Gonadotrophic pituitary incidentaloma as the cause premature ovarian insufficiency

Abstract

Objective: evaluate clinical significance pituitary incidentalomas, apparently derived from gonadotropocytes.
 Design: follow-up study. Patients. Three observations of pituitary microadenomas in patients whose cause for treatment was prolonged amenorrhea. Diagnosed uterine hypoplasia, decreased ovarian reserve, decreased bone mass. Patients combined expressed psycho-emotional symptoms (depression, neuroticism up to mental disorders in one case). The diagnosis of a gonadotrophic incidentaloma is suspected after exclusion of clinical and laboratory signs of prolactinoma, somatotrophic, corticotrophic and thyrotrophic adenoma.
 Results. In two cases, the clinical picture of severe estrogenic failure was combined with high concentrations FSH, LH and low concentrations of anti-mullerian hormone (AMH). The increase in gonadotrophines, obviously, was both a reaction to a decreased production of estrogens, and the result of their hypersecretion by adenoma. In the observed cases there was no development of ovarian cysts, characteristic for patients with gonadotrophic adenomas, which can be explained by a reduced ovarian reserve. In the third case marked initially normal secretion of FSH and LH, not corresponding to a low concentration of sex steroids. Further there was a complete cessation of the secretion of FSH and LH with a simultaneous rapid decrease in the secretion of AMH. Given the small size of adenomas, in all cases selection of tactics for dynamic observation. All patients were prescribed hormone replacement therapy.
 Conclusion. For patients with premature ovarian failure, it is advisable to carry out MRI with contrast enhancement to exclude pituitary adenoma.

Ovarian insufficiency and secondary amenorrhea in a patient with a novel variant within GDF9 gene

“…The implication of a gonadotropinsecreting adenoma in the patient's clinical presentation of POI can neither be confirmed nor excluded, especially in the absence of histological analysis (biopsy) of the pituitary lesion. Albeit the possible implication of both gonadotropin-secreting adenomas and Rathke cyst in POI, 15,16 GDF9 genetic defects are considered more likely to cause POI especially since GDF9 appears to participate also in a mechanism that modulates FSH b-subunit gene expression, 17 and GDF9, BMP15, and FSH seem to regulate AMH expression in granulosa cells. 18 Within this context, dysfunctional GDF9 molecules in this patient may explain FSH level fluctuations and low AMH levels whereas the observed hyperprolactinemia can be attributed to a mild pressure of the pituitary lesion to the pituitary stalk.…”