Gout is increasing in prevalence throughout the world, particularly in developed countries. The causes are dietary--purine-rich foods, high saturated fats, fructose-containing drinks and alcohol. Gout is also drug-related and associated with increased obesity, hypertension, insulin resistance and metabolic syndrome. Although very readily treated, there is evidence that physicians fail to optimi...

L-Lactate, the only known anaerobic end-product in decapod crustaceans (Gade, 1983), increases haemocyanin oxygen-affinity (Tnichot, 1980; Mangum, 1983; Bridges and Morris, 1986). In exercised blue crabs, Callinectes sapidus, the decrease in haemocyanin oxygen-affinity induced by metabolic acidosis via the Bohr shift was substantially balanced by the opposing effect of L-lactate (Booth etal, 19...

Under inpatient controlled conditions 4 patients with gout and hypertension were treated with varying doses of tienilic acid, a new uricosuric diuretic. Plasma urate levels were reduced by an average of 50% in association with significantly increased urinary urate excretion. A twice-daily regimen was considerably more effective than a single morning dosage in reduction of plasma urate, though b...

Serum Vitamin A, total protein, serum electrophoresis, were determined in pediatric patients with urolithiasis (mostly bladder stones) and compared to that of normal healthy volunteers. The level of Vitamin A in healthy volunteers was found to be significantly (P<0.001) higher than that of patients with urolithiasis. The amount of total serum protein, how­ever, was not significantly different i...

Ammonium acid urate urolithiasis is a quite rare condition. Our literature review of ammonium acid urate urolithiasis suggests that ammonium acid urate urolithiasis should be regarded as a general medical complication related to anorexia nervosa, and purging by laxative abuse might be a crucially important risk.

Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomati...

Investigation of the genetic basis of hyperuricaemia is a subject of intense interest. However, clinical studies commonly include hyperuricaemic patients without distinguishing between 'over-producers' or 'under-excretors' of urate. The statistical power of studies of genetic polymorphisms of genes encoding renal urate transporters is diluted if 'over-producers' of uric acid are included. We pr...

ments suggest that at physiological concentrations, only urate contributes to the artifactually high pre-dialysis values. When a standard serum sample was increased in concentration (in vitro) from 11.6 to 54 mmol/L in urea, from 97 to 1130 mmol/L in creatinine, and from 0.31 to 1.38 mmol/L in urate, values for apparent SFA were unaffected by urea or creatinine changes, but rose 13% in the pres...

Hyperuricemia results from an imbalance between the rates of production and excretion of uric acid. Longstanding hyperuricemia can lead to gout, which is characterized by the deposition of monosodium urate monohydrate crystals in the joints and periarticular structures. Because such deposits are resolved very slowly by lowering plasma urate with available drugs or other measures, the symptoms o...