High serum concentrations of lipoprotein (a) [Lp(a)] are considered a
risk factor for premature atherosclerosis. Besides apolipoprotein B-10
0, Lp(a) consists of apolipoprotein (a) [apo(a)], which shows a remark
able size polymorphism, The serum concentration of Lp(a) is considerab
ly influenced by this apo(a) phenotype, Because Lp(a) is synthesized i
n the liver, we wondered whether and to what extent Lp(a) levels might
be affected by acute liver disease, We compared Lp(a) serum concentra
tions in 74 patients (54% male, 46% female; mean age, 46 years) with a
cute viral hepatitis (32, 28, and 14 with hepatitis A, B, and C, respe
ctively) with those in 404 healthy controls (57% men, 43% women; mean
age, 47 years). In addition, the intraindividual course of Lp(a) conce
ntration during and after acute hepatitis was followed in a subgroup o
f 23 patients (15, 6, and 2 with hepatitis AB, and C, respectively), D
uring acute hepatitis, median Lp(a) concentrations in the patient grou
p were significantly diminished compared with controls (7 vs, 17 mg/dL
; P < .0001, Mann-Whitney test), Any bias by an unequal isoform distri
bution was excluded because there was no significant difference in the
isoform distribution between patients and controls (P > .10, chi(2) t
est), Furthermore, the decrease in Lp(a) concentration during acute he
patitis was independent of the molecular weight of the apo(a) isoform,
Longitudinally observed patients showed a marked increase in Lp(a) co
ncentration during convalescence (7 to 32 mg/dL; P < .0001, Wilcoxon t
est). Our results show that acute hepatitis is associated with decreas
ed Lp(a) serum levels. Further studies are needed to evaluate whether
Lp(a) serum concentration might be clinically useful as a parameter of
liver function.