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).