The efficacy of pravastatin as reducing plasma cholesterol, LDL-CH and Apo B is widely proved. Other molecules within the Apolipoprotein family are recently emerging to have a predictive and/or causative role in atherosclerosis such as particularly Lp(a). The aim of this study was to evaluate the effects of pravastatin therapy in patients affected by primary hypoercholesterolemia on apoprotein and Lp(a) plasma levels. We investigated the effects of pravastatin on 15 patients, seven female and eight male patients, mean age 50.23 +/- 17.2 (range 21-71 years) with primary hypercholesterolemia, of which 7 patients affected by familial hypercholesterolemia and 8 patients by polygenic hypercholesterolemia, were selected. Five weeks after suspension of lipid-lowering drugs and on a normocaloric-fat diet, were given 20 mg pravastatin/day for 12 weeks. The following parameters were measured basally, on the 6th week and the 12th week on pravastatin therapy and after five weeks from drug withdrawal: cholesterol (CH), triglicerides (TG), high density and low density lipoprotein cholesterol (HDL-CH and LDH-CH) measured enzymatically, apoproteins A1, B, C2, C3, E measured radial immunodiffusion technique (RID) and Lp(a), measured as apoprotein(a) with immunoradiometric assay (RIA). Our data confirm pravastatin efficacy in decreasing CH (from 305.6 +/- 43.4 mg/dl to 266.2 +/- 47.7 mg/dl, p < 0.01) LDL-CH (from 223.9 +/- 56.4 mg/dl to 187.2 +/- 59.8 mg/dl, p < 0.01) and Apo B (from 170.4 +/- 27.5 to 152.4 +/- 25.2, p < 0.02); non influence was observed on HDL-CH and apoproteins A1, C2, E and Lp(a). Pravastatin determined a significant increase only on Apo C3 (from 8.35 +/- 2.7 to 10.3 +/- 3.1, p < 0.04). The above data confirm the beneficial effect of pravastatin in greatly decreasing CH and LDL-CH considered as major risk factors for coronary artery disease, but also point to a role of pravastatin in regulating the apoproteins equilibrium, an aspect that surely merits further studies.