Aggravation of Broad-ß Disease (Type 3 Hyperlipoproteinemia) by Hypothyroidism

A man with peripheral atherosclerosis manifested concurrent postsurgical hypothyroidism and braod-β disease (type 3 hyperlipoproteinemia). In the presence of both, low-density lipoprotein levels remained normal, but very low-density lipoprotein (VLDL) levels were markedly increased, β-migrating, and rich in cholesterol. During replacement therapy with levothyroxine, cholesterol and triglyceride levels were initially reduced to normal, and the diagnosis of broad-β disease became uncertain. Its persistence was suggested by the relative prominence of Sf12-100 lipoproteins, the cholesterol-rich composition of VLDL subfractions and of chylomicrons persisting late after an orally administered fat load, the preponderance of slower-migrating lipoproteins in the Sf20-60 subfraction. With time, moderate hyperlipoproteinemia returned, and broad-β disease was again clearly evident. Thus, secondary factors may interact with the primary metabolic defect to influence the chemical, and possibly clinical, expression of broad-β disease.