Gout and hyperuricemia. (1/541)

Gout is a condition characterized by the deposition of monosodium urate crystals in the joints or soft tissue. The four phases of gout include asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout. The peak incidence occurs in patients 30 to 50 years old, and the condition is much more common in men than in women. Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle. Acute gout most commonly affects the first metatarsal joint of the foot, but other joints are also commonly involved. Definitive diagnosis requires joint aspiration with demonstration of birefringent crystals in the synovial fluid under a polarized light microscope. Treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, corticosteroids and analgesics. In patients without complications, NSAID therapy is preferred.  (+info)

Sparing effect of hemiplegia on tophaceous gout. (2/541)

The sparing effect of hemiplegia on the development of tophaceous gout is described. The useless upper limb had no tophaceous deposits and the partially paralysed lower limb had only limited urate deposits. Disuse was presumably the major contributor to the limited deposition of urates on the paralysed side.  (+info)

Diagnosis and management of gout. (3/541)

Gout is a disease resulting from the deposition of urate crystals caused by the overproduction or underexcretion of uric acid. The disease is often, but not always, associated with elevated serum uric acid levels. Clinical manifestations include acute and chronic arthritis, tophi, interstitial renal disease and uric acid nephrolithiasis. The diagnosis is based on the identification of uric acid crystals in joints, tissues or body fluids. Treatment goals include termination of the acute attack, prevention of recurrent attacks and prevention of complications associated with the deposition of urate crystals in tissues. Pharmacologic management remains the mainstay of treatment. Acute attacks may be terminated with the use of nonsteroidal anti-inflammatory agents, colchicine or intra-articular injections of corticosteroids. Probenecid, sulfinpyrazone and allopurinol can be used to prevent recurrent attacks. Obesity, alcohol intake and certain foods and medications can contribute to hyperuricemia. These potentially exacerbating factors should be identified and modified.  (+info)

Rheumatic disease and the Australian aborigine. (4/541)

OBJECTIVE: To document the frequency and disease phenotype of various rheumatic diseases in the Australian Aborigine. METHODS: A comprehensive review was performed of the archaeological, ethnohistorical, and contemporary literature relating to rheumatic diseases in these indigenous people. RESULTS: No evidence was found to suggest that rheumatoid arthritis (RA), ankylosing spondylitis (AS), or gout occurred in Aborigines before or during the early stages of white settlement of Australia. Part of the explanation for the absence of these disorders in this indigenous group may relate to the scarcity of predisposing genetic elements, for example, shared rheumatoid epitope for RA, B27 antigen for AS. In contrast, osteoarthritis appeared to be common particularly involving the temporomandibular joint, right elbow and knees and, most probably, was related to excessive joint loading in their hunter gatherer lifestyle. Since white settlement, high frequency rates for rheumatic fever, systemic lupus erythematosus, and pyogenic arthritis have been observed and there are now scanty reports of the emergence of RA and gout in these original Australians. CONCLUSION: The occurrence and phenotype of various rheumatic disorders in Australian Aborigines is distinctive but with recent changes in diet, lifestyle, and continuing genetic admixture may be undergoing change. An examination of rheumatic diseases in Australian Aborigines and its changing phenotype may lead to a greater understanding of the aetiopathogenesis of these disorders.  (+info)

Collagenase, cathepsin B and cathepsin L gene expression in the synovial membrane of patients with early inflammatory arthritis. (5/541)

OBJECTIVE: To examine the expression of the matrix metalloproteinase, MMP-1, and the cysteine proteases, cathepsin B (CB) and cathepsin L (CL), in the synovial membrane (SM) of patients with early inflammatory arthritis. METHODS: Samples of SM were obtained by blind needle biopsy or needle arthroscopy from inflamed knees of 28 patients with early inflammatory arthritis (mean disease duration 10.2 months, range 2 weeks-18 months). Sixteen patients had rheumatoid arthritis (RA), nine psoriatic arthritis and there was one each with ankylosing spondylitis, gout and an undifferentiated arthritis. Comparison was made with tissue from two patients with established erosive RA and three normal synovial tissue samples. In situ hybridization was performed using digoxigenin-labelled RNA probes. RESULTS: MMP-1, CB and CL were expressed in all patients with early arthritis and in established erosive RA, whereas normal synovium showed only scanty expression. The three proteases were prominent in perivascular infiltrates and endothelial cells of early arthritis tissue. MMP-1 was observed primarily in the lining layer, but was also evident in the sublining area. CB and CL were expressed to a lesser extent in the lining layer, and were present mainly in the subintima. The three proteases were not found in lymphoid aggregrates. No differences were observed between the disease categories. CONCLUSIONS: The detection of MMP-1, CB and CL in the synovium shortly after symptom onset implies that the potential for joint destruction exists at a very early stage in the disease. In addition, the perivascular and endothelial cell expression suggests a role for these proteases in mononuclear cell influx to the inflamed synovium and in angiogenesis.  (+info)

