Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We recently conducted a cross-sectional survey of the prescribing practices of rheumatologists and a random sample of family physicians. While in general there was agreement as to the preferred management of gout, family physicians were (a) more likely to use phenylbutazone, (b) more liberal in their use of allopurinol, (c) less likely to cover the introduction of allopurinol with antiinflammatory agents or to titrate the dose against the serum uric acid, or to adjust the dose according to the serum creatinine. A small number of physicians continued to routinely use urate lowering drugs in the treatment of entirely asymptomatic hyperuricemia.
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PMID:A survey of current prescribing practices of antiinflammatory and urate lowering drugs in gouty arthritis in the province of Ontario. 818 60

Published experiences with severe toxicity with intravenous colchicine have been reviewed. All reported cases reflect inappropriate use of the drug. Therapeutic rules for colchicine have been derived from this information: (1) Single intravenous doses should not exceed 2-3 mg, and cumulative total doses for an attack should not be more than 4-5 mg. (2) Patients should receive no more colchicine by any route for 7 days. (3) Colchicine doses must be reduced in the presence of renal or hepatic disease, and in the older patient with apparently normal renal function. (4) Intravenous colchicine doses should be half the size of oral ones. (5) Absolute contraindications to intravenous colchicine therapy for acute gout include combined renal and hepatic disease, creatinine clearances below 10 cc/min, and extrahepatic biliary obstruction.
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PMID:Review: systemic toxicity associated with the intravenous administration of colchicine--guidelines for use. 328 54

To determine the frequency of gout in our renal transplant population and to identify any predisposing factors, we retrospectively examined the outpatient records of all patients transplanted between January 1980 and July 1984 in whom the allograft functioned for at least 1 year. Two hundred forty-three charts were sufficiently complete to be evaluated. Of the 211 patients receiving corticosteroids and cyclosporine (CyA) as immunosuppression, 25 had at least one documented episode of gout (9.7% of total, 11.8% of CyA patients); no episodes occurred in the 32 patients receiving azathioprine and corticosteroid therapy (P = .05). The time from transplantation to the first episode of gout ranged from 4 months to 4 years. Of the patients without gout, 103 of the 186 receiving CyA (55.5%) and eight of 32 receiving azathioprine (25%) had asymptomatic hyperuricemia (serum uric acid greater than 8.5 mg/dL for men, greater than 7.0 mg/dL for women, P less than .01). The number of patients receiving diuretics in the CyA treated group was 142 of 211 (67%) v 12 of 32 (37.5%) in the azathioprine group. However, the increased incidence of gout or hyperuricemia in patients receiving CyA was not due to the effect of the diuretic alone. There was no correlation between the serum creatinine and uric acid in either the CyA or azathioprine group (r value for CyA group = -.06 and for the azathioprine group = -.26). Compared with patients receiving azathioprine, we conclude that there is an increased incidence of gout and/or hyperuricemia in renal transplant patients treated with CyA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The incidence of gout in renal transplant recipients. 331 90

Plasma uric acid was investigated in a population survey on diabetes and cardiovascular risk factors among Melanesians and Asian Indians in Fiji in 1980. Plasma uric acid levels were elevated in men and women with impaired glucose tolerance in both ethnic groups. The lowest plasma uric acid levels were found in diabetic patients, especially in diabetic men. Even though obesity was positively associated with plasma uric acid, it did not explain the high plasma uric acid level in persons with impaired glucose tolerance. Body mass index had a significant and independent impact on plasma uric acid levels both in nondiabetic and diabetic men and women. The strongest predictor of plasma uric acid in the multiple regression analysis in our study populations was plasma creatinine: it alone explained 9% of the variation in men and 2% in women; and 24% in Melanesians and 5% in Asian Indians. Our findings suggest a strong renal involvement in the balance of plasma uric acid and may also reflect certain dietary patterns, such as a high intake of protein, fats, and certain local vegetables. Although the prevalence of hyperuricemia was high, 27% in both Melanesian men and women, 22% in Asian Indian men, and 11% in Asian Indian women, clinical gout was uncommon. Many predictor variables and their interactions were analyzed along with the reasons for the high plasma uric acid levels in persons with impaired glucose tolerance and for the low plasma uric acid levels in diabetic patients.
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PMID:Plasma uric acid level and its association with diabetes mellitus and some biologic parameters in a biracial population of Fiji. 333 86

