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)

Introduction. Therapeutic doses of colchicine in patients with renal compromise and cyclosporine therapy may result in increased plasma concentrations of colchicine and colchicine toxicity. Case Report. A 60-year-old heart transplant patient with chronic renal failure and cyclosporine-induced immunosuppression was started on colchicine for suspected gout. Four days later, he developed multi-organ failure with rhabdomyolysis, liver damage, polyneuropathy, and cardiotoxicity. Colchicine intoxication was suspected and plasma levels were 7 ng/mL 36 hours after the sixth dose. Neutropenia with an absolute neutrophil count of 700 cells/mm3 was observed five days after colchicine discontinuation. Drug discontinuation, supportive care, antibiotic therapy for a concurrent infection, and G-CSF administration resulted in recovery and he was discharged from the hospital 3 weeks later. Discussion. Cyclosporine co-administration increases colchicine toxicity by a dual mechanism: cyclosporine inhibits P-glycoprotein resulting in increased intracellular colchicine concentrations and decreased hepatic and renal excretion of the drug and cyclosporine interacts with CYP3A4 to decreases the hepatic elimination of colchicine. On the other hand, colchicine may increase cyclosporine neurotoxicity by an addictive mechanism. Conclusions. Shortterm administration of therapeutic colchicine doses may cause life-threatening side effects in cyclosporine-treated patients with renal failure.
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PMID:Colchicine-induced toxicity in a heart transplant patient with chronic renal failure. 1860 82

Treatment of gout and hyperuricemia can be difficult in patients with chronic renal failure. At present, there is no study available comparing the efficacy of the most widely used agent, allopurinol, and the uricosuric benzbromarone for the control of hyperuricemia in patients with renal insufficiency. We describe an open, randomized, actively controlled, comparative trial in patients with clearance of creatinine from 20 to 80 mL/ min/1.73 m(2). Patients were randomized to take benzbromarone (100-200 mg/day) or allopurinol (100-300 mg/day). Outcome variables were the following: reduction of serum urate (Sur), Sur & tl; 6 mg/dL (357 micromol/L), reduction of gouty bouts and reduction of tophi. During 9-24 months of follow-up 36 patients were studied.The reduction of Sur was higher with benzbromarone, and only 1 of 17 patients taking benzbromarone did not achieve Sur < 6 mg/dL versus 7 of 19 taking allopurinol. Patients who did not reach optimal Sur levels with allopurinol were more frequently taking diuretics and showed lower fractional excretion of urate and higher initial Sur levels than patients with proper control of Sur. Seven patients with suboptimal control of serum urate were changed to benzbromarone 100 mg/day, which showed efficacy similar in those who were initially randomized to benzbromarone. A reduction of gouty bouts and size of tophi was observed after proper control of Sur. Allopurinol is effective in controlling hyperuricemia, but patients with higher initial Sur levels or taking concomitant diuretic therapy are less prone to reach therapeutic goals.Benzbromarone is useful for the control of hyperuricemia in patients with renal insufficiency even with concomitant diuretic administration; patients benefited include those who previously had no improvement by taking allopurinol.
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PMID:Treatment of chronic gout in patients with renal function impairment: an open, randomized, actively controlled study. 1907 56

Spontaneous ruptures of the extensor mechanism of the knee are very rare. They tend to increase considerably in patients with metabolic diseases such as chronic renal failure, hyperparathyroidism, diabetes, gout, and systemic lupus erythematosus. The reported case regards a 48-year-old man with chronic, spontaneous and simultaneous quadriceps, and contra-lateral patellar tendon rupture. The patient suffered from chronic renal failure and for the past year from tertiary hyperparathyroidism. Ruptured tendons were repaired and both knee were evaluated monthly for the next 12 months. Good functional recovery was achieved on both knees without relapse. This case emphasizes the importance of long-term high parathyroid hormone level in the etiology of tendons ruptures.
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PMID:Simultaneous chronic rupture of quadriceps tendon and contra-lateral patellar tendon in a patient affected by tertiary hyperparatiroidism. 1938 13

