Dyslipoproteinaemia in hypothyroidism of pituitary origin: effects of L-thyroxine substitution on lipoprotein lipase, hepatic lipase, and on plasma lipoproteins.
We have studied the effects of L-thyroxine substitution on lipoprotein concentrations, on the activities of lipoprotein lipase (LPL) and hepatic lipase (HL), and on the elimination rate of exogenous triglyceride in a homogeneous group of patients with hypothyroidism of pituitary origin. All were deficient of sex hormones but not of corticosteroids during the observation period. Before treatment total plasma cholesterol, LDL cholesterol, and triglyceride levels were significantly higher than in a euthyroid control group but not as high as in patients with overt primary hypothyroidism. The activities of LPL and HL were also intermediate between those of euthyroid and overt primary hypothyroid subjects, and there was a significant reduction of the elimination rate of exogenous triglyceride. No changes were found for HDL cholesterol levels. When the patients with secondary hypothyroidism were compared to patients with primary hypothyroidism, matched for thyroid function levels, age, sex, and weight, there were no differences with regard to plasma lipoprotein concentrations or post-heparin lipase activities. In 3 patients with secondary hypothyroidism the lipoprotein profiles were studied by zonal ultracentrifugation and found to agree well with changes observed in primary hypothyroidism. L-thyroxine substitution produced a normalization of lipase activities and lipoprotein concentrations in patients with secondary hypothyroidism. We conclude that there are no fundamental differences in the disturbances of the lipoprotein metabolism in primary and secondary forms of hypothyroidism.[1]References
- Dyslipoproteinaemia in hypothyroidism of pituitary origin: effects of L-thyroxine substitution on lipoprotein lipase, hepatic lipase, and on plasma lipoproteins. Valdemarsson, S., Hedner, P., Nilsson-Ehle, P. Acta Endocrinol. (1983) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg