Kein Einfluß von Digitalis auf Sexual-und Nebennierenrindenhormone bei gesunden Probanden und bei Patienten mit Herzinsuffizienz

Summary Digoxin was studied to see whether it impairs adrenal function and feminizes male subjects by changing plasma sexual hormones; both have been reported on previously. In eight healthy male subjects neither estrone (38.7±7.7 vs 35.4±3.2 pg/ml) nor estradiol (35.8±6.4 vs 32.2±3.9 pg/ml) nor testosterone (6.32±0.74 vs 6.45±0.73 ng/ml) were found to be altered by digoxin administration (plasma levels 1.55±0.27 ng/ml) lasting 35 days. The same was true of free testosterone (147±24 vs 142±19 pg/ml) and free estradiol (657±77 vs 615±78 fg/ml). Even maximal stimulation of the adrenal and gonadal glands by adrenocorticotropic hormone (ACTH) and human chorionic gonadotropin (hCG) did not exhibit any digoxin-induced alterations in the synthesizing capacity of steroid hormones, as shown by plasma cortisol (increase from 128±18 to 389±18 ng/ml) and testosterone (from 5.96±0.90 to 10.33±1.19 ng/ml). Furthermore, seven subjects on digoxin were observed over a period of 150–210 days; they did not show any increase of estrogens. This was also found in three subjects when estrogen levels were elevated initially due to extreme obesity. Also, 35 patients who took -methyldigoxin (n=8), -acetyldigoxin (n=20) and digitoxin (n=7) from 1 to 9 (x:1.9) years demonstrated normal plasma concentrations of gonadal and adrenal steroids, irrespective of duration of application or the digitalis compound. However, our studies showed that sexual hormones are correlated to cardiac performance: with decreasing cardiac index, testosterone (r: 0.86;P<0.01) and estradiol (r: 0.68;P<0.05) decreased significantly. We conclude that digoxin does not exert any influence on plasma sexual steroids. Since no competition between digoxin and estradiol receptors was found, it may even be the digitalis compound of choice when feminization is expected due to other complications. Furthermore, on digoxin the adrenal gland is capable of synthesizing cortisol sufficiently.

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