Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asymptomatic hyperuricemia should be treated only if the plasma uric acid levels are around 10 mg/100 ml or more on several determinations. In addition, patients on a purine-free diet who excrete more than 600 mg uric acid per 24 h should be treated. In both cases, treatment is intended to be prophylactic against gouty nephropathy. At present there is no evidence that primary hyperuricemia alone is a risk factor for early atherosclerosis and especially coronary artery disease. However, more attention should be paid to the accompanying risk factors such as obesity, hyperlipoproteinemia, diabetes mellitus and hypertension.
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PMID:[Which uric acid value is in need of treatment?]. 126 67

Four patients of pure gouty nephropathy are presented. Gout was of over five years duration and asymptomatic nephropathy manifested as non-oliguric acute renal failure. Diseases commonly associated with it like uric acid stones, urinary tract infections, hypertension, diabetes mellitus, hyperlipidemid, obesity and nephrosclerosis were absent. Reduction in serum uric acid level resulted in prompt improvement in renal functions. Early detection and control of hyperuricemia may help in restoration of renal functions.
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PMID:Non-oliguric acute renal failure in gout. 139 13

Thirty patients with gouty arthritis were studied over 3 years. The diagnosis was established with the help of polarised light microscopy. All the patients were males, with a median age of 45 years. They belonged to the middle or upper socio-economic class and were obese (mean body mass index 29.7). Chronic alcoholism, diabetes mellitus and hypertension were present in one patient each. No patient had symptomatic coronary artery disease. Although 6 patients had a history of renal colic, only one had gouty nephropathy with chronic renal failure. Six patients had a positive family history of gout. The disease involved mostly the joints of the lower extremity and podagra was observed in 70% of patients. Eight patients had tophi at various sites. There were 17 'over producers' and 13 'under excretors' of uric acid. The treatment consisted of patient education, symptomatic control with non steroidal anti-inflammatory drugs and/or colchicine and antihyperuricaemic therapy. The overproducers were treated with allopurinol while the under excretors were treated with [corrected] sulfinpyrazone. In general, there was a good response to therapy as indicated by lowering of serum uric acid and the number of painful episodes per year. The overall profile of the disease appears similar to that seen in the West.
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PMID:Clinical profile, therapeutic approach and outcome of gouty arthritis in northern India. 238 54