TNF-alpha (TNF-α) levels are elevated in patients with polymyalgia rheumatica. This important inflammatory cytokine is at the start of the inflammatory cascade (Tortora 2003). In mouse fibroblasts, TNF-α increases nuclear factor (NF)-kappa B in the cells, which stimulate the production of IL-6 (Shibanuma 1994). Thus, blocking TNF-α may help patients with polymyalgia rheumatica avoid or reduce corticosteroid use.
In one study, 7 patients with polymyalgia rheumatica and diabetes mellitus or osteoporosis were treated with Infliximab (Remicade®), a prescription TNF-α blocker. After 6 months they experienced clinical improvement and had significantly decreased IL-6 and erythrocyte sedimentation rate levels (Migliore 2005). The authors suggest that Infliximab may be used as a steroid-sparing agent, and it may also be useful as a first-line treatment in patients who should avoid corticosteroids.
In another study, 4 patients with polymyalgia rheumatica who had relapsed were treated with Infliximab (3mg/kg) at weeks 0, 2, and 6 (Salvarani 2003). Three of the 4 patients went into remission by week 2, and the fourth was able to tolerate a lower prednisone dose. Together, these small-scale studies suggest that blocking TNF-α may be useful for treating polymyalgia rheumatica.
A major therapeutic goal in treating polymyalgia rheumatica and giant cell arteritis is to reduce the dosage of steroid to help reduce side effects (Hellmich 2005). Because of the risk of blindness and other consequences of arterial inflammation (such as thrombosis and aneurysms), high doses of corticosteroids are used when giant cell arteritis is suspected. Although these high doses bring with them the additional risk of significant side effects, most clinicians feel the risk associated with giant cell arteritis justifies this approach (Chang 1983; Weyand 2004).
Methotrexate. Methotrexate is a folate antagonist with anti-inflammatory, immunosuppressive, and antiproliferative actions (Majumdar 2001). Studies of methotrexate in addition to prednisone have been contradictory; some studies suggest that methotrexate decreases total steroid dose needed by patients (Ferraccioli 2000; Caporali 2004).
Methotrexate increases homocysteine levels (Aksu 2001), so people taking methotrexate should consider supplementing with vitamins B6, B12, and folate to lower homocysteine (Sunder-Plassmann 2000; Guthikonda 2006).
Pentoxifylline. Pentoxifylline (PTX), an anti-inflammatory drug used for more than 20 years (Pollice 2001; Abdel-Salam 2003), is well tolerated (Lin 2005). PTX suppresses inflammation by decreasing synthesis and secretion of cytokines, including interleukin-1, IL-6, interleukin-8, and TNF-α (Mandell 1995; Graninger 1995; Dorazil-Dudzik 2004; Neuner 1994; Pollice 2001). While no published studies of PTX in patients with polymyalgia rheumatica or giant cell arteritis exist, it is possible that PTX will be a treatment for polymyalgia rheumatica in the future. Research shows that a combination of fish oil (omega-3 fatty acids), alpha-linolenic acid, and PTX can reduce synthesis of IL-6 (McCarty 1999).
Osteoporosis prevention and bone preservation are important facets of treatment for polymyalgia rheumatica. Both the disease itself and the corticosteroids used to treat it are known to increase bone loss (Dolan 1997). All patients, especially postmenopausal women, need to take calcium and vitamin D to avoid problems associated with osteoporosis (Barilla-LaBarca 2002). In some cases, prescription medications are needed to reverse osteoporosis (Gerster 1998; Richy 2005; Turbin 1999).
Bisphosphonates. Bisphosphonates are prescription drugs that slow the rate at which calcium is removed from the bones; they have been shown to increase bone mass and strength (Adachi 2000).