Reports on hormone analysis in androgenic hairloss in the female show partly contradicting results. Elevated as well as normal-range androgen levels have been found. The present study aimed at the investigation of a possibly more differentiated hormonal constellation by hormone analysis and additional determination of the hypophyseal level by the thyrotropin-releasing hormone (TRH) test. In 46 female patients with androgenic hairloss blood sampling for hormone analysis was performed. Determination of the androgens testosterone (T), androstenedione (A), dehydroepiandrosterone sulfate (DHEAS), 17-hydroxy-progesterone acetate (17-OHP) and free testosterone (FT), of sex-hormone-binding globulin (SHBG), estradiol (E₂), cortisol (F) and the hypophyseal luteinizing hormone (LH) and follicle-stimulating hormone (FSH) was performed by standard radioimmunoassay methods. The TRH-test is based on feedback mechanisms between the hypothalamic TRH which stimulates hypophyseal TSH and PRL release. Thus, even mild forms of hypothyroidism or hyperprolactinaemia can be detected. The control group for the TRH test consisted of 45 volunteer females without hairloss or any other hormonal or menstrual disturbances. Statistical analysis was performed according to the Wilcoxon two-sample test. The results of the study show no significant elevation of androgens in females with androgenic hairloss, but a more complex condition with involvement of the glandula suprarenalis and the hypophyseal level. Significantly elevated TSH levels prior to and after TRH stimulation in the hairloss group indicate that hypothyroidism may be an important hormonal disturbance in androgenic hairloss. Interactions between hypothyroidism and androgen metabolism are possible at various links. The TRH test was shown to serve as an important criterion for additional information on hormonal involvement in androgenic hairloss and may open new treatment approaches in the future.

Women with a normal menstrual cycle (n = 21, controls), polycystic ovary syndrome (n = 10) and hypogonadotropic amenorrhea (n = 3) were stimulated with clomiphen-citrate (4th day to 8th day of the cycle) and with human menopausal gonadotropin (8th day to 11th day). The vascular impedance of the ovary carrying the dominant follicles was monitored by endovaginal pulsed Doppler flow measurement. Simultaneously, serum levels of LH, E2 and 17-OHP were assayed. Contrary to controls, women with polycystic ovary syndrome or hypogonadotropic amenorrhea showed decreased hormone levels and no lowering of the vascular impedance. In controls, the lower pulsatility index is caused by neovascularization around the dominant follicle and by E2-induced vasodilatation in the ovarian artery.

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