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Historically, treatment of rheumatoid arthritis (RA) has been conservative and symptom or patient-complaint oriented. Newer approaches use disease-modifying antirheumatic drugs (DMARDs), sometimes known as slow-acting antirheumatic drugs (SAARDs), to slow the progression of the disease earlier in its course. Some of these drugs may be used as initial therapy and some may be used in combinations to reduce the side effects or adverse reactions.
This article reviews the incidence, etiology, and pathophysiology of rheumatoid arthritis (RA), along with signs and symptoms, laboratory, and other diagnostic parameters of the disease. Criteria utilized for defining RA are discussed. While the primary cause is unknown, theories implicate genetic, hormonal, viral, bacterial, autoimmune, atmospheric, and environmental factors. Recent studies focus on the role of immune complexes, endothelial cells, and antibodies in the disease process.
Osteoarthritis (OA) is a joint disorder that is characterized by increased degradative and decreased synthetic processes. The pathogenetic factors that have been demonstrated to influence the progression of OA are cytokines and nitric oxide. This new information serves to further elucidate the factors involved in the etiology of osteoarthritis and will aid in the development of pharmacological tools to treat this disease. As our understanding of the pathogenesis of OA grows, so does our appreciation that it is not simply a disease of passive joint degeneration. Unfortunately, therapies aimed at modifying the progression of the disease remain frustratingly difficult to identify. Primary therapy for OA thus is still largely aimed at controlling the symptoms of the disease while minimizing drug side effects. New agents with the potential to slow disease progression are beginning to emerge however. These will be discussed along with the agents that should be used first line to control symptoms.
Juvenile rheumatoid arthritis (JRA) is a common disorder of childhood that can be potentially devastating physically and psychologically. Over the last several decades, therapy for JRA has changed little. Therapy for advanced JRA is based on trial and error due to the lack of significant clinical trials for both old and new pharmaceutical agents. The following article is a brief overview of the disease and a review of the different treatment options available today with a look at some of the future developments in JRA research.
Gout is recognized by sudden onsets of joint pain and swelling caused by imbalances in production and excretion of uric acid. Hyperuricemia is a risk factor for gout, however, not all patients with hyperuricemia will develop gout. Other risk factors include hypertension, renal insufficiency, obesity, excessive alcohol consumption, high purine diets, and medications such as thiazide diuretics and low dose aspirin. Management of gout and hyperuricemia can be achieved through inhibiting urate synthesis, enhancing urate excretion, or both. Medications to treat gout include NSAIDs, colchicine, and glucocorticosteroids. Chronic therapy with uricosuric agents or xanthine oxidase inhibitors may be necessary for those with recurrent attacks.
Systemic lupus erythematosus (SLE) is a chronic, multiple-organ system inflammatory disorder associated with immune system dysfunction. Autoantibodies are produced that react with self-antigens in cell membranes and nuclear and cytoplasmic constituents to produce tissue damage. Commonly observed clinical manifestations include arthritis, myalgia, fever, cutaneous lesions, cytopenia, and renal, CNS, and cardiopulmonary involvement. Minor manifestations can be managed with relatively nontoxic agents such as nonsteroidal anti-inflammatory drugs, topical corticosteroids, and antimalarials. Severe disease involving the kidneys, CNS, and cardiopulmonary systems requires the aggressive use of more toxic agents such as high-dose corticosteroids, azathioprine, and cyclophosphamide. Other supportive and ancillary therapies are also required to manage the complications frequently associated with SLE.
Alternative therapies are widely used for the treatment of arthritis. Some examples of these are acupuncture/acupressure, animal venoms, copper bracelets, dimethyl sulfoxide, herbal products, magnets, and nutritional therapy. Many products used for alternative therapies are not regulated in the United States and can vary greatly in their content. They may contain toxic contaminants, induce allergic reactions, or interact with prescription medications. Much of the support for their use is based on testimonials and poorly controlled trials. The Office of Alternative Medicine was established under the National Institutes of Health to promote study and evaluation of unconventional therapies.
The purpose of this review is to discuss the range of physical therapy interventions for the individual presenting with arthritis. Rehabilitation of the individual with arthritis is a complex process. Individuals with arthritis present with the impairments of pain, joint contractures, decreased strength, and diminished cardiovascular endurance. These impairments negatively impact the functional status of an individual with arthritis. These issues should be addressed with an individualized physical therapy treatment plan utilizing a variety of therapeutic modalities and exercise. The ultimate goal of rehabilitation is a return to function.
Access to the Internet provides us with an incredible amount of information about the rheumatic diseases. There are numerous arthritis organizations, professional associations, educational institutions, research and professional journals and patients with Web sites devoted to the rheumatic diseases. Some are reviewed and listed here.