A 56-year-old woman presented with a 6 month history of bullae and whitish plaques of the fingers. She had chronic renal failure, but no joint pains or evidence of arthritis. An aspirate of fluid from a bulla revealed uric acid crystals and serum uric acid was elevated at 16.2 mg/dL. A diagnosis of tophaceous gout was made.
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PMID:Whitish bullae on the fingers: what is the diagnosis? Tophaceous gout. 1972 83

GLUT9 is a novel, facilitative glucose transporter isoform that exists as two alternative splice variants encoding two proteins that differ in their NH(2)-terminal sequence (GLUT9a and GLUT9b). Both forms of GLUT9 protein and mRNA are expressed in the epithelia of various tissues; however, the two splice variants are expressed differentially within polarized cells, with GLUT9a localized predominantly on the basolateral surfaces and GLUT9b expressed on apical surfaces. Protein expression of GLUT9 drops under conditions of starvation but increases with addition of glucose and under hyperglycemic conditions. The substrate specificity of GLUT9 is unique since, in addition to transporting hexose sugars, it also is a high-capacity uric acid transporter. Several recent large-scale human genetic studies show a correlation between SNPs mapped to GLUT9 and the serum uric acid levels in several different cohorts. The relationship between GLUT9 and uric acid is highly clinically significant. Elevated uric acid levels have been associated with metabolic syndrome, obesity, diabetes, hypertension, and chronic renal failure. Although some believe uric acid is elevated as a result of these diseases, there is now evidence that uric acid may play a role in the pathogenesis of these diseases. It is also known that GLUT9 is expressed in articular cartilage and is a uric acid transporter, and thus it is possible that GLUT9 plays a role in gout, a disease of uric acid deposition in the joints. In addition, some studies have suggested that intake of fructose plays an important role in causing elevated serum uric acid levels, especially in diabetes and obesity. It is possible that GLUT9, which seems to be both a fructose and a uric acid transporter, plays an important role in these conditions associated with hyperuricemia.
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PMID:Facilitative glucose transporter 9, a unique hexose and urate transporter. 1979 40

Percutaneous radiofrequency thermal ablation (RFA) is considered an effective technique for providing local control in the majority of Hepatocellular carcinoma (HCC) patients. Although RFA is generally well tolerated, recent studies have reported complications associated with RFA. We describe a case of acute gouty arthritis in a 71-year-old man with chronic renal failure who was treated with RFA for a HCC lesion and who had hepatitis B-associated cirrhosis and mild renal insufficiency. Regular surveillance of the patient detected a 3.5 cm HCC lesion. Because the patient had declined surgery, RFA was chosen for therapy. On the third post-procedural day, the laboratory results showed increases in his uric acid and potassium levels, which were compatible with a tumor lysis syndrome. On the 6th post-procedural day, the patient complained of new right knee pain. Subsequent joint aspiration revealed monosodium urate monohydrate crystals. We made the diagnosis of acute gouty arthritis arising from tumor lysis and liver infarction caused by HCC ablation, which was aggravated by acute renal insufficiency. After adequate hydration and administration of oral colchicines, the patient's right knee pain subsided and the uric acid serum level returned to normal. This is the first described case of acute gouty arthritis after RFA for a HCC lesion in a patient with underlying chronic renal insufficiency. To avoid hyperuricemia and an acute attack of gout after RFA therapy for HCC, early identification of patients at risk is warranted, such as those with a large tumor, rapid tumor growth, and renal insufficiency, and preventative measures should be considered.
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PMID:A case of gouty arthritis following percutaneous radiofrequency ablation for hepatocellular carcinoma. 2013 29

