This study examines the effect of nicotinic acid (1 g t.d.s.) on serum
Lp(a) concentration in a group of patients with type II hyperlipidaem
ia selected on the basis of a plasma Lp(a) concentration greater than
30 mg/dl. Reductions in total cholesterol, triglyceride, LDL-cholester
ol and Lp(a) were 16.3%, 25.5%, 23.7% and 36.4%, respectively, with an
increase in HDL cholesterol of 37.3%. The reduction in Lp(a) concentr
ation did not correlate with any other lipoprotein changes. In order t
o establish the mechanism of the fall in Lp(a) concentration, in vivo
turnover of autologous Lp(a) was studied in three subjects before and
whilst taking nicotinic acid. The fractional catabolic rate in Lp(a) w
as unaltered in the subjects on therapy, indicating that nicotinic aci
d did not increase catabolism of Lp(a) but decreased the synthetic rat
e. Since nicotinic acid was poorly tolerated we examined the effect of
acipimox, an analogue of nicotinic acid on lipoproteins using a place
bo controlled double-blind crossover design in a group of hyperlipidae
mic patients again selected with plasma Lp(a) concentration greater th
an 30 mg/dl. Acipimox was better tolerated than nicotinic acid but the
percentage changes in lipoprotein concentrations were smaller.