The negative association between gout and rheumatoid arthritis is well accepted. Agudelo et al proposed that persistent hyperuricemia might protect against or decreae the expression of rheumatoid inflammation. To test this proposal, we investigated the relationship between the serum uric acid level and the Lansbury's activity index in patients with rheumatoid arthritis (RA).180 consecutive patients with RA were retrospectively studied for at least a year. The following results were obtained:
1) In comparison with normal control, the patients with RA showed significantly lower level of serum uric acid (P< 0.01).
2) In initial observation, there was no correlation between the uric acid level and the activity index.
3) Among 180 patients,15 developed persistent hyperuricemia.
4) There was an insignificant, negative correlation (r=-0.24) between the serum uric acid level and the activity index in those 15 RA patients.
5) A significant improvement, however, in both activity index and ESR during hyperuricemia was noted.
6) The above results suggest the proposal by Agudelo et al is right and apropriate.

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We have purified adenylate cyclase (AC) and cytidylate cyclase (CC) from rat brain. The nucleotide cyclase activities were evaluated by determining cyclic AMP or cyclic CMP by enzyme immunoassay (EIA) which had been developed in our laboratory.
Triton X-100 (0.3%) soluble fractions containing AC and CC were subjected to dodecyl - Sepharose 4 B column chromatography. Further purification was carried out with Sepharose 6 B gel filtration. AC and CC were separated by affinity chromatography with ATP- and CTP- Sepharoses. These findings suggested that AC and CC are different enzyme species.

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The measurement of oxypurines concentrations steadily becomes important because of the usefulness for the diagnosis of hypoxia, ischemic heart disease and malignant diseases as well as the abnormality of purine metabolism like xanthine oxidase defici ency.
But question arises as to whether measurement of the oxypurines concentrations in plasma and serum showed the real concentration in the blood, because it has been reported previously that oxypurines concentrations increased in plasma or serum samples when whole blood samples were stored at room temperature for some time without separation in serum or plasma and blood corpuscles.
Therefore, we examined changes, in plasma concentration of oxypurines as a function of time for 48 hours between venous puncture and centrifugations of whole blood staying at 4°C or incubatimgat 37°C.
We also studied on the cause of difference in plasma oxypurines concentrations between these two groups of samples. Hypoxanthine concentration in plasma was increased even one hour after sampling when whole blood samples were stored at 4°C or at 37°C. In the two groups, however, no significant increase in the plasma concentration of xanthine occurred until 6 hours after venous puncture. Thereafter, both hypoxanthine and xanthine concentrations in plasma continued to increase during the 48-hour period in both, groups. After 48 hours, both hypoxanthine and xanthine concentrations in the plasma were higher in the samples incubated at 37°C than in those stored at 4°C.
The increase in the concentrations of these oxypurines was thought to result from purines catabolism in blood cells, catabolism being more accelerated in the samples incubated at 37°C than in those stored at 4°C because the hypoxanthine concentration in blood cells continued to increase along with increase in hypoxanthine concentration in plasma during 48 hours observation, and was always 2 to 5 times as high as that in plasma in both groups.
In addition, we investigated whether uric acid, hypoxanthine and xanthine concentrations in plasma increased when platelet rich plasma was stored at 4°C for 24hours, because platelets were known to have xanthine oxidase. After 24 hours, the hypoxanthine concentration in plasma increased significantly but those of uric acid and xanthine did not.

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Four purine bases, adenine, guanine, hypoxanthine and xanthine in various Japanese alcoholic beverages were quantitatively analyzed using high-performance liquid chromatography(HPLC). All samples were hydrolyzed at 100°C for 1 hr with 60-70% perchloric acid. The hydrolyzed samples were neutralized with potassium hydroxide and subjected to cation exchange HPLC for analysis of guanine, hypoxanthine and xanthine, and to reversed phase HPLC for adenine. Total purine contents were as follows; beer: 4.35~6.86 mg/dl whisky: 0.12 mg/dl, brandy: 0.38mg/dl, shouchu: 0.03 mg/dl, sake: 1.21 mg/dl, wine: 0.39 mg/dl respectively. Beer was shown to contain large amounts of purine bases compared with other alcoholic beverages. However, purine contents in Japanese beer were approximately half those of imported beer.

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We studied the effects of muscular exertion on uric acid metabolism in a patient with type VII glycogenosis (muscle phosphofructokinase deficiency), who had hyperuricemia.
Atter mild leg exercise on a bicycle ergometer, plasma inosine and hypoxanthine concentrations increased greatly, as did the plasma uric acid concentration, which showed a delayed response. Urinary excretion of uric acid did not decreased during exercise, but increased during the post-exercise period.
When the patient came to our clinic, the plasma hypoxanthine and uric acid concentrations were markedly elevated. By bed rest, plasma hypoxanthine level was normalized in a short time, and the plasma uric acid level decreased gradually but markedly within two days. In the same manner, urinary excretion of these metabolites was reduced by bed rest.
These findings indicate that large amounts of inosine and hypoxanthine are released from exercising muscle into circulating blood in patients with type VII glycogenosis, and thus hyperuricemia may develop due to overproduction of uric acid.

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Two male siblings with xanthinuria due to xanthine oxidase deficiency are reported. The propositus, a 29-year-old man, had gastroduodenal ulcer. Routine laboratory studies showed an extremely low serum uric acid level (0.1mg/dl)and decreased urinary excreti on of uric acid (4.9 mg /dl 36.8 mg/day), indicating reduced uric acid synthesis. Similar findings were obtained in his elder brother. Further biochemical analyses showed elevated serum levels of xanthine (proposi tus 0.44 mg /dl and his brother 0.40 mg /dl vs. normal controls < 0.02 mg/dl)and hypoxanthine ( 0.14 mg/dl and 0.10 mg /dl vs.0.03 mg/dl), and concomitantly increased urinary excretions of xanthine (51.2 mg/dl and 29.0 mg/dl vs.1.0 mg/dl)and hypoxanthine (15.5 mg /dl and 9.9 mg /dl vs.0.3 mg/dl). Xanthine oxidase activity in duodenal mucosa extracts was undetectable in the propositus and extremely low in his brother ( 0 and 0.2 mU/g tissue vs. normal controls 20.6mU/g tissue). Thus, the diagnosis of hereditary xanthinuria due to xanthine oxidase deficiency was established.

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