Darnis F

Liver adenoma and focal nodular hyperplasia in a man with high endogenous sex steroids.

The authors report the case of a 29-yr-old man presenting with both hepatocellular adenoma and focal nodular hyperplasia. The patient had never been treated with androgens or estrogens. Investigations revealed the existence of high plasma levels of androgens and estrogens. In addition, the patient presented features compatible with the syndrome of partial androgen resistance. We propose that the hepatic lesions could be secondary to an abnormally high secretion of sex steroids. We suggest that in the absence of known intake of either estrogens or androgens, the existence of hepatocellular adenoma or focal nodular hyperplasia, or both, should indicate a search for abnormal secretion of sex steroids.

Perhexiline Maleate-Associated Hepatic Injury Prevalence and Characteristics

In order to assess the prevalence and characteristics of perhexiline maleate (PM)-associated hepatic injury, we have conducted a study in 46 patients on PM therapy (100-400 mg/day) for angina pectoris

Hepatic Uptake of Sex Steroids in Men With Alcoholic Cirrhosis

We attempted to determine to what extent the degree of liver function impairment might affect the hepatic uptake and, as a consequence, alter the systemic plasma levels of endogenous sex steroids in male patients with alcoholic cirrhosis. The plasma levels and hepatic uptake of the steroids dehydroepiandrosterone, androstenedione, testosterone, dihydrotestosterone, estrone, estradiol, progesterone, and 17-hydroxyprogesterone were assessed. Systemic plasma levels of testosterone and dehydroepiandrosterone were significantly (p less than 0.05) reduced, whereas those of androstenedione, estrone, and estradiol were significantly (p less than 0.05) elevated in men with alcoholic cirrhosis when compared to controls. Sex hormone binding globulin levels were also significantly elevated (p less than 0.01). The hepatic uptake of sex steroids depended on the degree of liver function impairment as shown by the linear significant relationship between their hepatic extractions and that of indocyanine green (r = 0.74-0.92, p less than 0.05; except for dihydrotestosterone, r = 0.17, not significant). In addition, the hepatic uptake of sex steroids depended on the binding affinity to sex hormone binding globulin. The higher the affinity for sex hormone binding globulin, the lower the hepatic uptake influenced by liver function impairment. It was estimated that hepatic clearances accounted for only 20%-50% of the metabolic clearance of sex steroids. No significant relationship between plasma levels of sex steroids and their hepatic clearance was found. We show here that in alcoholic cirrhosis the extent of hepatic uptake of sex steroids depends partly on the degree of liver function impairment and partly on the degree to which they are bound to sex hormone binding globulin. Production rate or peripheral metabolism, or both, rather than hepatic uptake alone may account for the altered circulating levels of sex steroids.