Spontaneous Ovarian Hyperstimulation Syndrome Due to Extraovarian Pathologies

BRAVSLAVSKY D; ESCOBAR ME; ARCARI A; CLEMENT F; BALLERINOI MG; ROPELATO MG; BERGADA I; GRYNGARTEN M

Costa do Sauipe, Bahia

Congreso; XXI Annual Meeting of the Sociedad Latinoamericana de Endocrinologia Pediatrica SLEP); 2010

Sociedad Latinoamericana de Endocrinologia Pediatrica (SLEP)

To describe 3 adolescents with bilateral multicystic ovarian masses. 1-A 13 years old girl with abdominal distention and secondary amenorrhea. Referred for an oophorectomy. Ultrasound (US) showed enlarged multicystic ovaries (15x9 and 15x15cm). Biochemical assays: negative serum âsubunit chorionic gonadotrophin(âHCG), Estradiol 8643pg/ ml, LH<0.05IU/l, FSH:25.7IU/l, prolactin 66ng/ml. MRI revealed pituitary adenoma. Transsphenoidal surgery confirmed FSH secreting adenoma. Spontaneous ovarian hyperstimulation syndrome (SOHS) remitted after tumor resection. 2-A 13 year old girl admitted after complete mola hydatiform evacuation suffering from progressive abdominal girth. âHCG: 171000IU/l. US: bilateral multicystic enlarged ovaries (18x10 and 18x10cm). Miometrial infiltration. Estradiol 3800pg/ml, LH< 0.1UI/l, FSH<0.1UI/l and âHCG 31000UI/l. Lung metastases. SOHS due to trophoblastic gestational neoplasia.Treated with chemotherapy. 3-A 15 year old girl admitted after surgical acute abdomen due to multicystic bilateral ovarian masses. Giant cysts relapsed after resection. She had clinical signs of hypothyroidism and galactorrhea. TSH>100ìU/ml, T4<1.0ìg/dl, LH<0.05UI/l, FSH:8.1UI/l. SOHS remitted after treatment with thyroid hormone. Follicular recruitment occurs through stimulation of FSH receptor either by hypersecretion of FSH itself or by promiscuous activation of âHCG or TSH. Massive luteinization of enlarged stimulated ovaries leads to the development of SOHS. Giant multicystic ovaries must alert about SOHS that improves after treatment of its etiological cause.