SUBJECTS uric acid

Haig, A. "Uric Acid. An Epitome of the Subject" Churchill London, 1906. p 99. 

On purine-free diets individuals excrete 300 to 600 mg. of uric acid per day, which excretion incidentally is subject to daily fluctua-... 

Estrogen is uricosuric and that is most probably the reason why premenopausal women do not have primary gout. Estrogen hormone replacement therapy in post-menopausal women lowered serum uric acid (SUA). Consequently, the prevalence of primary gout in these subjects is similar to what is seen in pre-menopausal women. 

In six healthy subjects, ampicillin caused an increase in urinary uric acid excretion this effect was attributed to competition for active renal tubular reabsorption of urate (SEDA-13, 212). 

Don BR. The effect of trimethoprim on potassium and uric acid metabolism in normal human subjects. Clin Nephrol 2001 55 45-52. 

Plasma Diabetes without nephropathy, diabetic nephropathy III, IV, and V Healthy subjects 50 patients 88 HPLC-UV- MS/MS Adenosine, inosine, uric acid, xanthine, and creatinine (44)... 

The following study demonstrates the effect of dietary protein on uric acid. In the study, human subjects consumed diets containing no protein, normal levels of protein, and extremely high levels of protein. The diets were chemically defined and did not contain purines. The protein-free diet supplied 0.9 g N/day. The normal-protein diet supplied 13 g l>J/day, The extremely high-protein diet supplied 62 g N/day. The feeding trials were 2 weeks in duration. The norma I-protein diet contained 90 g of egg albumin, which was supplemented with 162 g of soy protein plus 156 g of casein in the high-protein diet. 

Studies by CJifford ft /if. 197ft) revealed the effect of purine consumption on uric acid levels. The purines were supplied to human subjects in the form of ribonucleic acid (RNA) 4g/day). Purine consumption resulted in a near doubling of plasma levels of uric acid and a 2.5-fold increase in urinary uric acid, Thi.s demonstrates the need for avoiding purine rich foods in treating hyperuricemia and gout, it has been recommended that the maximal safe limit of RMA in the diet is 2,0 g/day (Clifford ef ai, 1976). 1)115 amount of RNA can be supplied by 340 g cf sardines, 415 g of dried lentils or pinto beans, or 500 g of chicken liver. As few people consume, or would be willing to consume, 500 g of liver per day the limitation of dietary RNA to safe levels would not be expected to be a common concern,... 

Most diuretics cause hyperuricemia. Increased reabsorption of uric acid (along with other solutes) in the proximal tubule as a consequence of volume depletion is one reason however, diuretics also compete with uric acid for excretory transport mechanisms. There is a small increased risk of acute gout in susceptible subjects (73). In the large outcome trials, about 3-5% of subjects treated with diuretics for hypertension developed clinical gout... 

Triamterene has been reported to cause photosensitivity reactions, increase in uric acid concentration, and blood dyscrasias.91 Nephrolithiasis may occur in susceptible patients. Megaloblastic anemia has been reported in patients with depleted folic acid stores such as those with hepatic cirrhosis. In a study conducted on rats, daily treatment of the animals with doses of 1.5, 3 and 4.5 mg/lOOg over the period of three weeks caused severe degenerative changes of renal cortical and medullary tubules resembling osmotic nephrosis.93 Reversible acute renal failure from combined triamterene and indomethacin in healthy subjects is reported.94 It is recommended that this potentially nephrotoxic association be avoided. 

Examination of the urine of subjects receiving EATDA showed that several, if not all, of the urinary purines were excreted in increased amounts. There was, furthermore, no change in the mode of excretion of urates or in the proportion disposed of extrarenally (S12). The suggestion has been made (K18) that the fundamental mechanism of action of these compounds is the blocking of the incorporation of newly synthesized adenine into polynucleotides and/or coenzymes, with the production of an undefined deficiency state. This block could stimulate a compensatory increase in purine biosynthesis. The excess purines would not be utilizable and, therefore, would be excreted from the cells, and the normal degradation by enzymes would convert this material to uric acid. 

B19. Bishop, C., Gamer, W., and Talbott, J. H., Pool size, turnover rate, and rapidity of equilibration of injected isotopic uric acid in normal and pathological subjects. 

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