APOLIPOPROTEIN(A) PHENOTYPES AND LIPOPROTEIN(A) CONCENTRATIONS IN PATIENTS WITH HYPERTHYROIDISM

Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL) particle in which apolipoprotein B-100 (apoB) is attached to a glycoprotein called apolipoprotein(a) [apo(a)]. Apo(a) has several genetically determined phenotypes differing in molecular weight, to which Lp(a) concentratio ns in plasma are inversely correlated. High plasma levels of Lp(a) are associated with atherosclerotic diseases. It is therefore of interest to study whether factors other than the apo(a) gene locus are involve d in the regulation of Lp(a) concentrations. We measured plasma concen trations of Lp(a) and other lipoproteins and determined apo(a) phenoty pes in 31 patients with hyperthyroidism, before and after the patients had become euthyroid by treatment. The mean concentration of LDL chol esterol rose from 2.67 to 3.88 mmol/l (P < 0.01), apoB rose from 0.79 to 1.03 g/l (P < 0.01), and the median Lp(a) concentration increased f rom 9.74 to 18.97 mg/dl (P < 0.01) on treatment. Lp(a) concentrations were inversely associated to the size of the apo(a) molecule both befo re (P < 0.01) and after treatment (P < 0.01). The increase in Lp(a) wa s significant in patients with high molecular weight apo(a) phenotypes (n=9; P < 0.01) and in patients with low molecular weight apo(a) phen otypes (n=16; P < 0.01), but not in those with apo(a) ''null types'' ( n=6; P=0.5). The low levels LDL cholesterol and apoB in untreated hype rthyroidism may result from increased LDL receptor activity. The incre ase in Lp(a) levels were not correlated with the increase in LDL chole sterol or apoB. Most other clinical evidence indicates that the LDL re ceptor is not important in Lp(a) catabolism, and we suggest that the l ow Lp(a) levels seen in thyroid hormone excess are caused by an inhibi tion of Lp(a) synthesis.