Rheumatoid Arthritis
Rheumatoid arthritis is a chronic syndrome characterized by non-specific, usually symmetric inflammation of the peripheral joints, potentially resulting in progressive destruction of articular and periarticular structures (Berkow 1992, 1305). It is generally considered to be an autoimmune disease in which the immune system attacks the cartilage and joint linings. The synovial membrane becomes inflamed, proliferates and thickens, forming villi that encroach upon space in the joint. The inflammatory membrane then produces an abnormal granulation tissue, called pannus that adheres to the surface of the articular cartilage. At the point of contact between the pannus and the hyaline cartilage, proteolytic enzymes are released and begin to digest the articular cartilage and subchondral bone, leading to joint deformities.
Diagnosis of RA
According to the Merck Manual, any four criteria must be present to diagnose rheumatoid arthritis; criteria 1 through 4 must have been present for at least 6 weeks:
- Morning stiffness for at least one 1 hour
- Arthritis of at least three joints
- Arthritis of hand joints
- Symmetric arthritis
- Rheumatic nodules
- Serum rheumatoid factor, by a method positive in more than 5% of normal control subjects
- Radiographic changes (erosions, decalcification) (Berkow 1992, 1307)
Diagnostic factors in laboratory investigations include elevated ESR (Erythrocyte Sedimentation Rate), normocytic anemia, rheumatoid factor (usually IgM subclass, but also IgG and IgA), elevated immunoglobulins, and lowered serum complement. Investigations of the synovial fluid itself should reveal low viscosity, high cell count (mostly neutrophils), low glucose, high protein and positive RF (Rheumatoid Factor) (Berkow 1992, 1307).
Medical Treatment of RA
Complete bed rest is occasionally indicated for short periods during the most active painful stage of the severe disease. In less severe cases regular rest periods are recommended.
Nonsteroidal antiinflammatory drugs (NSAIDs) such as acetylsalicylic acid (ASA), ibuprofen and celecoxib are the traditional cornerstones of medical treatment, along with acetaminophen. All of these drugs except acetaminophen inhibit the cyclooxygenase-2 (COX-2) pathway, thereby preventing the synthesis of the PgE2 series of prostaglandins that promotes inflammation. Acetaminophen in contras exerts its analgesic activity through the inhibition of the nitric oxide pathway and neurotransmitter receptors including N-methyl-D-aspartate and substance P. Side effects for these drugs are numerous including nausea, vomiting, gastrointestinal irritation and ulceration, tinnitus, vertigo, leukopenia, thrombocytopenia, anemia, edema, skin eruptions, asthma, and mental confusion. The side effects of acetaminophen specifically include renal tubular necrosis, renal failure and hepatoxicity (Berkow 1992, 1308-9).
Corticosteroids are also employed and will provide dramatic results initially, although they do not prevent destruction of the joint and will eventually become of less benefit with chronic use. Side effects are weight gain, water and sodium retention, high blood pressure, osteoporosis, thinning of the skin, cataracts, acne, muscle weakness, immunosuppression, stomach ulcers and depression (Berkow 1992, 1310-11).
Immunosuppressive drugs such as cyclosporine and azathioprine are used in rheumatoid arthritis unresponsive to NSAIDs, and function mostly by inhibiting and suppressing white blood cells and the immune response. Side effects due to azathioprine include gastrointestinal disturbances, heartburn, immunosuppression, bleeding and bruising, and malignancy. A side effect due to cyclosporine is kidney damage. Methotrexate is also employed to inhibit cell growth and is used as an antineoplastic drug as well. Possible side effects include mucosal ulceration and bone marrow suppression (Berkow 1992, 1311). Immunomodulators (e.g. abatacept), Interleukin Receptor Inhibitors (e.g. anakinra, tocilizumab), and Tumor Necrosis Factor (TNF) Inhibitors (e.g. infliximab) also inhibit the immune response by suppressing the activity of proteins and cytokines such as CD80, TNF-alpha and interleukins 1 and 6 that participate in the immune response (King and Worthington 2010). All these drugs have serious side-effects including immunosuppression and risk of serious infection.
Remittive drugs such as gold and penicillamine are used in patients suffering from serious rheumatoid arthritis. It is not entirely clear how they work but may produce clinical remission and a decrease in tissue destruction. Side effects to gold include pruritis, dermatitis, stomatitis, thrombocytopenic purpura and aplastic anemia as well as diarrhea, hepatitis, pneumonitis and neuropathy. Marrow suppression, proteinuria, nephrosis as well as fatalities due to penicillamine have been reported (Berkow 1992, 1309-10).
Exercise to restore muscle mass and preserve normal range of motion is also encouraged, as well as orthopedic shoes for those so affected. Surgery and joint replacement is indicated in severe degeneration and must be undertaken while the disease is active.
Ayurvedic Treatment of RA
The classic text on diagnosis called the Madhava Nidana provides three basic causes of amavata, a condition described in Ayurveda that is very similar to the clinical description of rheumatoid arthritis:
- Weakness of digestion: The digestive fire is one of the prime motivators of all human function, ensuring the proper absorption and metabolism of nutrition. When digestion is impaired ama accumulates, the doshas become vitiated, and the vitality (ojas) diminishes.
- Incompatible foods in the diet: Incompatible foods include foods consumed out of season or without respect to local bioclimactic factors; unfamiliar foods (asatmya, i.e. opposite of the healthy norm [satmya], i.e. non-traditional foods; spoilt and contaminated foods; food additives; refined flour; feed-lot and farmed meat, etc.