Quadriceps tendon rupture is an uncommon injury; the incidence of simultaneous bilateral quadriceps tendon rupture is extremely rare. Two distinct categories-individuals older than 50 years and between 27 and 54 years-have been described. Bilateral quadriceps tendon rupture is more common in patients older than 50 years and is thought to be the result of tendon weakening due to obesity and arteriosclerosis-induced fibrotic changes, or previous injury.In younger individuals, bilateral simultaneous quadriceps rupture is less frequent and has been associated with anabolic steroid use, but more frequently with underlying comorbid medical conditions such as chronic renal failure, hyperparathyroidism, endocrine disorder, gout, diabetes and obesity, which predispose the patients to tendon rupture. Our case report is unique because we report the simultaneous bilateral quadriceps tendon rupture following minor trauma in an otherwise healthy 43-year-old man with no predisposing comorbidity.
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PMID:Bilateral quadriceps tendon rupture: a rare finding in a healthy man after minimal trauma. 2034 79

A case of fluvastatin-induced rhabdomyolysis after coadministration of colchicine is reported. A 77 year old man with ischemic heart disease, chronic pericardial effusion, diabetes mellitus, dyslipidemia, arterial hypertension, chronic renal failure (stage 2 of classification of chronic kidney disease of National Kidney Foundation) and chronic gout presented with a generalized muscle pain. The patient had been taking 80 mg/day of fluvastatin for 4 years, and, for four weeks before presentation, he had also been taking a dose of colchicine (1.0 mg daily) for an exacerbation of gout. Investigations confirmed the diagnosis of rhabdomyolysis. Discontinuation of fluvastatin and colchicine therapy and adequate fluid administration resulted in the resolution of clinical and biochemical features of rhabdomyolysis. Although neuromuscular adverse effects of fluvastatin and colchicine are well recognized, rhabdomyolysis is rare, making this is only the second case reported of fluvastatin and colchicine co-administration induced rhabdomyolysis in literature.
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PMID:Rhabdomyolysis induced by co-administration of fluvastatin and colchicine. 2111 May 12

Objective. To evaluate the association between the purported risk factors for chondrocalcinosis and gout and the risk of pseudogout in the general population. Methods. We conducted a case-control study nested within a UK general practice database (The Health Improvement Network) by identifying incident cases of pseudogout between 1986 and 2007 and up to 10 control subjects matched to each case, based on age, sex and follow-up time. We evaluated the purported risk factors for chondrocalcinosis (i.e. OA, RA, hyperparathyroidism and diuretics) and established risk factors for gout (as comparison exposures) using conditional logistic regression analysis. Results. We identified 795 cases of pseudogout and 7770 matched control subjects. The risk of pseudogout was associated with hyperparathyroidism [odds ratio (OR) 4.87; 95% CI 2.10, 11.3], OA (OR 2.91; 95% CI 2.48, 3.43) and loop diuretic use (OR 1.35; 95% CI 1.09, 1.67). RA, thiazide diuretic use, BMI and other gout risk factors were not associated with the risk of pseudogout, except for chronic renal failure (OR 2.29; 95% CI 1.30, 4.01). Conclusion. This general population study based on physician-recorded pseudogout suggests that most of the previously observed associations with chondrocalcinosis are replicable with the risk of pseudogout, but there are notable differences, such as thiazide diuretics, RA and chronic renal failure, highlighting the need to study the clinical outcome, pseudogout. Avoiding loop diuretics may help individuals with recurrent pseudogout.
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PMID:Risk factors for pseudogout in the general population. 2288 40

Allopurinol is a drug that has been used for decades to lower serum urate levels in patients with gout or chronic renal failure and in cancer patients undergoing chemotherapy at risk of tumor lysis syndrome. Patients may develop cutaneous hypersensitivity reactions, ranging from mild rashes to potentially fatal severe cutaneous adverse reactions (SCARs) namely drug hypersensitivity syndrome, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN). Recent studies have demonstrated the association between human leukocyte antigen (HLA) B*58:01 allele and allopurinol-induced SCARs, which might explain ethnic differences in their incidences. Genotyping is now required before starting abacavir and carbamazepine so as to identify individuals susceptible to SJS. However, no genetic screening is advocated before commencement of allopurinol. The lack of availability of a rapid and inexpensive screening test for the HLA-B*58:01 allele is one of the obstacles to such screening. Development of a test that is quick, accurate, and cost-effective is warranted.
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PMID:Pharmacogenetics of allopurinol--making an old drug safer. 2338 51


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