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Triiodothyronine rapidly lowers plasma lipoprotein (a) in hypothyroid subjects
R P Dullaart1, J J van Doormaal, K Hoogenberg
1Department of Endocrinology, University Hospital, Groningen, Netherlands.
Background:
Increases in plasma low-density-lipoprotein (LDL) cholesterol and apolipoprotein B (apo-B) are well known in primary hypothyroidism, but it is uncertain whether thyroid dysfunction is associated with elevated levels of the atherogenic lipoprotein (a) (Lp(a)).
Methods:
The effect of short-term hypothyroidism on plasma Lp(a) was studied in 14 patients who had undergone a total thyroidectomy because of a well-differentiated thyroid carcinoma. They were studied 2 weeks after withdrawal of triiodothyronine (T3) therapy and 7 (5-9) weeks after resumption of T3 treatment (75-100 micrograms T3 daily). Fourteen euthyroid subjects served as controls.
Results:
In the hypothyroid phase the athyreotic patients had higher levels of Lp(a) (105 [12-536] vs. 42 [1-321] mg/l, p < 0.05), apo-B (p < 0.001) and LDL cholesterol (p < 0.001) as compared with the euthyroid control subjects. T3 therapy lowered Lp(a) by 29% to 50 (12-535) mg/l, p < 0.01. Apo B and LDL cholesterol fell by 42% (p < 0.001) and by 53% (p < 0.001), respectively. After resumption of T3 therapy the levels of Lp(a), apo-B and LDL cholesterol were not different from those of the control subjects. The mean percentual decreases in Lp(a) and in apo-B were similar, although the individual changes in Lp(a) were more variable.
Conclusions:
Short-term hypothyroidism increases plasma Lp(a) and T3 therapy rapidly lowers Lp(a) together with apo-B and LDL cholesterol. Our findings support the hypothesis that thyroid hormone regulates plasma Lp(a) and apo-B in a parallel manner. Elevated concentrations of Lp(a) in combination with LDL cholesterol may be involved in the increased risk of cardiovascular disease assumed to be associated with hypothyroidism.