Polymyalgia rheumatica pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]
Overview
The underlying pathophysiology of polymyalgia rheumatica (PMR) remains unknown.[1] 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.[2][3][4] It has also been hypothesized that PMR is associated with infections such as parainfluenza virus type 1,[5] mycoplasma pneumoniae, chlamydia pneumoniae, and parvovirus B19.[6] In addition, histological exam of synovial biopsies of affected individuals revealed mild synovitis with predominance of CD4 T cells and macrophages.[7]
Pathophysiology
- PMR is a chronic inflammatory disease of the articular and periarticular structures of the cervival region, shoulder girdle and hip girdle. The cause of PMR remains unknown; however, there is evidence in the literature of possible involvement of genetic and environmental factors. This hypothesis is supported by the seasonal and geographical variations of the prevalence of PMR. In fact, the incidence of PMR is the highest among patients from northern European descent and Scandanavian countries, which suggests a genetic and/or environmental role in the pathophysiology of PMR.
- Several genes have been reported to be involved in PMR, such as:
- HLA DRB1
- Interleukin 6
- Interleukin 1 receptor antagonist
- Intercellular adhesion molecule 1
- In addition, the association between PMR and infections is another hypothesis for the development of PMR. This hypothesis is supported by the highest incidence of PMR in the time of some infection epidemics. Some of the infections that have been linked to PMR are:
References
- ↑ Kermani TA, Warrington KJ (2013). "Polymyalgia rheumatica". Lancet. 381 (9860): 63–72. doi:10.1016/S0140-6736(12)60680-1. PMID 23051717.
- ↑ 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.
- ↑ Duhaut P, Bosshard S, Calvet A, Pinede L, Demolombe-Rague S, Dumontet C; et al. (1999). "Giant cell arteritis, polymyalgia rheumatica, and viral hypotheses: a multicenter, prospective case-control study. Groupe de Recherche sur l'Artérite à Cellules Géantes". J Rheumatol. 26 (2): 361–9. PMID 9972970.
- ↑ Elling P, Olsson AT, Elling H (1996). "Synchronous variations of the incidence of temporal arteritis and polymyalgia rheumatica in different regions of Denmark; association with epidemics of Mycoplasma pneumoniae infection". J Rheumatol. 23 (1): 112–9. PMID 8838518.
- ↑ Meliconi R, Pulsatelli L, Uguccioni M, Salvarani C, Macchioni P, Melchiorri C; et al. (1996). "Leukocyte infiltration in synovial tissue from the shoulder of patients with polymyalgia rheumatica. Quantitative analysis and influence of corticosteroid treatment". Arthritis Rheum. 39 (7): 1199–207. PMID 8670331.