After partial hepatectomy (about 70%) in rats, the activities of adenylate cyclase, guanylate cyclase, and cytidylate cyclase and contents of cAMP, cGMP, and cCMP in the regenerating livers were assayed by enzyme immunoassays, which were recently established by our laboratory.
cAMP contents in regenerating livers at 4-16 hr after hepatectomy were about 2.5-3 times greater than those in normal livers, but adenylate cyclase activities were not changed during this experimental period. cCMP contents and guanylate cyclase activities were almost the same levels as prehepatectomy levels. cCMP contents in the regenerating liver has been shown to increase at 4 hr and 16 hr after hepatectomy in biphasic manner. Cytidylate cyclase activities remain unchanged.
These findings were identical to those reported by other investigators using RIA technique. It was confirmed that cyclic nucleotides were exactly and simply assayed by these enzyme immunoassays.

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The influences of steroid hormone on the uric acid metabolism were evaluated by measuring serum and urine uric acid, uric acid clearance (Cua) and uric acid creatinine clearance ratio (Cua/ Ccr) in 10 control subjects and 14 patients being treated with prednisolone.
In patients being treated with prednisolone, serum uric acid was 3.8=E0.9mg/d1 (mean: LSD), urine uric acid was 3917E139mg/day, Cua was 7.49±2.67m1/min and Cua/Ccr was 12.7±4.8%.
In control subjects, serum uric acid was 5.5±0.9mg/d1, urine uric acid was 361±146mg/day, Cua was 4.30±1.95m1/min and Cua/ Ccr was 8.5±2.9%.
There were significant differences in serum uric acid (P0.01), Cua (P<0.05) and Cua/Ccr (P<0.05) between patients being treated with prednisolone and control subjects, but no significant differences in urine uric acid.
Serum uric acid significantly more decreased (P<0.05) and Cua and Cua/Ccr significantly more increased (P<0.01) in patients after treated than in before treated.
These results indicate that prednisolone may decrease the production of uric acid and may increase the renal clearance of uric acid.

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The author measured the serum uric acid (SUA) in 15 patients with leukemia and gained the following findings.
(1) Hyperuricemia with the SUA levels over 8.0 mg/dl was found in 4 of 15 cases. Hypouricemia with the SUA levels below 2.0 mg/dl was not found.
(2) There were not significant correlations between SUA levels and white blood cell (WBC) counts, serum lactic dehydrogenase (LDH) and hemoglobin. However, the patients with hyperuricemia showed the WBC counts over 5×10⁴/mm³.
(3) After the administration of antileukemic agents, the almost parallel reduction of SUA, WBC counts and serum LDH was observed. Hypouricemia appeared in a few patient during the treatment of these drugs.

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Twentythree massive obese subjects, twelve men (2077±21%IBW)and eleven women (194±24%IBW), were hospitalized and put on a low-calorie diet (600-1000kcal) for intensive weight reduction. Serum levels of uric acid, lipids and lipoproteins were determined before and during weight-loss.
Massive obese subjects had higher uric acid levels 8.0±2.0mg/dl in male,6.2±1.7mg/dl in female, and hyperuricemia group was acompanied with higher triglyceride levels,234-1-127mg/dl in male,210+29mg/dl in female before treatment than normal control. Urinary uric acid did not increase in massive obese patient,465±277mg/day in male and 498±252mg/day in female when compared with control subjects,601±146mg/day and 499±168mg/day, respectively. While the ratio of uric acid clearance to creatinine clearance were significantly decreased 4.7±3.1% in male and 8.4+4.5% in female than those in control subjects. Therefore it is likely that hyperuricemia in massive obese subjects is mainly attributable to a reduced renal clearance of uric acid.
During weight reduction, body weight and fat cell volume were decreased slowly in all period. It was confirmed using CT scan ning method that reduction of weight was exclusively due to the reduction of fat tissue and no destruction of lean body mass occured. Serum cholesterol, triglyceride and HDL-cholesterol levels fell rapidly with weight-loss for 2-4 we eks. In contrast to the changes in serum lipid levels, uric acid levels were not consistent during weight reduction, indicating that the associa tion between uric acid metabolism and lipid metabolism did not link directly in massive obese subjects.

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Changes in serum urate concentration (S-UA), urine flow (U_flow) and urinary urate excretion rate (U_UA) after sodium (Na)or potassium (K) administration were detected in Japanese young athletes. Subjects (n=11, male,19-22 yrs) drank 500 ml of 0.6%saline (Na solution) or 1.2% potassium gluconate (K solution)within 10 minutes after more than ten hours' overnight fasting and water depletion. Experimental temperature was 23±2°C, and the humidity was 40-65%.
S-UA, U_flow, urinary urate (cU_UA), Na (cU_Na), K (cU_K) concentrations and creatinine clearance (C_cr) were measured throughout the experiment, from one hour before till five hours after drinking.

