Low Lipoprotein (A) Levels During Acute Viral Hepatitis

Abstract

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...

Lipids changes in liver cancer

“…Serum Lp(a) level changes during inflammatory disease (Maeda et al, 1989); and also liver damage is linked to reduced Lp(a) serum levels (Malaguarnera et al, 1996;Kostner, 1983). Geiss et al(1996) longitudinally observed patients showing a marked increase in Lp(a) concentration from 7 mg/dl in acute stage to 32 mg/dl in convalescence, and acute hepatitis is associated with decreased Lp(a) serum levels.…”

Impact of Viral Hepatitis on Apo- and Lipoprotein Status in Blood

“…Liver is the major source of circulating Lp(a) [18][19][20][21] . Although several studies report a close association of serum Lp(a) level with cardiovascular and thrombotic disorders, only few studies have described a possible relation between Lp(a) and liver diseases [22] . These studies demonstrated AVH with diminished Lp(a) serum concentration [22] .…”

Lipoprotein (a): impact by ethnicity and environmental and medical conditions

“…Thus, patients with liver cirrhosis and hepatitis have lower Lp(a) concentrations compared with healthy controls (209)(210)(211)(212)(213)(214)(215). Geiss et al (216) reported a 41% reduction in Lp(a) concentration in patients with acute hepatitis A, B, and C, and the decrease was independent of apo(a) isoform size. Notably, a significant increase in Lp(a) concentrations was seen in those patients with chronic active hepatitis C that responded completely to a 6 month interferon treatment regimen, raising the possi bility of an inflammationmediated effect or improved liver function (210).…”