1016/j.humimm.2008.10.011. PMID 19026700.
- ↑ Cimmino MA, Caporali R, Montecucco CM, Rovida S, Baratelli E, Broggini M (1990). "A seasonal pattern in the onset of polymyalgia rheumatica". Ann Rheum Dis. 49 (7): 521–3. PMC 1004141. PMID 2383076.