Serum uric acid: correlation with biological, clinical and behavioral factors in Japanese men. (6/541)

Cross-sectional associations between biological, clinical and behavioral factors and serum uric acid (SUA) levels were examined in 2,438 Japanese male office workers aged 20 to 59 years in Osaka, Japan. Stepwise regression analysis for SUA was carried out for all persons and repeated excluding those under medication for hypertension, hyperuricemia or diabetes mellitus. The results were essentially the same without change in the sequence of the seven most important variables. When 150 men under medication were excluded, independent correlates with SUA levels were, in order of relative importance, history of gout, log triglyceride, creatinine, hemoglobin A1c (negative association), body mass index, total protein, alcohol intake, age (negative association), and total cholesterol. 32.7 percent of total variation in SUA was accounted for by these variables combined. Our data suggest that weight and serum lipids control and avoiding excessive drinking may be beneficial in the prevention of hyperuricemia.  (+info)

The epidemiology study of hyperuricemia and gout in a community population of Huangpu District in Shanghai. (7/541)

OBJECTIVE: To investigate the prevalence of hyperuricemia and gout in a community population of Huangpu District in Shanghai. METHODS: In the target community, 2037 dwellers were interviewed with relevan questionnares from house to house. According to even house number 1017 blood samples were taken for serum uric acid (SUA) levels measured with the uricase-peroxidase enzymatic method. RESULTS: The prevalence of hyperuricemia was 14.2% in men (SUA > 70 mg/L, 62 cases), 7.1% in women (SUA > 60 mg/L, 41 cases), 10.1% in both sexes. Seven gout patients were all men. The prevalence of gout in 2037 dwellers in Huangpu District was 0.77% in men and 0.34% in both sexes. CONCLUSIONS: The mean SUA level in each age group in this survey was much higher than that of a previous study 1 carried out in Shanghai, Beijing and Guangzhou in 1980 (P < 0.05). And the prevalence of hyperuricemia was increased rapidly (in men: from 1.4% in the survey of 1980 to 14.2% in our survey; in women: from 1.3% in the survey of 1980 to 7.1% in our survey). Compared with Idonesia data in 1992, the prevalence of hyperuricemia and gout in our survey was lower than that in Indonesia (P < 0.05), which suggests that racial and genetic predispositions are key causative factors.  (+info)

Contribution of a missense mutation (Trp64Arg) in beta3-adrenergic receptor gene to multiple risk factors in Japanese men with hyperuricemia. (8/541)

Epidemiological data reveal that hyperuricemia is a risk factor of atherosclerosis. The risk is possibly caused by a link between hyperuricemia and insulin resistance-related metabolic syndrome. Recently it has been proposed that a missense mutation (Trp64Arg) in the beta3-adrenergic receptor (beta3-AR) gene may contribute to the accumulation of multiple risk factors related to insulin resistance. The present study was undertaken to further clarify an association between the Trp64Arg mutation and the metabolic syndrome in 47 Japanese men with hyperuricemia, who are substantially at high risk of atherosclerosis. One patient (2%) had the homozygous mutation, 12 (26%) were heterozygous for the mutation, and 31 (72%) had no mutation found by the PCR-RFLP analysis. The Trp64Arg mutation was not related to past maximal body mass index (BMI), BMI and waist/hip ratio. The subjects with the heterozygous mutation showed a slightly higher incidence of impaired glucose tolerance and diabetes mellitus in the 75 g oral glucose challenge (67%), as compared with those without the mutation (39%). Serum insulin response at 60 min and the sum of serum insulin in the glucose challenge were greater in the former subjects than those in the latter subjects (P=0.041 and 0.076, respectively). An increase in serum lipoprotein(a) was also observed in the subjects with the heterozygous mutation, but the Trp64Arg mutation was not associated with other dyslipidemia, blood pressure or ischemic changes on the electrocardiogram. These results indicate that the heterozygous mutation of Trp64Arg in the beta3-AR gene partly contributes to the accumulation of multiple risk factors in male subjects with hyperuricemia. A larger prospective study is necessary to elucidate a possible role of the Trp64Arg mutation in atherosclerotic diseases in future.  (+info)