It is known that metabolic disorders of uric acid (UA), in particular hyperuricemia (HU), are associated with vascular complications of type 2 diabetes mellitus (DM 2). Previously, the authors established a relationship between the I/D polymorphism of the angiotensin-converting enzyme (ACE) gene and vascular lesions in patients with DM 2 living in Chuvashia. It was of interest to find out how the I/D polymorphism of the ACE gene and metabolic disorders of MC in patients with diabetes mellitus 2 (residents of Chuvashia) are related. ACE gene polymorphism was determined by the I/D polymerase reaction method in 104 patients with diabetes mellitus 2, in 46 of whom UA metabolism was studied in depth. The UA was determined spectrophotometrically in the blood and in daily urine, and the total and fractional renal clearance of the UA was calculated. There were no significant differences in the parameters of UA metabolism depending on the I/D polymorphism. A steady tendency towards a decrease in renal UA clearance was established in the DD genotype. In patients with the DD genotype in comparison with carriers of the I allele (genotypes ID and DD), a lower mean value of UA clearance was recorded (M 10.0, Me 8.4 ml/min versus M 12.4, Me 11.7 ml/min; Z=1.1, p=0.28) and a higher prevalence of its low (<9 ml/min) values: 60% (9 out of 15) versus 34.6% (9 out of 26) (χ2=2, 18, p=0.14). It should be assumed that with an increase in the number of examined patients, the relationship of the DD genotype with a reduced UA clearance will acquire statistical significance. With the DD genotype, according to many authors, the maximum ACE activity is rectified. The authors suggest that an increase in ACE activity contributes to a decrease in UA transit through the kidneys in the DD genotype

The values of the purine metabolites in preeclampsia and acute cerebral stroke were compared. A total of 33 patients with preeclampsia and 350 patients with an acute cerebral stroke were examined. The blood and liquor guanine, hypoxanthine, adenine, xanthine, and uric acid were determined by a direct spectrophotometry, in addition to conventional laboratory parameters. It has been established that there are clinicalpathobiochemical parallels between preeclampsia and the cerebral stroke, including by the features of purine metabolism. It is known that the most pronounced adverse metabolic indicator (marker, predictor) for both preeclampsia and the cerebral stroke is hyperuricemia. It was revealed that the favorable sign for stroke is the high values of oxypurines (hypoxanthine, xanthin, and uric acid) in the cerebrospinal fluid, and for preeclampsia their low levels. It has been shown that cerebrospinal fluid is not only the medium of administration of the drugs for spinal anesthesia, but also a source of valuable diagnostic and prognostic information, including in preeclampsia. Preeclampsia is metabolically like stroke with an unfavorable significance of hyperuricemia and diametrically antagonistic to stroke with a favorable value not increased, but a reduced concentration of hypoxanthine, xanthin, and uric acid in cerebrospinal fluid. The level of uric acid and other purines in patients suffering from a preeclampsia and in patients suffering from a cerebral stroke should be determined not only in the blood serum, but also, as far as possible, in cerebrospinal fluid.