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Lipoprotein(a) has many similarities to low density lipoproteins but possesses a unique protein moiety called apolipoprotein(a). The plasma concentration of lipoprotein(a) is mainly under genetic control and most of diets and hypolipidemic drugs do not change its level. Only nicotinic acid and neomycin are able to reduce its concentration. Epidemiological studies suggest that high level (greater than 30 mg/dl) of lipoprotein(a) is an independent risk factor for atherosclerosis of the coronary and carotid arteries. The risk is highest in patients with hypercholesterolemia. The atherogenic role of lipoprotein(a) is attributed to the lack of its recognition by the cellular receptors and its consequent diversion to the atherogenic "non receptor" pathway. Due to its strong homology with plasminogen, lipoprotein(a) could also favour thrombosis. It is suggested that its determination is of importance when evaluating a patient with atherosclerosis. Reducing high plasma levels of cholesterolemia appears to be mandatory when plasma lipoprotein(a) concentration is higher than 30 mg/dl.

An ultracentrifugation technique for isolation of the various lipoprotein fractions using a vertical rotor is described. By the use of a multiple discontinuous density gradient, very low density lipoproteins, low density lipoproteins and high density lipoproteins are sharply separated, without contamination of other lipoproteins or albumin. Centrifugation time is 80 min. The densities, electrophoretic mobilities, electron microscopic appearance and chemical composition are those of the expected classes of lipoproteins. Two different gradients are used to enhance the separation of very low density lipoproteins from low density lipoproteins on one hand and high density lipoproteins from infranatant on the other.

In the serum of many patients with sarcoidosis, alkaline phosphatase activity is increased due to sarcoid liver involvement. A study was carried out of various tests expressing intrahepatic cholestasis in 26 patients with sarcoidosis, 18 of them with a positive liver biopsy and 8 with a negative liver biopsy. SAP was elevated in 23% of the patients and its thermoresistance pointed to an hepatic origin. The predictive value of a positive test (PV-positive, the percentage of times that a positive test is in agreement with an involved liver) and the predictive value of a negative test (PV-negative, the percentage of times that a negative test will detect a nondiseased liver) were calculated. LP-X test is more reliable than SAP, which in turn is better than CB, BSP retention, and gamma-glutamyl-transpeptidase, in that order. LP-X seems to be more specific and more sensitive than alkaline phosphatase for predicting liver involvement in sarcoidosis.

The short-term effect of the blockade of the beta-adrenergic receptors on serum lipoproteins and the plasma activities of the enzymes involved in the metabolism of the serum lipoproteins: lipoprotein lipase (LPL), hepatic lipase (HL) and lecithin: cholesterol acyltransferase (LCAT) was evaluated in ten healthy normolipemic and normotensive subjects. In the first part of the study, the first three-day period of placebo was followed by another three-day period during which propranolol (120 mg/d) was given. In the second, third, and fourth part of the study, the same schedule was used but pindolol (15 mg/d), nadolol (160 mg/d), atenolol (100 mg/d) were given respectively instead of propranolol. The four drugs induced a significant blockade of the beta-adrenergic receptors as evaluated by the measurement of the double two-step test of Master (-45%). Despite similar blockade, the effect on serum lipid concentrations depended on the type of drug: propranolol induced an increase in triglycerides and apoprotein B-concentrations and a decrease in serum high density lipoprotein cholesterol (HDL-C) and apoprotein AI-concentrations. Pindolol provoked only a slight decrease of serum HDL-C concentration. Nadolol and atenolol elicited a lowering of the same magnitude in HDL-C. Except for a possible slight increase in plasma LCAT activity on propranolol, there was no significant change in the plasma activities of LPL, HL, and LCAT during the blockade of the beta-adrenergic receptors with the drugs used.(ABSTRACT TRUNCATED AT 250 WORDS)