A thorough physical examination should be performed on all patients presenting with joint pain, including examination of asymptomatic joints and other organ systems that might be involved. Joints should be examined for swelling, tenderness, deformity, instability, and limitation of motion. Comparisons with the patient's contralateral side can be made in all these parameters, as well as with the physician's joints as a control. Instability can be tested by moving adjacent bones in the direction opposite to normal movement and observing for greater-than-normal motion. Serial grip strength measurements can be made by asking the patient to squeeze a blood pressure (BP) cuff inflated to 20 mm Hg and however, because its presence or absence neither guarantees nor excludes development of arthritis testing for these antigens if not routinely performed. A National Institutes of Health (NIH) study found that genetic factors contributed 39% to 65% of OA variance. About 80% of patients with chondrodysplasias were found to have a type II collagen gene mutation likely linking these findings to OA (Prockop, 1998).
Inborn errors of metabolism are well known to cause diseases such as gout, in which uric acid is overproduced or underexcreted by the kidneys. Poorly controlled metabolic diseases such as diabetes or hemochromatosis might lead to arthropathies. Mechanical or traumatic factors cause OA in soccer players but not in long-distance runners, indicating that the type and direction of joint stress might be more important than the stress itself. Adduction moment is associated with OA disease severity. Obesity is also an identified factor in OA of the knee, possibly because of metabolic influences as well as mechanical forces (Eaton, 2004).
Infectious agents such as parvovirus B19, human immunodeficiency virus (HIV), Neisseria gonorrhoeae, Borrelia burgdorferi (Lyme disease), and streptococci (rheumatic fever) are all well-known causes of arthritides. Some speculate that dietary factors might contribute to autoimmune syndromes, and fasting or a vegan diet (or both) can lead to improvement in RA (Kjeldsen-Kragh et al., 1991; McDougall et al., 2002). The imbalance of omega-6 and omega-3 fatty acids in the standard American diet (a ratio of 30:1, as opposed to the ratio of 1:2 that is thought to have been present in Paleolithic diets) is also postulated to contribute to a more inflammatory state. Omega-6 fatty acids are preferentially converted to more inflammatory prostaglandins such as ara-chidonic acid, whereas omega-3 fatty acids can be converted into eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which contribute to anti-inflammatory series-3 prostaglandin production (Fig. 32-4). Omega-3 fatty acids are useful in RA, showing a decrease in use of nonsteroidal anti-inflammatory drugs (NSAIDs) and decreased levels of pain (Oh, 2005).
of these factors will help the family physician and rheuma-tologist modify the course of disease and eventually perhaps even prevent them.
Genetic factors have been identified for several arthritides. Presence of the human leukocyte antigen (HLA) system's HLA-DR4 antigen is associated with increased incidence and severity of RA. The HLA-B27 antigen is found in a higher percentage in patients with ankylosing spondylitis and other spondyloarthropathies than in the general population. Other factors are apparently involved,
Other medical systems, such as traditional Chinese medicine (TCM), may have completely different explanations for the changes seen in rheumatologic conditions. Although a conventional practitioner may not be aware of these, it is helpful to know about complementary modalities that may be beneficial (e.g., acupuncture helping patients with OA and fibromyalgia).
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