liver was supposed to be the major source of circulating Lp(a).
High serum concentrations of lipoprotein (a) [Lp(a)]This finding was confirmed by the observation that after liver are considered a risk factor for premature atherosclerotransplantation the recipient acquired the donor's apo(a) phesis. Besides apolipoprotein B-100, Lp(a) consists of apolinotype.12 poprotein (a) [apo(a)], which shows a remarkable size According to recent studies, [13][14][15] not the total Lp(a) particle, polymorphism. The serum concentration of Lp(a) is conbut apo(a) is secreted by the hepatocyte. In a second step, it siderably influenced by this apo(a) phenotype. Because is extracellularly linked to apo B-100, possibly on the liver Lp(a) is synthesized in the liver, we wondered whether cell surface.14 and to what extent Lp(a) levels might be affected by In chronic liver disease of different etiology, 16-23 a decreased acute liver disease. We compared Lp(a) serum concenLp(a) serum concentration has been found. However, the intrations in 74 patients (54% male, 46% female; mean age, fluence of acute liver damage on the Lp(a) concentration has 46 years) with acute viral hepatitis (32, 28, and 14 with not been studied systematically. The aim of our study was to hepatitis A, B, and C, respectively) with those in 404 investigate whether acute damage of the liver cell would also healthy controls (57% men, 43% women; mean age, 47 affect the Lp(a) serum concentration promptly. Therefore, we years). In addition, the intraindividual course of Lp(a) determined the Lp(a) serum concentrations in 74 patients concentration during and after acute hepatitis was folwith acute viral hepatitis compared with 404 healthy controls lowed in a subgroup of 23 patients (15, 6, and 2 with in a cross-sectional study. The apo(a) isoforms were deterhepatitis A, B, and C, respectively). During acute hepatimined in both groups to exclude any influence of an unequal tis, median Lp(a) concentrations in the patient group apo(a) isoform distribution. Furthermore, 23 patients were were significantly diminished compared with controls studied again after recovery from acute hepatitis (longitudi-(7 vs. 17 mg/dL; P õ .0001, Mann-Whitney test). Any bias nal study). by an unequal isoform distribution was excluded because there was no significant difference in the isoform distribution between patients and controls (P ú .10, x
PATIENTS AND METHODS test). Furthermore, the decrease in Lp(a) concentrationIn the cross-sectional study, patients were included if the clinical during acute hepatitis was independent of the molecular suspicion of acute viral hepatitis was confirmed by significant transweight of the apo(a) isoform. Longitudinally observed aminase levels and positive serological test results (antibody to hepapatients showed a marked increase in Lp(a) concentratitis B core antigen-immunoglobulin [Ig] M, antibody to hepatitis tion during convalescence (7 to 32 mg/dL; P õ .0001, Wil-A virus-IgM, antibody to hepatitis C virus; all tests from Abbott coxon test). Our results sh...