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Query: UMLS:C0018099 (gout)
5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The traditional Chinese antirheumatic herb Danggui-Nian-Tong-Tang (DGNTT) was studied comparatively with indomethacin and allopurinol to evaluate its anti-inflammatory and antihyperuricemic effects in patients with gout. Results in this study did not show any significant improvement in reducing the total number of painful and swollen joints, articular index and pain score (P > 0.05) by treatment with DGNTT. Unlike allopurinol, DGNTT did not lower the high serum level of uric acid. In vitro study in rats showed that DGNTT significantly inhibits the activity of beta-glucuronidase (P < 0.05) and lysozyme release (P < 0.01) from neutrophils. In conclusion, despite the effect of inhibition on enzyme release from neutrophils, DGNTT is not effective in treating acute arthritis or hyperuricemia.
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PMID:The anti-inflammatory and anti-hyperuricemic effects of Chinese herbal formula danggui-nian-tong-tang on acute gouty arthritis: a comparative study with indomethacin and allopurinol. 857 22

The identification of monosodium urate crystals in synovial fluid is essential for the definite diagnosis of gout. Neutrophils interact with urate crystals to produce inflammatory reactions associated with acute arthritis. Crystals activate monocyte-macrophages and synoviocytes to produce high levels of proinflammatory cytokines, like TNF alpha und interleukin-1 and different chemokines. High levels of interleukin-8, a powerful neutrophil attractant with activating properties, were demonstrated in the synovial fluid of patients with acute gout arthritis.
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PMID:[Uric acid crystals and chemotactic cytokines--pathogenesis of an acute gout attack]. 944 14

Although the prevalence of tophaceous gout has decreased in the past few years, the disease still exists, and without accurate diagnosis and therapy, it can still result in destructive arthritis. However, use of urate-lowering drugs may reduce plasma urate concentrations enough to allow resorption of tophi and prevent painful tophaceous gout. Some patients may have mechanical problems from tophi, despite adequate control of acute arthritis; in such situations, joint replacement or surgical excision of tophi may be necessary.
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PMID:Stopping progression to tophaceous gout. When and how to use urate-lowering therapy. 986 Dec 61

The clinical features and laboratory findings of 91 Thai patients (33 males and 58 females) with CPPD crystal deposition disease were studied. Their average age was 71.54 years. Acute monoarthritis and oligoarthritis were the two most common forms of presentation and were seen in 89 per cent of cases. The knee, wrist and ankle were the three most common joints involved. Associated diseases were common and included hypertension (30 cases), renal insufficiency (23 cases), chronic obstructive pulmonary disease (17 cases), coronary heart disease (13 cases) and diabetes mellitus (12 cases). Eleven patients had malignancies. Five patients had concomitant gout and CPPD crystal deposition disease. The knee and the wrist were the two most common sites of chondrocalcinosis. Of 67 patients who had thyroid function tested, 2 had hyperthyroidism and 5 had hypothyroidism. Hypomagnesemia was seen in 19 per cent. None had hypercalcemia, hypophosphatasia, hemochromatosis or hyperparathyroidism. In contrast to the western series, acute arthritis in our series responded well to oral colchicine alone.
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PMID:Calcium pyrophosphate dihydrate crystal deposition: a clinical and laboratory analysis of 91 Thai patients. 1044 78

Gout is a metabolic disease characterized by recurrent episodes of acute arthritis. High blood levels of uric acid lead to inflammation, joint swelling, and severe pain. Treatment is aimed at relieving the acute attack and preventing recurrent episodes of gouty arthritis.
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PMID:Gouty arthritis: not just a big toe problem. 1141 Jul 63

Gout is a common disease arising due to abnormal purin metabolism and excessive accumulation of uric acid in the blood (hyperuricemia) and manifesting with attacks of acute gouty arthritis. In long duration of gout uric acids accumulate in the bones and periarticular tissues as tophuses. Repeat attacks lead to development of chronic gouty arthritis. Purins restriction diet is an important component of gout treatment. Treatment of acute arthritis should be started early, in initial pains before the development of the attacks. Gouty arthritis in the presence of continuous hyperuricemia, tophyses and urolithiasis is treated with allopurinol. Its intake should be long and controlled by the blood level of uric acid. Balneotherapy is recommended for patients with chronic gouty arthritis associated with cardiovascular diseases, urolithiasis.
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PMID:[Gout: current views. Stage oriented treatment]. 1189 31

