Steroid Production

Steroid production by testicular tumors has been investigated both in vitro and in vivo.

Cortisol production by the testicular tumor was demonstrated in vivo by testicular venous sampling after stimulation with ACTH in a patient with nonclassic CAH (35) and, surprisingly, also in a patient with salt-wasting (36).

17-Hydroxyprogesterone production by a testicular tumor was demonstrated in vivo by testicular vein sampling after ACTH stimulation (37).

11-Hydroxylated steroids, like 21-deoxycortisol (21-DF), 21-deoxycorticosterone (21-DB), and 1ip-hydroxy-A4-androstenedione (11P-OHA), have been demonstrated in vitro (37,38), as well as in vivo (37,39,40). 11-Hydroxylase activity is usually restricted to the adrenal gland. Clark et al. demonstrated 11-hydroxylase activity in vitro in a testicular tumor from a patient with salt-wasting CAH (38). That study identified abundant angiotensin II receptors but no gonadotropin receptors in tumor membranes. In vivo, 11-hydroxylase activity was demonstrated by testicular vein sampling by Blumberg-Tick et al. (40). Combes-Moukhovsky et al. showed that stimulation with human chorionic gonadotropin (hCG) increased secretion of 11-hydroxylated steroids (39). In humans, LH/hCG receptors have been found not only in the testes but also in the normal adrenal cortex (41).

Testosterone production was shown in vitro by Franco Saenz et al. (36) but only after stimulation with ACTH or hCG. Interestingly, testosterone production was more responsive to ACTH stimulation than to hCG stimulation. The authors hypothesized the presence of specific receptors for ACTH and hCG in the same cells, a defective receptor with loss of specificity or the presence of two different cell lines. In vivo, Kirkland et al. showed increased testosterone production after ACTH infusion into the testicular artery (42).

Benvenga et al. hypothesized from longitudinal observations in a single patient that at least three distinct types of testicular tumors in CAH can be discriminated, based on their response to dexamethasone-induced ACTH suppression (43). The first type was ACTH dependent, in both growth and steroidogenesis. The second type was only partially responsive to ACTH, because growth suppression lagged behind the prompt suppression of steroidogenesis. In addition, this type was responsive to LH/hCG. In the third type, growth is unresponsive to dexamethasone-induced ACTH suppression, unresponsive to gonadotropins, and has lost the property to synthesize cortisol.

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