- Lack of physical activity: Physical exercise (vyama) is considered an important aspect to dinacharya, the daily regimen recommended in Ayurveda. A lack of exercise predisposes one to amavata because the circulation of blood to and the removal of wastes (ama) from the periphery is impaired.
The treatment of inflammatory joint disease is threefold:
- support and enhance digestion (agni)
- facilitate the removal of ama from the body
- repair damaged tissues and restore vitality (ojas)
The initial treatment often begins with enkindling agni, the digestive fire. This can be achieved by a short period of fasting, sudation therapy and the use pungent and bitter herbs. Fasting is particularly appropriate during a time of exacerbation: the food should be light, little and liquid. Weak ginger tea with a little lemon and honey and a simple diet of kichari (mung and rice soup) is best. Dipanapachana herbs to stimulate the appetite (‘dipana’) and ‘eat up’ (‘pachana’) the accumulated ama include Guduchi (Tinospora cordifolia), Guggulu (Commiphora mukul), Lasuna (Allium sativum), Haritaki (Terminalia chebula), Shunthi (Zingiber officinalis) and Yavani (Trachyspermum ammi). One important formula for amavata is Yogaraja guggulu, the Ayurvedic text the Chakradatta stating that it "stimulates the digestive fire, promotes energy and strength, and overcomes vatika (vata) disorders even if located in the joints and marrow" (Sharma 2002, 250). The Ayurvedic Formulary of India suggests a recommended dose of 3 grams, twice daily (1978, 58-59). While Yogaraja guggulu is best used for the chronic pain of RA, another guggulu called Kaisara guggulu is frequently used concurrently to reduce active inflammation.
The elimination of ama in the joints is best facilitated by applying an oil to the affected area, such as castor oil, and followed with dry heat. Medicated oils used in amavata include Kottamchukadi taila and Mahanarayana taila. Once the oil has been applied, heated brick dust, heated sand, or powdered rock salt may be wrapped inside a linen bag and applied to the affected area to enhance blood flow. It is important to note however, that counterirritant therapies should never be used in during active inflammation. Warm water and medicated enemas are used to remove ama in the digestive tract and correct the flow of vata. Gentle laxative called aperients such as Triphala and bulk laxatives like Isabgol (Plantago psyllium) improve the tone of the colon as well as cleanse the dhatus. Hatha yoga and regular exercise also becomes important at this time as it increases circulation to and away from the affected areas, although the person would do well to take care and not engage in any strenuous exercise that may damage the joints further.
Western herbal treatment of RA
Treatment of RA in the Western herbal tradition is along the similar line as Ayurvedic therapies, focusing on measures to restore digestion, promote elimination and restore integrity to the joints.
Digestive remedies are frequently given in the form of a bitter tonic, which functions by improving digestion, especially of proteins by increasing HCl acid production, which may protect against undigested proteins that can irritate the gut wall and stimulate immune reactions. An excellent bitter tonic is Devil’s Claw (Harpagophytum procumbens) which contains the iridoid glycoside harpogoside that has significant analgesic effects. Other useful bitter tonics include Gentian (Gentiana lutea) and Barberry (Berberis vulgaris), which may also be combined with carminatives such as Caraway (Carum carvi) and Fennel (Foeniculum vulgare) to enhance digestion.
To cleanse and detoxify the tissues, a number of remedies are used in tandem including diuretics, alteratives and cholagogues. Diuretics such as Birch leaf (Betula alba) and Celery seed (Apium graveolens) are useful as the kidneys are the body's primary way to eliminate acids that may build up in the joints. Alteratives and cholagogues such as Yellowdock (Rumex crispus), Burdock (Arctium lappa), Dandelion root (Taraxacum officinalis), and Barberry (Berberis vulgaris) are all useful for cleansing and facilitating elimination, clearing the body of accumulated toxins. In addition to these remedies, circulatory stimulants such as Prickly Ash berry (Zanthoxylum spp) and Ginger root (Zingiber officinalis) are used increase blood flow to the affected areas, breaking up stagnation in the joints, as well as have diaphoretic actions that promote elimination.
Joint restoratives typically utilize herbs that contain an abundance of minerals that help to restore joint integrity, including seaweeds (e.g. Laminaria, Fucus, Macrocystis spp.), Nettle (Urtica dioica) and Horsetail (Equisetum arvense). White Bryony (Bryonia dioica) is a potentially toxic herb that is considered to be a restorative specific to the serous membranes by nourishing and increasing the secretion of synovial fluid, the 1:3 dry plant tincture dosed at between 5-10 drops thrice daily.
Supplementary measures undertaken to relieve pain may include a variety of anti-inflammatory, analgesic, muscle relaxant and sedating herbs including White Willow bark (Salix alba), Black Cohosh (Actaea racemosa), Kava (Piper methysticum), Wild Yam (Dioscorea villosa) and Jamaican Dogwood (Piscidia erythrina).
Supplementation with antioxidants can help with repair of tissues and prevent further damage to tissues and cells by free-radicals generated in a toxin producing diet and a stressful environment. Vitamin C and E, as well as selenium, zinc, super oxide dismutase, N-acetyl cysteine, manganese and bioflavonoids are all useful antioxidants.
Topical applications in Western herbal medicine include poultices, baths, lotions, plasters and salves. Counterirritants can be used during remissive phases to promote local circulation, including Kelp (Fucus spp.), Cayenne (Capsicum spp), Jimsonweed (Datura stramonium) and Ginger root (Zingiber officinalis). During active inflammation useful topical herbs include St. John’s Wort (Hypericum perforatum) and Lobelia (Lobelia inflata).
For more information on RA and dietary therapies, please refer to the section on autoimmune disease.
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