A. Djerassi et al., GONADOTROPH ADENOMA IN A PREMENOPAUSAL WOMAN SECRETING FOLLICLE-STIMULATING-HORMONE AND CAUSING OVARIAN HYPERSTIMULATION, The Journal of clinical endocrinology and metabolism, 80(2), 1995, pp. 591-594
The clinical manifestations of gonadotroph adenomas are almost always
neurological, consequences of their large size, and are rarely endocri
nological. We report an exception, a 39-yr-old woman whose gonadotroph
adenoma caused supranormal serum concentrations of FSH, which resulte
d in the development of multiple ovarian cysts, persistent elevation o
f her serum estradiol concentration, and endometrial hyperplasia. She
initially presented because of amenorrhea at age 30 yr and was treated
for an intrasellar mass by transsphenoidal surgery at age 31 yr and a
gain at age 36 yr. Before and after the second operation she had persi
stently supranormal plasma estradiol concentrations (>1840 pmol/L) and
endometrial hyperplasia. When she was evaluated at age 39 yr, transva
ginal ultrasound showed multiple ovarian cysts and endometrial thicken
ing. Her plasma estradiol level was markedly supranormal (2160 pmol/L)
, FSH was mildly supranormal (17.8 IU/L), and alpha-subunit was marked
ly supranormal (23.3 mu g/L). Characteristic of gonadotroph adenomas,
her LH beta level increased by 69% in response to TRH. Neither FSH nor
cr-subunit decreased in response to administration of the GnRH antago
nist, Nal-Glu-GnRH (5 mg/12 h for 4 weeks). Excised adenoma tissue exh
ibited morphological features of a gonadotroph adenoma. This patient a
ppears to be unique, in that her gonadotroph adenoma caused slightly,
but persistently, supranormal concentrations of FSH, which caused ovar
ian stimulation, including supranormal plasma estradiol concentrations
, multiple ovarian cysts, and endometrial hyperplasia. We propose that
gonadotroph adenomas be considered in the differential diagnosis of p
atients who have this constellation of abnormalities.