This article presents three patients suffering from complications related to tophi deposited within the hand and wrist synovium and flexor tendons. One patient had no previous history of gout or acute arthritis, with uricemia within normal values upon admission. The pathophysiology and treatment of gout in these special circumstances are discussed.
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PMID:Gouty involvement of flexor tendons. 1272 10

The characteristic phenomena of acute gouty arthritis are acute arthritis in a middle-aged male, associated with serum uric acid above 6 mg. per 100 cc. and a satisfactory response to colchicine. Roentgenographically observable changes do not occur early. In recent years uric acid metabolism has been studied by means of isotope techniques utilizing labeled substances. Uric acid is excreted in relatively constant amounts by humans and is little affected by variations in dietary intake, except for purine or nucleic acid substances. Persons with gout have a greater total amount of uric acid and a lower turnover than normal persons. In the treatment of acute attacks of gout colchicine is still the most practical single drug, even though its pharmacologic action remains unknown. Benemid (probenecid) is a powerful uricosuric agent of low toxicity which has been subjected to extensive clinical trial for three years. It causes inhibition of the resorption of urate from the glomerular filtrate; the site of action is believed to be the tubular cells. The author's usual dose is 2 gm. a day. This has caused a lowering of the uric acid in the serum and an increase in the urinary output.
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PMID:Diagnosis and treatment of gouty arthritis. 1308 23

In 99% of the cases, the underlying cause of gout is an inborn disorder of uric acid excretion. In addition to acute arthritis, clinical consequences include tophi, chronic destruction of joints, and ulcers. The patient is endangered by the frequent renal involvement, with hypertension and renal insufficiency. Furthered by such exogenous factors as overweight, high-calorie, purine-rich foods and immoderate consumption of alcohol, hyperuricemia may develop. Basic treatment comprises dietary measures and, up to a serum uric acid concentration of 8.5 mg/dl, should be the sole measure required. The aim is to achieve a permanent lowering of uric acid concentrations in the blood to < 6.5 mg/dl. This may be achieved by reduction of overweight (including regular exercise), an energy-adapted diet with only moderate amounts of fat, restriction--or, better, banishment--of alcohol, an ovolactovegetarian diet low in purine (care must be taken with high-purine vegetablesl), moderate intake of readily assimilated carbohydrates, and adequate amounts of calorie-free liquids.
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PMID:[Avoid purine-rich foods, drink a lot, reduce weight. The most important recipes against hyperuricemia]. 1452 70

Gout is the most frequent cause of acute arthritis in men over 40 years of age. In the recent years, gout incidence has been increasing in developed countries probably due to dietary changes, alcohol consumption, ageing of population and also application of high-risk medications. Hyperuricemia is one of the symptoms of hyperinsulinism and metabolic syndrome. The level of uricemia correlates with the degree of insulin resistance. Correlation of uric acid levels and the risk of coronary and cerebral accidents were reported both in diabetic and non-diabetic population. It has not been explained satisfactorily whether this is the direct result of hyperuricemia or concurrently present symptom of metabolic syndrome. The study describes symptomatology of clinical signs of gout and discusses about appropriate therapeutic approach in each stage of the disease. New therapeutic possibilities that are still in the stage of clinical studies are mentioned. Also, we focus on alternative dietary recommendations for hyperuricemia and gout patients. The reason of changes in dietary regime is the effort to alleviate the signs of metabolic syndrome. The study emphasises the practical significance of screening of metabolic syndrome signs during examination of gout patients so that appropriate targeted therapeutic intervention could be performed. On the contrary, increased risk of gout-induced movement disorders should be taken into account in patients with diagnosed insulin resistance.
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PMID:[Gout and diabetes]. 1677 Oct 97


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