Automated Analysis of Uric Acid

A B S T R A C T The effects of administration of drug combinations on uric acid excretion were studied in order to test the hypothesis that a portion of renal tubular reabsorption of uric acid occurs distal to the uric acid secretory site.Oral administration of pyrazinamide (3 g) during probenecid uricosuria (probenecid 500 mg every 6 h) decreased urate excretion from 463 isg/min following probenecid medication alone to 135 /Ag/min following probenecid plus pyrazinamide (P <0.01). When a greater uricosuric effect was induced with a 2 g oral dose of probenecid, the decrement in urate excretion which followed pyrazinamide administration (3 g) was more pronounced (2,528 u'g/min following probenecid alone, 574 t&g/min following probenecid plus pyrazinamide).Results were similar when an 800 mg oral dose of sulfinpyrazone was given in place of probenecid (1,885 ig/min following sulfinpyrazone alone, 475 /hg/min following sulfinpyrazone plus pyrazinamide). Thus, apparent urate secretion (measured as the decrease in excretion of urinary uric acid resulting from pyrazinamide administration) appeared to vary, depending upon the degree of inhibition of reabsorption produced by probenecid or sulfinpyrazone.When small doses of aspirin were administered in place of pyrazinamide to produce secretory inhibition, the results were similar.Neither probenecid nor pyrazinamide significantly altered urate excretion when administered to patients with serum salicylate levels above 14 mg/100 ml.These results are interpreted as suggesting that renal tubular reabsorption of uric acid occurs at least in part at a postsecretory site and that a portion of secreted urate is reabsorbed. During maximum probenecid-or sulfinpyrazone-induced uricosuria, inhibition of urate secre-

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“…Y.). Uric acid was determined by an automated enzymatic spectrophometric technique (12). Salicylate was determined by the method of Keller (13).…”

Section: Methodsmentioning

confidence: 99%

Evidence for a Postsecretory Reabsorptive Site for Uric Acid in Man

Diamond¹,

Paolino²

1973

J. Clin. Invest.

129

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“…Compared to the 2 h level recommended by the WHO in 1980 [211, the sensitivity of our criterion was 80% and the specificity was 82%, justification at that time for the level adopted. When the National Diabetes Group [22] and the WHO Expert Committee produced new criteria, it was decided that it would be wiser not to change the method and diagnostic criteria in the last round in 1980-1982. Serum uric acid levels were determined by a method modified by Crowley [23]. Blood was collected and stored at -15~ and assayed for total serum cholesterol and triglyceride concentrations as reported previously [24].…”

Section: Subjects Materials and Methodsmentioning

confidence: 99%

Type 2 (non-insulin-dependent) diabetes mellitus, migration and westernisation: The Tokelau Island Migrant study

Østbye

Welby²,

Prior³

et al. 1989

Diabetologia

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Summary. The migration of Tokelauans from a traditional atoll in the Pacific to urban New Zealand is associated with an increased prevalence and incidence of Type 2 (non-insulindependent) diabetes mellitus over the period [1968][1969][1970][1971][1972][1973][1974][1975][1976][1977][1978][1979][1980][1981][1982]. During the same period, a lesser but definite increase is seen among non-migrants in Tokelau. The age standardised prevalence rates rose from 7.5 and 11.7 to 10.8 and 19.9 per 100 respectively in the male and female migrants compared with an increase from 3.0 and 8.7 to 7.0 and 14.3 per 100 in the nonmigrant males and females respectively. The incidence of diabetes is shown to be consistently higher in the migrants compared to the non-migrants giving relative risks of 1.5 in males and 1.9 in females. The factors most likely contributing to this difference, are changes to a higher calorie, high protein diet, higher alcohol consumption, a greater weight gain and altered levels of physical activity in the migrants. A number of populations in the Pacific have been shown to have a low rate of diabetes in their traditional setting, but may have a genetic predisposition for diabetes which responds to factors in the urban industrialised environment and life-style. The social and economic changes taking place in Tokelau are also clearly increasing the risk of diabetes. To reverse these trends and prevent the development of complications of Type 2 diabetes, it will be important to institute preventive programmes and to follow up the population in both environments for long-term outcomes, including mortality.

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“…Creatinine and uric acid clearances were performed and calculated using standard clearance techniques. Uric acid was determined by an automated enzymatic (uricase) spectrophotometric method (Crowley and Alton, 1968). Creatinine was determined by Autoanalyser method llb.…”

Section: Methodsmentioning

confidence: 99%