The therapeutic efficacy of cyclosporine (CsA) as an immunosuppressive agent was complemented by a modest, long-term incidence of toxic complications in 402 renal allograft recipients engrafted one to five years prior to analysis. The overall patient and graft survivals at one year were 97% and 84% (actual), and at five years 92% and 67% (actuarial). The immunosuppressive therapeutic index was excellent: only 12% of allografts were lost from rejection, with 5% of patients succumbing to infection. While infections were common, tending to emanate in the urinary tract or to be viral in etiology, they were generally mild and readily controlled. Only four patients displayed malignancies; none succumbed to this cause. The most common toxic complication was hypertrichosis, which was accentuated in pediatric patients. While tremors occurred in 20% of patients, primarily during the first three months, other neuroectodermal complications of parethesias, depression, somnolence, and seizures were rare. Hepatotoxicity, which was noted in 50% of patients, particularly recipients of cadaveric grafts, generally was first seen as a transaminase elevation, at least partially reversible by dose-reduction and abating by the third year. Associated disturbances of cholelithiasis and pancreatitis were occasionally observed. Nephrotoxicity was the only persistent, long-term complication. Hypertension occurred in 72% of patients during the first month, 36% in the second year, and about 15% thereafter. Hyperuricemia, which occurred in about 30% of recipients during the first two years, was occasionally associated with symptomatic gout. The mean serum creatinine level remained elevated throughout the follow-up period at 1.8-1.9 mg/dl, suggesting persistent, but nonprogressive, drug-induced renal injury. The present analysis documents the relative safety of CsA for long-term therapy, and highlights the need for new approaches to ameliorate drug-induced nephrotoxicity.
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PMID:Complications of cyclosporine-prednisone immunosuppression in 402 renal allograft recipients exclusively followed at a single center for from one to five years. 354 76

After longterm treatment (mean duration 7.2 years) with antihyperuricemic drugs, ten tophaceous gouty patients requested withdrawal of the medication because they had not felt any arthritic pains for years, the tophi had disappeared, and they disliked the idea of taking the medicine daily for the rest of their lives. Five patients (Group I) had no recurrence of either arthritis or tophi during follow-up for 18 to 52 months (average duration 33 months). Five patients (Group II) had a recurrence of arthritis 5 to 29 months (average 15.8 months) after cessation of therapy and two of them developed tophi again at 29 months and resumed treatment. Group II patients tended toward obesity, more severe hyperuricemia and an earlier age onset of gout, as compared with Group I patients. The creatinine concentration determined before, during, and after treatment showed no change. On the basis of the present findings it seems justified to withdraw medication in cases of tophaceous gout in remission when aggravating factors such as obesity and severe hyperuricemia are absent. Attacks of gout and tophi are likely to recur, but so far in our series the duration of the symptom-free period without medication is almost three years for Group I patients, who are now considered as "asymptomatic hyperuricemics".
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PMID:Withdrawal of longterm antihyperuricemic therapy in tophaceous gout. 358

The plasma concentrations of oxipurinol, the chief metabolite of allopurinol, were studied in 66 patients with gout in whom the dose of allopurinol varied between 100 and 400 mg per day. Renal function ranged from normal to moderately impaired. Plasma oxipurinol concentrations correlated directly with both allopurinol dosage and with renal glomerular function as reflected by the plasma creatinine concentration. Plasma oxipurinol concentrations between 30 and 100 mumol/l were generally effective in controlling hyperuricaemia. However, oxipurinol concentrations usually rose above this range if the daily dose of allopurinol exceeded 300 mg in patients with plasma creatinine concentrations of 0.2 mmol/l or more. In patients with normal renal function, a rise of the plasma xanthine concentration to between 6 and 9 mumol/l suggested a satisfactory degree of xanthine oxidase inhibition. These measurements are particularly useful in patients who are still hyperuricaemic despite the usual doses of allopurinol.
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PMID:Plasma oxipurinol concentrations during allopurinol therapy. 369 Jan 40

