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When compared to values obtained in 40 normalweight normolipemic healthy control subjects, serum uric acid levels were found to be significantly increased in 68 subjects with type II-b and especially in 68 subjects with type IV hyperlipoproteinemia. A much lesser increase of uricemia occurred in 22 patients with type II-a. A significant positive correlation between uricemia and serum triglyceride level could be demonstrated but no such correlation was found with serum cholesterol. Overweight and hypertensive hyperlipemic subjects were presenting higher levels of serum uric acid than normalweight normotensive ones. On the other hand, clinical atherosclerosis and diabetes mellitus had no additive effects upon uricemia in hyperlipoproteinemic patients. It is suggested that hyperinsulinism and accelerated turnover of lipoproteins, often encountered in obese and hypertriglyceridemic subjects, might lead to an enhanced synthesis of purines and subsequently increased production of uric acid.

Both gamma-glutamyltransferase (gammaGT) and pseudocholinesterase (PCE) were found to be increased in hypertriglyceridemic subjects. High values of gammaGT were noted in alcoholic subjects and especially in those with either increased serum triglyceride or alanine aminotransferase higher than 16 mU/ml, while PCE was not significantly changed in alcoholic subjects. Although both enzymes were strongly correlated with the logarithm of serum triglyceride and the prebeta electrophoretic fraction, there were striking differences concerning their behavior in various hypertriglyceridemic subjects. PCE activity was high even in moderate hypertriglyceridemias but its correlation with serum triglyceride had a tendency to flatten with increasing concentration of triglyceride. However, increase of gammaGT was rather characteristic for gross hypetriglyceridemia. Short-term, triglyceride-lowering therapy was accompanied by a tendency to normalization of gammaGT, while PCE values were not influenced. An attempt was made to interpret these changes of serum-enzyme activity in hypertriglyceridemia in connection with mechanisms of lipoprotein synthesis and with the pathogeny of hyperlipemic conditions.