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The patient was a 24-year-old woman. Her parents were consanguineous. She had had abdominal distension and low stature from her childhood. She had often had nasal bleeding. She had never had convulsion or disturbances of consciousness. She had arthralgia at her right foot joint and was referred to our hospital.
She was 140 cm tall and weighed 43 kg. She had a round face and reddish cheeks. The liver edge felt at about 3 cm below the right costal margin. She had hyperuricemia (13.2 mg/dl), hyperlactemia (58 mg/dl) and hyperlipidemia. The fasting plasma glucose level was subnormal (65 mg/dl). Blood lactate level was decreased by an oral glucose load. The plasma glucose was not increased after an oral load of 90 g of fructose or galactose. Glucose 6-phosphatase activity of intestinal mucosa was decreased to less than 10% of the normal control. Glycogen content of intestinal mucosa was increased to 10.3 mg/g (the normal control,1.5).
Blood uric acid was increased and serum inorganic phosphate was decreased after glucagon injection. Hyper-reaction of serum uric acid in fructose tolerance test disappeared after the administration of allopurinol. Clearance ratio of uric acid to creatinine was low. Hyperuricemia in our case may be due to enhanced purine metabolism and low excretion of uric acid.

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We encountered 337 cases of gout for these ten years and found complication of urolithiasis in 44 cases (13.3%) of them. We studied these cases by dividing them into two groups: gout cases (G group) and complicated ones with urolithiasis (G+S group).
The age of the first gouty attack was about 5 years earlier in G+S group than in G group. Both serum urate level and urinary urate excretion were significantly higher in G+S group than in G group. However, there was no significant difference between the two groups in creatinine clearance and uric acid clearance. Stones were obtained from 15 cases out of G+S group. The components of these stones were uric acid in 5 cases; uric acid and calcium oxalate in 2 cases; calcium oxalate in 4cases; and calcium oxalate and calcium phosphate in 4 cases. The results thus obtained were found considerably different from those reported by Gutman.
These findings l e d us to consider as regards effects of hyperuricemia or hyperuricosuria on urolithogenesis that besides occurrence of uric acid stone in acidic urine, excessive monosodium urate in urine may accelerate formation of urinary stones consisting of such components as calcium stone or cystine stone.

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Materials: Two cases of gout in association with rheumatoid arthritis were made a investigation into purine metabolic system to obtain its etiological hints, because such these cases were very rare in frequency and it's clinical cause were still not know. The former case, a male aged 72 years, had previously in episode of gouty attack in addition with polyarthralgia. Diagnostic radiological pictures were observed punched out lesion and erosive changes in bones. The serum uric acid level was determined at the value of 10.3 mg/dl, besides rheumatoid factor was positive. Synovia procured from the wrist joint by open biopsy was histologically proved typical rheumatoid changes. The latter case, a male aged 47 years, had also an episode of gouty attack and polyarthralgia. Clinical features were demonstrated a lot of gouty nodules and some erosive changes were radiologically present in bones. Rheumatoid factor was positive at a titer of 1: 1024. Aspiration material from the nodule was revealed unequivocal MSU crystals under the microscopic observation.
Method: The contents of adenosien deaminase (ADA) activity in lymphocytes and erythrocytes were measured in each cases to study the enzymatic activity of purine metabolic system.
Results: The contents of ADA activity in erythrocytes were as high as those of simple gout. The contents of ADA in lymphocytes were higher than those of gout or rheumatoid arthritis respectively.
Conclusion: From the investigation, the etiology of these cases is speculated to be based on the anomalies of enzymatic activity in purine metabolic system.

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Blood sample obtained from a girl of 7 years old who received a diagnosis of urolithiasis of 2,8-dihydroxyadenine was subjected for enzymological studies on purine nucleotide biosynthesis including APRTase, HGPRTase, PRPPsynthetase.
APRTase activity in erythrocyt e s was 0.45nmoles/mg prot. /hr (2.5 per cent of normal) in the patient, and 4.75, 3.94, 6.20nmoles/mg prot. /hr (ranging from 20 to 31 per cent of norm al) in her clinically healthy brother, father and mother respectively. But HGPRTase activity in erythrocytes was 73.2, 70.0 nmoles/mg prot/hr (within normal range) and PRPPsynthetase activity in erythrocytes was 36.0,31.8 nmoles/mg prot. /hr (within normal range) in the patient and her mother respectively.
These findings suggested that the patient is homozygote and families are heterozygotes for this enzyme defect and the expression in phenotype is variable. In this case, however, the possibility of acceleration of IMP production is not excluded, because PRPP concentration in erythrocytes is thought to be elevated than that of normal subjects.
This possibility is now under investigation using high performance liquid chromatography.

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The serum uric acid were determined in pregnancy, labour, puerperium and toxemias. The results were as follows.
(1) The serum uric acid levels increase up t o the termination of pregnancy and reach to the maximum levels after labour. But they decrease gradually in puerperium.
(2) Very high serum uric acid levels were observed in toxemia of pregnancy. In this case, the cause of hyperuricemia was thought to be due to the decrease of uric acid clearance.

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A 62-year old man was admitted to this hospital with fever and gingival bleeding.
On admission, the white blood cell (WBC) count was 10,200/mm³,92% of which being myeloblasts. The serum uric acid (SUA) level was 3.2 mg/dl. After the administration of antileukemic agents, the SUA level decreased to 0.9 mg/dl at minimum with the decrease of WBC, and at that time the urinary excretion of urate and the uric acid clearance (C_UA) was about 900mg/day and 25.6 ml/min respectively. However, the SUA level and C_UA returned to normal during remission.
The above results indicate that impaired tubular dysfunction was the main factor responsible for the fall in the SUA level.

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Vol. 6 (1982) No. 2 p. 144

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