People with polymyalgia rheumatica, the synovial membranes and bursae, which line and lubricate the joints, become inflamed, causing pain and discomfort, no permanent damage to either the joints or the muscles is associated with polymyalgia rheumatica. Corticosteroids are generally used as first-line therapy. However, corticosteriod drugs are associated with significant side effects, including osteoporosis.
Nutritional therapy offers an important adjunct approach to polymyalgia rheumatica. Inflammation associated with the disease causes impairment of the adrenal hormone system, causing a deficiency in vital hormones that need to be replaced.
A significant number of people with polymyalgia rheumatica also suffer from a condition known as giant cell arteritis . Giant cell arteritis involves inflammation of the temporal artery . Aneurysms can form and, blindness is a possible consequence. Up to 75 percent of patients with giant cell arteritis may have aortitis
Diagnosis of Polymyalgia Rheumatica
Patients are usually more than 60 years old (Beers MH et al 2005). It is twice as common in women as in men
The main diagnostic criteria for polymyalgia rheumatica are hip and shoulder pain, For example, patients with polymyalgia rheumatica usually have an elevated erythrocyte sedimentation rate. C-reactive protein and IL-6 are also elevated in patients with polymyalgia rheumatica. These pro-inflammatory indicators, however, are elevated in response to inflammation anywhere in the body and cannot be used to definitely diagnose polymyalgia rheumatica.Treatment with steroids usually begins promptly. Most patients respond very quickly to corticosteroids. In fact, if the symptoms don’t resolve rapidly, your physician may want to conduct additional tests to determine whether the diagnosis was correct.
Inflammation and the HPA Axis
Probably caused by an autoimmune reaction in which the body’s immune system is activated against itself . The inflammation that leads to symptoms, have a profound effect on the hypothalamic-pituitary-adrenal (HPA) axis, which is intimately involved in maintaining levels of vital hormones such as dehydroepiandrosterone (DHEA) and cortisol.
DHEA is a vital adrenal hormone that is converted into other hormones, including estrogen and testosterone. DHEA administered with glutamine and arginine allowed for lower dosages of prednisone (a corticosteroid) among women with polymyalgia rheumatica.
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 . All patients, especially postmenopausal women, need to take calcium and vitamin D to avoid problems associated with osteoporosis (Barilla-LaBarca ML et al 2002). In some cases prescription medications are needed to reverse osteoporosis (Gerster JC et al 1998; Richy F et al 2005;
Calcium and vitamin D. Calcium is important to maintain adequate serum calcium so that bone demineralization can be prevented. Vitamin D or a vitamin D analog is necessary for the body to absorb and utilize calcium. Studies have shown that vitamin D analogs (alfacalcidol or calcitriol) are readily converted to active form in the body (Reginster JY et al 2005; Richy F et al 2005).
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 JD et al 2000a,b).
Vitamin K. Vitamin K consists of vitamins K1 and K2; vitamin K3 is a synthetic form (Bern M 2004). Maintaining adequate vitamin K levels is crucial for bone mineralization, blood clotting, cell growth, and blood vessel health (Bern M 2004). Vitamin K1 (phylloquinone) has anti-inflammatory effects, while synthetic vitamin K3 does not (Eichbaum FW et al 1979).
TNF-alpha (Tumor Necrosis Factor) levels are elevated in patients with polymyalgia rheumatica. This important inflammatory cytokine is at the start of the inflammatory cascade (Tortora GJ et al 2003). In mouse fibroblasts, TNF-alpha increases nuclear factor (NF)-kappa B in the cells, which in turn stimulates the production of IL-6 (interleukin-6) (Shibanuma M et al 1994). Thus, blocking TNF-alpha may help patients with polymyalgia rheumatica avoid or reduce corticosteroid use.
N-acetylcysteine. N-acetylcysteine (NAC) is a well-known antioxidant that also helps regulate production of inflammatory cytokines. In one study, NAC modulated IL-6 production through an NF-kappa B mechanism (Shibanuma M et al 1994).
