Xanthine oxidase does not exist in blood usually, but appears often in blood in pathological states such as hemorrhagic hypotensive rabbit, traumatic shock rat and severe patients after extracorporeal circulation and in I. C. U.
Xanthine oxidase converts the hypoxanthine to xanthine to uric acid. It is reported that superoxide occures in the course of uric formation and therefore oxygen consumption increases. Superoxide and its derivatives, so called, active oxygens, oxidizes organic substances in the body and damages the cellular and subcellular membranes.
In our experiment, the formation of uric acid in vitro was accelerated by the increase of both xanthine and xanthine oxidase, po2 descended and β-glucuronidase was released then, and these findings were inhibited by adding of allopurinol.

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As a simple method for analysing urate metabolism abreviation in hyperuricemia of gouty patients, inosine loading test has been investigated.
Eight hundred mg of inosine was injected intravenously into 282 patients with gout and 32 controls (normal subjects and non gouty patients with normal renal function). Urine samples for 60 min. before and after the injection, respectively, and blood samples immediately before and 60 min. after the injection were collected, respectively. Serum uric acid level (Sua), urinary urate excretion (Uua), and creatinine clearance (Ccr), were determined and uric acid clearance (Cua), and clearance ratio (R=Cua /Ccr), were calcurated before and after the injection, respectively.
Serial determination of Sua after the injection of inosine revealed that Sua began to be immediately elevated and reached to a plateau level in 20-30 min. after the injection. The increments at the plateau level of Sua were approximately 2.0 mg/d1 which suggested that the urate pool was enlarged approximately 500 mg in size by the injection. Only 1.8% of inosine injected was detectable in urine collected for 120 min. after the injection. These findings suggested that inoshin injected intravenously was rapidly converted to urate without significant loss of oxypurine and the injection was resulted in a stoichiometric expansion of the urate pool. The elevation of Sua resulted in a parallel increase of Uua with Sua. Therefore, Cua was not changed significantly by the injection. Increments of Sua of gouty patients were exactly the same to that of the control, but increments of Uua in gouty patients were significantly lower than those of the control. Among patients with gout, the increments of Uua in patients of underexcretion type were significantly less than those in patients of overproduction type.
In patients under allopurinol treatment, few increase of Sua and Uua were observed by the inosine loading but in patients under benzbromarone treatment the increment of Sua by inosine loading was significantly lower than that of the control. However, the increments of Uua in patients under the benzbromarone treatment were significantly higher than those of the control, which reflecting action mechanism of the urate production inhibitor and the uricosuric agents, respectively.
These findings indicates that the inosine loading test is a valuable method for estimating urate excretion and also for urate production such as for evaluation of efficacy of allopurinol.

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Associations of various variables such as obesity, hypertriglyceridemia, hypercholesterolemia, hypertension, habitual alcohol intake, administration of antihypertensive drugs and hyperglycemia related to hyperuricemia were studied on 2,583 male employees of various enterprises. 93 cases (31.4%) out of 296 with serum uric acid of more than 7 mg/dl were associated with two or more variables. Frequently observed combinations of variables were that of habitual alcohol intake and obesity (37 cases out of 296,12.5%), of habitual alcohol intake and hypertriglyceridemia (18 cases,6.0%), of habitual alcohol intake, obesity and hypertriglyceridemia (17 cases,5.7%)and of obesity and hypertriglyceridemia (13 cases,4.3%). In 171 cases with hyperuricemia out of 1,580 in which blood pressure was also investigated, frequently observed combinations were that of hypertension and habitual alcohol intake (15 cases,8.7%) and of hypertension, alcohol intake and obesity (12 cases,7.0%). It was suggested that the prevalence of hyperuricemia and the mean serum uric acid levels in group with two or more variables were higher than those with a single variable.

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We reported two cases of 2,8-dihydroxyadenine stone. We studied the clinical and biochemical manifestations of them. APRTase activity and therapy were discussed. We emphasized the importance of differential diagnosis from uric acid stone and of preventive therapy.

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Hyperuricemia is a common finding in acute leukemia. However, recently, hypouricemia was watched with interest in acute leukemia.
In our study, hypouricemia was noted in 66.1% (11 cases). Its value is higher than previous reports.
Renal clearance studies were performed on these cases. A significant correlation between C_UA and %TRP was found, and same correlation between C_UA and C_β2-microglobulin was found. These data showed that hypouricemia was induced from proximal tubular dysfunction.
Few cases revealed hyponatremia with hypouricemia, but there was no data to be responcible for SIADH.

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