[Severe postmenopausal hyperandrogenism due to an ovarian lipoid cell tumor: a case report]. / Descrizione di un caso clinico di severo iper-androgenismo postmenopausale dovuto a un tumore ovarico a cellule lipidiche.

The case of a 62-year-old woman with severe post-menopausal hirsutism is described. Her clinical history revealed regular menstrual periods until menopause at the age of 50, hysterectomy for fibromatosis at 58 years, non-insulin dependent diabetes mellitus, hypertension, obesity, severe hirsutism, which had developed in the previous 3 years, with a deeping of the voice. Examination showed android obesity, hypertension and severe hirsutism involving the face and the trunk. Endocrine evaluation pointed out regular adrenal function, serum total and free-testosterone in the adult male range, with normal androstenedione, DHEAS and 17OHP levels. Estradiol was slightly increased and LH and FSH were inappropriately low for her post-menopausal age. Computed tomography of the abdomen showed regular adrenal glands, and a radio-labeled cholesterol scan was negative. A further pelvic transvaginal ultrasonography revealed a small cystic formation near the right ovary and a slight increase in the size of the left ovary. The patient underwent bilateral ovariectomy. Histological examination showed a lipoid cell tumor within the left ovary. Immunohistochemical studies were positive for inhibin and cytokeratin. After surgery, serum testosterone fell to normal levels, gonadotropins increased to menopausal levels, confirming that the tumor was able to produce both LH, and FSH-inhibiting factors, and hirsutism greatly improved. Periodic hormonal tests remained normal and CT of the abdomen and pelvic ultrasonography did not show alterations at a 3 years follow-up.

Use of a long-acting gonadotrophin-releasing hormone analogue in a postmenopausal woman with hyperandrogenism due to a hilus cell tumour.

OBJECTIVE: The aim of this study was to prove the utility of GnRH analogues for the suppression of androgen secretion in a postmenopausal woman with a suspected virilizing ovarian tumour. DESIGN AND METHODS: We present a case of a 72-year-old woman with virilization of recent onset. Hormonal studies revealed a fourfold increase in serum testosterone levels, normal dehydroepiandrosterone sulphate concentrations and high levels of serum 17-hydroxyprogesterone levels. Computed axial tomography scan of the ovaries was normal and the adrenal glands showed a discrete enlargement. The long-acting GnRH analogue, triptorelin, was injected initially (3.75mg i.m.) and serum hormone levels were measured weekly throughout one month. RESULTS: GnRH produced a decrease in serum testosterone levels to normal values, in parallel with the suppression of serum LH and FSH concentrations. The patient was treated for three months with triptorelin and she experienced an amelioration of the hyperandrogenic symptoms. In order to achieve a diagnosis, the patient was submitted to a laparotomy that revealed a small hilus cell tumour in the left ovary. CONCLUSION: GnRH analogues may offer a good therapeutic option in some states of gonadotrophin-dependent hyperandrogenism of ovarian origin.

Gynandroblastoma in pregnancy: case report and review of literature.

Gynandroblastoma is an extremely rare tumor, composed of sex cord and stromal cells of both ovarian (granulosa-theca) and testicular (Sertoli-Leydig) types. We believe that its occurrence during pregnancy has not been previously reported. The patient was a 32-year-old woman who during her pregnancy was noted to have a progressively enlarging, unilocular left ovarian cyst. Beginning at 18 weeks gestation, the fetus required multiple platelet transfusions for severe alloimmune thrombocytopenia. A viable baby girl was delivered by cesarean section at 39 weeks gestation. At that time, an ovarian cystectomy also was performed. When the histology of the tissue subsequently became known, a left salpingo-oophorectomy was performed for gynandroblastoma. One year later, at the time of laparoscopic sterilization, the examination of the pelvis was normal.

An ovarian lipid cell tumour causing virilization and Cushing's syndrome.

We report a 73-year-old woman with rapidly developing symptoms and signs of Cushing's syndrome and high urinary free cortisol. She was virilized and hirsute with testosterone levels which became exceptionally high. ACTH was suppressed and CT scan of the adrenals and pelvis showed no abnormality. Ultrasound scanning showed enlargement of the left ovary. Venous catheter studies suggested a left ovarian source. A 2-cm diameter lipid cell tumor was removed from the left ovary laparoscopically. Histology was initially benign, and clinical and biochemical cure of Cushing's syndrome was rapid. However, the neoplastic nature of the ovarian tumour was demonstrated 12 months later when peritoneal metastases were detected and there was then clinical and biochemical relapse.

[Ovarian steroid cell tumors: a bilateral form]. / Tumeurs ovariennes à cellules stéroïdiennes: à propos d'une forme bilatérale.

The authors report a case of bilateral ovarian steroid cell tumour, not otherwise specified (as subclassified now by Scully). For two years a 46-year-old woman had androgenic manifestations. Only plasma testosterone level was increased. A hysterectomy with bilateral ovariectomy was performed. The first diagnosis was bilateral Leydig cell tumour, but no Reinke crystal was found. The final diagnosis was steroid cell tumour, not otherwise specified. No significant nuclear atypia or mitotic activity were found and two-year follow-up was favourable. The authors discuss the difficulty to class some ovarian tumours between Leydig cell tumour and steroid cell tumour, not otherwise specified as defined by Scully.

Gynandroblastoma of the ovary.

A gynandroblastoma of the ovary in a 17-year-old girl is reported. Primary amenorrhoea, hirsuties and slight clitoral enlargement were associated with the tumour and high levels of circulating testosterone were found. This is the first gynandroblastoma in which Reinke crystalloids have been identified in the Leydig cell component. The criteria for the diagnosis of this tumour and its histogenesis are discussed.