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Testicular Function in Type II Hyperlipoproteinemic Patients Treated with Lovastatin (Mevinolin) or Neomycin

Molecular Disease Branch, National Heart, Lung, and Blood Institute, and the Developmental Endocrinology Branch, National Institute of Child Health and Human Development (R.J.S.), National Institutes of Health Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: W. H. Farnsworth, Molecular Disease Branch, National Heart, Lung, and Blood Institute, Building 10, Room 7N-117, National Institutes of Health, Bethesda, Maryland 20892.

Steroid synthesis requires cholesterol derived from de novo synthesis or plasma lipoproteins. Low density lipoproteins appear to be the major contributor of cholesterol for steroid synthesis in man. Patients with disorders of low density lipoproteins or the low density lipoprotein receptor have reduced cortisol production in response to ACTH. Therapeutic agents designed to lower plasma cholesterol could, therefore, adversely affect steroid hormone production. Lovastatin (mevi-nolin) is a new hypolipidemic agent which blocks cholesterol synthesis by competitive inhibition of 3-hydroxy-3-methylglu-taryl coenzyme A reductase. In beagle dogs, lovastatin at 40–180 times the clinically effective dose in man, has been associated with an increase in spontaneous testicular atrophy. Accordingly, the effect of lovastatin on testicular function and lipoprotein levels was studied in 16 hyperlipidemic men in a randomized, double blind, cross-over study with another hypolipidemic agent, neomycin. Serum testosterone, PRL, LH, and FSH; LHRH-stimulated LH and FSH concentrations; and testicular size were measured, and semen analyses were made. We found no evidence that lovastatin had adverse effects on testicular function despite significant alterations in plasma lipoprotein concentrations.

Received January 14, 1987.

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