Summary:Purpose: To evaluate the changes in serum sex hormones of gonadal or adrenal origin, the gonadotropic hormones, and sex hormone-binding globulin (SHBG) in men and women with chronic temporal lobe epilepsy (TLE), who are undergoing monotherapy with carbamazepine or receiving carbamazepine in combination with other anticonvulsant drugs.Methods: Gonadal hormones (estradiol, testosterone, free testosterone, and inhibin B), adrenal hormones [cortisol, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and 17a-hydroxyprogesterone], and gonadotropic hormones (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) were measured in 22 women and 26 men with TLE. The study also measured prolactin; human growth hormone and its major mediator, insulin-like growth factor-I; thyroid hormones (free thyroxine and free triiodothyronine); thyroid-stimulating hormone (TSH); and SHBG. The results were compared with those obtained from 60 healthy women and 106 healthy men.Results: In the female patients, TSH, DHEAS, follicularphase LH, and luteal-phase estradiol were significantly lower than in the control groups, with prolactin and SHBG significantly higher. In the male patients, DHEAS, 17a-hydroxyprogesterone, free testosterone, inhibin B, and the testosteroneLH ratio were significantly lower than in the control group, with LH, FSH, and SHBG significantly higher. Increased FSH in 31% of the men indicates an impairment of spermatogenesis; lowered inhibin B in 12% indicates an impaired Sertoli's cell function; and the decreased testosteroneLH ratio in 50% indicates an impaired Leydig's cell function. Conclusions:The case patients had endocrine disorders, mainly concerning the gonadotropic and gonadal functions in both sexes; the adrenal function, with lowered DHEAS levels in both sexes; and lowered 17a-hydroxyprogesterone levels in the men. SHBG levels were increased in patients taking anticonvulsant medications.

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Adrenomyeloneuropathy (AMN) is a disorder due to a disturbance in the peroxisomal b-oxidation of saturated very long chain fatty acids. It is characterized by symptoms of the nervous as well as the endocrine systems, especially the adrenal cortex and the gonads. We investigated the testicular function in 49 male AMN patients aged 36.2 Ϯ 1.5 years (range, 18.5-59 years). Twenty-four of these patients were suffering from adrenocortical insufficiency. Twenty-five AMN patients showed neurological symptoms without ' Addison's disease'. To register the frequency and the degree of gonadal impairment, LH and FSH, testosterone, free testosterone and inhibin-B were determined. Gonadotropin concentrations were significantly higher in AMN patients than in healthy controls (LH, 8.0 Ϯ 1.2 vs 2.77 Ϯ 0.11 IU/l; FSH, 10.1 Ϯ 1.6 vs 4.0 Ϯ 0.17 IU/l; P < 0.001). Serum LH was elevated in 31 patients (63.3%); 28 patients (57.1%) showed elevated serum FSH indicating deficient spermatogenesis. Mean testosterone did not differ significantly between patients and healthy controls, but mean free testosterone was significantly lower in patients than in controls (16.3 Ϯ 1.0 vs 28.5 Ϯ 1.68 pg/ml, P < 0.002). Inhibin-B concentrations did not differ between AMN patients and healthy men. The testosterone/LH ratio reflecting an impairment of the Leydig cells was significantly lower in AMN patients than in controls (P < 0.01). An impairment of the Leydig cells and/or of the Sertoli cells was evident in 81.6% of AMN patients. Twenty-one of thirty-nine patients (53.8%) admitted erectile dysfunction.These data indicate that endocrine dysfunction in AMN is not only confined to adrenocortical functions, but testicular dysfunctions also frequently occur, thus permitting the term 'adreno-testiculomyelo-neuropathy'.

Possible protective effects of D-Tryptophan-6 luteinizing hormone releasing hormone (D-Trp-6-LH-RH) against irradiation-induced testicular damage were investigated for the first time in patients with seminoma. After unilateral orchiectomy 12 men were allocated to receive the long-acting gonadotropin releasing hormone (GnRH) agonist D-Trp-6-LH-RH prior to and for the duration of radiotherapy. Eight patients with the same disease served as a control group. In contrast to several trials to protect spermatogenesis from chemotherapy by GnRH agonists, we first suppressed the pituitary-testicular axis before starting the treatment. As a new schedule this adjuvant GnRH agonist treatment was combined with cyproterone acetate for the first 20 days to diminish the amount and the duration of the initial stimulation of gonadotropins and testosterone. Irradiation started after suppression of the pituitary-gonadal axis. In all patients luteinizing hormone and testosterone were completely suppressed throughout the treatment compared to the controls, whereas the initial suppression of follicle-stimulating hormone was not completely maintained until radiotherapy was completed. At the follow-up at 18 months after completion of therapy, all patients reached their initial concentration of gonadotropins, testosterone, and motile spermatozoa independently of D-Trp-6-LH-RH treatment. With the dose and schedule investigated, the GnRH agonist showed no protective effects against testicular damage caused by radiotherapy.