Endocrine Abstracts

Background: Ovarian granulosa cell tumours are rare, aggressive, hormonally active neoplasms.

Case: A 16-year-old, nulliparous, Eastern European woman presented with a 9-month history of secondary amenorrhoea and a 2-month history of galactorrhoea. She denied headache or visual symptoms. Past medical history was unremarkable with menarche at age 14 and a previously normal menstrual cycle. She had never used hormonal contraception. Only medications were paracetamol and ibuprofen. On examination, visual fields were full and cranial nerves were intact. General examination was unremarkable. Pituitary bloods demonstrated suppressed gonadotrophins (LH <0.1 IU/l, FSH <0.1 U/l) and an elevated serum prolactin at 7081 mIU/l (ref range 102–496 mIU/l). A macroprolactin screen was negative. Serum oestradiol was significantly elevated at 7442 pmol/l and serum β HCG was undetectable. Thyroid function tests and a short synacthen test were satisfactory. MRI of the pituitary showed no focal abnormality. We considered a malignant ovarian source for the high serum oestradiol. Serum inhibin was elevated at 2734.7 ng/l. MRI of the pelvis showed a 4.8 cm mass within the right ovary, no evidence of metastatic disease and a normal uterus and left ovary. The patient underwent a right-sided salpingo-oophorectomy. Histology confirmed the mass to be a juvenile granulosa cell tumour (FIGO stage 1a). On immunohistochemical analysis, tumour cells did not express prolactin. The patient defaulted from follow-up after surgery.

Conclusion: We present a case of juvenile granulosa cell tumour producing oestradiol and inhibin. Based on immunohistochemistry, we postulate that observed hyperprolactinaemia and the subsequent clinical sequelae were caused by oestrogenic stimulation of pituitary lactotroph cells, a biochemical state analogous to pregnancy. Our case illustrates an uncommon but important cause of hyperprolactinaemia, which, if missed, could have significant adverse consequences for the patient.