Plant extracts. A number of plant extracts have also been shown to decrease NF-kappa B, including stinging nettle extract (Riehemann K et al 1999); helenalin from arnica flowers (Lyss G et al 1997); a spiroketal compound found in chamomile and Plagius flosculosus (Calzado MA et al 2005); oleandrin from oleander (Manna SK et al 2000b); resveratrol from grapes and other fruits (Manna SK et al 2000a); 1’-acetoxychavicol acetate (ACA) from Languas galanga (Ichikawa H et al 2005); curcumin (Jobin C et al 1999); ergolide from Inula britannica (Whan HJ et al 2001); rocaglamides extracted from Aglaia (Baumann B et al 2002); and tetrandrine from Han-Fang Chi, a Chinese herb used to treat rheumatic disorders (Ho LJ et al 2004).
Unfortunately, data are scant regarding the effect of many dietary supplements in polymyalgia rheumatica, perhaps because few research dollars are being directed at natural remedies for this condition. Because of the significant side effects associated with drugs prescribed for polymyalgia rheumatica, however, Life Extension recommends that patients do everything possible to reduce their use of these drugs, including pursuing natural remedies that have been proven to reduce inflammatory cytokine levels.
Fish oils. The inclusion of omega-3 fish oils in the diet has been shown to help with autoimmune and inflammatory diseases (Kelley DS 2001; Simopoulos SP 1999, 2002) by suppressing synthesis of TNF-alpha (Endres S et al 1989). Vitamin E and fish oil work together to decrease pro-inflammatory cytokines, including IL-6 and TNF-alpha, in mice (Venkatraman JT et al 1999a,b). Omega-3 fish oils have been useful in patients with a variety of inflammatory diseases, including rheumatoid arthritis and atherosclerosis (Simopoulos SP 1999). Studies in humans with rheumatoid arthritis suggest that fish oil and vitamin E decrease inflammation in humans (Tidow-Kebritchi S et al 2001). Moreover, fish oil supplementation has shown anti-inflammatory effects, including decreased use of anti-inflammatory drugs, for patients with a variety of other chronic inflammatory diseases (Simopoulos SP 2002).
Vitamins C and E. Vitamin E is an antioxidant with anti-inflammatory actions. The alpha-tocopherol form of vitamin E can decrease inflammation that contributes to atherosclerosis (Singh U et al 2005). Alpha-tocopherol supplementation has been shown to decrease C-reactive protein levels (Singh U et al 2005). Vitamin C is an antioxidant (Das 1989) that also has anti-inflammatory properties and blocks NF-kappa B activation by TNF (Bowie AG et al 2000).
Methylsulfonylmethane. Sulfur is a mineral found in several amino acids, the building blocks of all the proteins in the body. Methylsulfonylmethane (MSM) is a natural metabolite of dimethyl sulfoxide (Richmond VL 1986). MSM is used as a dietary supplement by many people and is naturally found in fruits, vegetables, grains, and animals (cow’s milk is a rich source) (Parcell S 2002; Richmond VL 1986). MSM has been studied in patients with a variety of conditions, including arthritis, allergies, and fibromyalgia, among others. MSM appears to have little or no toxicity (Horvath K et al 2002).
Studies have shown that MSM can decrease pain and increase mobility in patients with osteoarthritis (Kim LS et al 2006).
Curcumin and ginger. Curcumin has been shown to reduce NF-kappa B in a wide variety of settings, including autoimmune diseases and cancer. It is a well-known antioxidant and anti-inflammatory (Yadav VS et al 2005). Ginger has also been documented to reduce multiple inflammatory chemicals, including NF-kappa B and many others, and to be effective against a variety of inflammatory diseases, including autoimmune diseases that are characterized by an elevation of NF-kappa B (Aggarwal BB et al 2004).