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Polymyalgia Rheumatica

Inflammation and the HPA Axis

The hallmark of polymyalgia rheumatica is inflammation, probably caused by an autoimmune reaction in which the body’s immune system is activated against itself (Brito 1994; Cimmino 1997; Gitlits 2000; Meyer 1996; Schmits 2002). In people with polymyalgia rheumatica, inflammatory chemicals (including interleukin-6 (IL-6) and tumor necrosis factor-alpha [TNF-α]) are released into the bloodstream. Besides causing the inflammation that leads to symptoms, these chemicals have a profound effect on the hypothalamic-pituitary-adrenal (HPA) axis, which is intimately involved in maintaining levels of vital hormones (eg, dehydroepiandrosterone [DHEA] and cortisol). Among people with polymyalgia rheumatica, it appears the HPA axis is depressed due to elevated levels of IL-6 (Cutolo 2002). As a result, DHEA levels are low (de la Torre 1995; Nilsson 1994; Cutolo 2002; Straub 2000).

DHEA is a vital adrenal hormone that is converted into other hormones, including estrogen and testosterone. Low levels of DHEA have been associated with a wide variety of diseases, including inflammatory, autoimmune diseases such as rheumatoid arthritis and polymyalgia rheumatica.

DHEA replacement therapy has been shown to inhibit inflammatory cytokines and decrease IL-6 levels (Straub 1998; Straub 2000b). In one study, DHEA administered with glutamine and arginine allowed for lower doses of prednisone (a corticosteroid) among women with polymyalgia rheumatica (Meno-Tetang 2001; Petri 2002). DHEA also protects against the risk of infection caused by reduced immunity in steroid-treated animals (Gennari 1997) and increases bone density (Villareal 2000).