We aspirated synovial fluid from the knees of 50 patients with asymptomatic, nontophaceous gout, in whom synovial fluid monosodium urate (MSU) crystals had previously been documented in the knees or other joints. Fifty-eight percent of these asymptomatic patients had MSU crystals in their knee joints. Serum uric acid levels, serum creatinine levels, volume of synovial fluid aspirated, and cell counts of the aspirated fluid did not differentiate the MSU crystal-positive group from the group without MSU crystals. Clinical factors such as alcohol abuse, coronary heart disease, hypertension, duration of gout, duration of the intercritical period, and drug therapy did not differentiate the 2 groups. Nineteen patients consented to aspiration of their other knee. Seven of these patients (37%) had MSU crystals bilaterally, and 6 patients (32%) had them unilaterally. The implications of the persistence of MSU crystals (including those in intracellular locations) in many patients, despite normalization of serum uric acid levels, should be determined. Knee joint aspiration is a sensitive method for the demonstration of MSU crystals in asymptomatic patients. The procedure might also be useful in documenting these crystals in patients who have had attacks of arthritis with features consistent with a diagnosis of gout, but in whom MSU crystals have not been documented.
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PMID:Monosodium urate crystals in the knee joints of patients with asymptomatic nontophaceous gout. 380 Oct 71

To quantify the consequences of asymptomatic hyperuricemia, this study examined rates for a first episode of gouty arthritis based on 30,147 human-years of prospective observation. A cohort of 2,046 initially healthy men in the Normative Aging Study was followed for 14.9 years with serial examinations and measurement of urate levels. With prior serum urate levels of 9 mg/dl or more, the annual incidence rate of gouty arthritis was 4.9 percent, compared with 0.5 percent for urate levels of 7.0 to 8.9 mg/dl and 0.1 percent for urate levels below 7.0 mg/dl. With urate levels of 9 mg/dl or higher, cumulative incidence of gouty arthritis reached 22 percent after five years. Incidence rates were three times higher for hypertensive patients than for normotensive patients (p less than 0.01). The strongest predictors of gout in a proportional hazards model were age, body mass index, hypertension, and cholesterol level, and alcohol intake. When the serum urate level became a factor in the model, none of these variables retained independent predictive power. At the final examination, only 0.7 percent of participants had a serum creatinine level of 2.0 mg/dl or more, with no evidence of renal deterioration attributable to hyperuricemia. These data support conservative management of asymptomatic hyperuricemia.
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PMID:Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. 382 98

Interaction of thiazide diuretics and the serum uric acid and creatinine levels was studied in 3693 stepped care participants in the Hypertension Detection and Follow-up Program not receiving treatment at baseline. Among men grouped into quartiles by their level of uric acid at baseline, the upper quartile (average uric acid, 7.7 mg/dL [458 mumol/L]) had an average serum creatinine level of 1.2 mg/dL (106 mumol/L) and the lowest quartile (uric acid, 4.9 mg/dL [291 mumol/L]) had an average serum creatinine level of 1.1 mg/dL (97 mumol/L). Similar findings were present in women. Therapy with chlorthalidone or other thiazide-type diuretics tended to increase levels of uric acid and creatinine, but the increase in both was less in the upper quartile than in the lower quartile. Among individuals who were prescribed uric acid-lowering drugs, the level of serum creatinine increased just as much as in those whose uric acid level was not pharmacologically lowered. Baseline uric acid level was a weak predictor of mortality in men; the introduction of an interaction term for creatinine suggested that this effect was primarily restricted to those with elevated levels of both uric acid and creatinine at baseline. Change in uric acid level at one year after therapy was inversely correlated with mortality in men. There were few episodes of gout (only 15 recorded in five years among 3693 participants at risk). These results suggest that neither the baseline uric acid level nor the change in uric acid level produced by therapy injures the kidney. These results suggest no reason to lower uric acid levels pharmacologically in the treated hypertensive patient who is not gouty. They leave unanswered whether there is a predictive value to baseline uric acid level not explainable by other correlated cardiovascular risk factors.
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PMID:Is thiazide-produced uric acid elevation harmful? Analysis of data from the Hypertension Detection and Follow-up Program. 382 51


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