A VIRILIZING LEYDIG-CELL TUMOR OF THE OVARY ASSOCIATED WITH STROMAL HYPERPLASIA UNDER GONADOTROPIN CONTROL

Citation
Jam. Marcondes et al., A VIRILIZING LEYDIG-CELL TUMOR OF THE OVARY ASSOCIATED WITH STROMAL HYPERPLASIA UNDER GONADOTROPIN CONTROL, Journal of endocrinological investigation, 20(11), 1997, pp. 685-689
Citations number
12
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
03914097
Volume
20
Issue
11
Year of publication
1997
Pages
685 - 689
Database
ISI
SICI code
0391-4097(1997)20:11<685:AVLTOT>2.0.ZU;2-Z
Abstract
A 34-yr-old nulliparous black woman presented with hair loss, facial h irsutism, irregular menses and infertility associated with greatly inc reased serum total testosterone levels. The adrenal glands and the ova ries were normal on radiological and ultrasonographic investigation. C atheterization of the veins draining from the adrenal glands and the o varies yielded testosterone levels of 20.3 nmol/L and 20.0 nmo/L in th e right and the left adrenal veins, respectively, and 17.9 nmol/L and 27.4 nmol/L in the right and left ovaries venous plexus, respectively. Sequencial dexamethasone and ethynyl estradiol suppression test showe d a decrease in cortisol level with no change in total testosterone le vel on dexamethasone while an increase in testosterone from 10.5 nmol/ L to 20.1 nmol/L was observed ten days after ethynil estradiol had bee n associated to dexamethasone. When a gonadotropin-releasing hormone a gonist (gonadorelin 3.5 mg IM) was administered for 2 months, serum go nadotropins levels decreased to less than 2 IU/L, total testosterone t o 3.8 nmol/L and estradiol to less than 36 pmol/L. The patient was sub mitted to a pelvic exploratory laparotomy and a left salpingo-oophorec tomy was performed. A solid and circumscribed ovarian tumor of 1.0 cm in diameter was found. The pathological diagnosis was a Leydig cell tu mor with surrounding stromal hyperplasia. These findings may suggest t hat this tumor was gonadotropin-dependent being indirectly stimulated by ethynil estradiol, through a sensitization of the pituitary gonadot ropes and increase in gonadotropin levels and suppressed by a gonadotr opin-releasing hormone agonist. (C) 1997, Editrice Kurtis.