[Plasma lipids and apoproteins. The effect of cigarette smoking]. / Lipidi ed apoproteine plasmatiche. Influenza del fumo di sigaretta.

Cigarette smoking produces lipo-apoprotein modifications, which makes it more atherogenic. In this study we have evaluated lipids and apoproteins in 178 normolipidemic, healthy subjects, in relation to their smoking habits. In smokers we have found lower levels of HDL-cholesterol and apo A-I and higher levels of triglyceride and apo B. Number of cigarette smoked in a day directly correlated with triglycerides and apo B (r = 0.321 and 0.313 respectively) and inversely with HDL-cholesterol (r = -0.274). These alterations seem to be due to an inhibition that smoking could cause on lipolytic processes. Further studies need to establish influences that smoking-related alterations have in the atherosclerotic lesions of smokers.

Transient neonatal hypercholesterolemia. Lack of relationships with dehydroepiandrosterone sulfate.

In order to obtain new information about the relationship between transient neonatal hypercholesterolemia and adrenal gland function, we have studied 39 healthy babies found hypercholesterolemic at birth and 39 healthy controls with normal cholesterol levels. The results of this study have shown that levels of dehydroepiandrosterone sulfate in cord blood were not significantly different in the hypercholesterolemic subjects compared with normolipidemic controls (1.4 +/- 0.5 micrograms/dl vs 1.3 +/- 0.5 mu/dl). Moreover correlations between this hormone and levels of total and LDL-cholesterol were not only not statistically significant but even positive (respectively r = +0.207 and +0.195). These data suggest that dehydroepiandrosterone sulfate measurements in cord blood do not give any further information about transient neonatal hypercholesterolemia.

Inhibition of thromboxane biosynthesis and platelet function by simvastatin in type IIa hypercholesterolemia.

Thromboxane A2 (TXA2) biosynthesis is enhanced in the majority of patients with type IIa hypercholesterolemia. Because simvastatin (a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor) was previously shown to reduce platelet aggregation and TXB2 production ex vivo, we investigated TXA2 biosynthesis and platelet function in 24 patients with type IIa hypercholesterolemia randomized to receive in a double-blind fashion simvastatin (20 mg/d) or placebo for 3 months. The urinary excretion of 11-dehydro-TXB2, largely a reflection of platelet TXA2 production in vivo, was measured by a previously validated radioimmunoassay technique. Blood lipid levels and urinary 11-dehydro-TXB2 excretion were significantly (P < .001) reduced by simvastatin. In contrast, placebo-treated patients did not show any statistically significant changes in either blood lipids or 11-dehydro-TXB2 excretion. The reduction in 11-dehydro-TXB2 associated with simvastatin was correlated with the reduction in total cholesterol (r = .81, P < .0001), LDL cholesterol (r = .79, P < .0001), and apolipoprotein B (r = .76, P < .0001) levels. Platelets from patients with type IIa hypercholesterolemia required significantly (P < .01) more collagen and ADP to aggregate and synthesized less TXB2 in response to both agonists after simvastatin therapy. Bleeding time, platelet sensitivity to Iloprost, and blood lipoprotein(a) and HDL cholesterol levels were not significantly affected by either treatment. We conclude that enhanced TXA2 biosynthesis in type IIa hypercholesterolemia is, at least in part, dependent on abnormal cholesterol levels and/or other simvastatin-sensitive mechanisms affecting platelet function.