The endocrine activity of the postmenopausal ovary and the effect of pituitary down-regulation were studied in a group of 35 postmenopausal women. All women underwent oophorectomy with or without hysterectomy. Fifteen women received a single dose of a depot GnRH agonist (GnRHa) 2 weeks before operation, whereas 20 women formed the control group. Peripheral venous levels of LH, FSH, estrone, 17 beta-estradiol, testosterone (T), androstenedione (A), sex hormone-binding globulin, and dehydroepiandrosterone sulfate were measured 2 weeks before, during, and 6 weeks after surgery. Ovarian venous blood was sampled during surgery. In the GnRHa and control groups, ovarian venous levels of A and T were significantly higher, and those of dehydroepiandrosterone sulfate and sex hormone-binding globulin significantly lower, compared to the peripheral levels. A significant decrease in T was found in the peripheral and ovarian vein samples during pituitary down-regulation with GnRHa. Six weeks after operation, peripheral T levels were significantly lower than those during surgery in the group that was down-regulated at the time of oophorectomy. We conclude that the postmenopausal ovary produces significant amounts of A and T, although only T contributes significantly to its peripheral serum levels. T production by the postmenopausal ovary is in part stimulated by the high levels of circulating gonadotropins, although pituitary down-regulation does not completely abolish androgenic activity.
Summary
A 14‐year‐old girl presented with precocious sexual development, galactorrhoea and symptoms and signs suggestive of hypothyroidism. On physical examination a tumour was found in the lower abdomen. Serum gonadotrophins, especially luteinizing hormone, serum thyroid stimulating hormone and prolactin were elevated. Measurement of thyroid hormones and additional thyroid function tests confirmed the diagnosis of primary hypothyroidism. Ultrasound investigation revealed the mass in the lower abdomen to be of a cystic nature and to originate from the right ovary. Following the institution of thyroid substitution therapy, all symptoms disappeared, biochemical and hormonal abnormalities returned to normal and the ovarian size decreased to normal. A hypothesis is presented for non‐specific pituitary glycoprotein hormone synthesis secondary to the hypothyroidism, as the cause of the syndrome.
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