Post‐menopausal bleeding: Hydatidiform mole a rare cause

A 55-year-old nulliparous woman presented for investigation of breakthrough bleeding while on hormone replacement therapy. She had been on the combined oral contraceptive pill until age 53. Six months after ceasing the contraceptive pill she commenced cyclical combined hormone replacement therapy, switching to combined continuous therapy after 6 months and then owing to palpitations, changing to tibolone. In May 2002 she presented with a history of breakthrough bleeding for 5 weeks, after 6 months of treatment with tibolone. She also had generalised malaise including aching joints and palpitations. The patient was otherwise well and had no significant medical history. She had no personal or family history of gynaecological or other malignancy. She was a non-smoker and drank moderate amounts of alcohol. On examination she was a slim lady of stated age. The abdomen was soft. There was some bleeding from the cervix and the uterus was slightly bulky, but non-tender and there were no palpable adnexal masses. Haemoglobin was within the normal range and thyroid function tests were normal. Transvaginal and transabdominal pelvic ultrasound was performed and showed an anteverted uterus with a grossly abnormal endometrial echo pattern. The endometrium was heterogenous and 5 cm × 4 cm × 3 cm in size. There were areas of fluid echogenecity and loss of the boundary between the myometrium and endometrium. There was increased vascularity around the outside of this abnormal endometrium. No invasion outside the uterus was seen and the adnexae appeared normal. Owing to the high likelihood of endometrial malignancy, a hysteroscopy and curettage was performed. Standard saline hysteroscopy was carried out under general anaesthesia. Endometrial biopsy was performed, with profuse curettings obtained. Blood loss was not excessive and the patient was discharged home the same day. Histopathology of the curettings showed marked psuedo decidual change and Arias-Stella like change. These findings were thought to be consistent with exogenous hormone effect. No evidence of hyperplasia, neoplasia or endometritis was seen. One month later the patient represented to her general practitioner complaining of nausea and lumpy breasts, which had not improved since ceasing tibolone pre hysteroscopy. Her bleeding had also continued. Abdominal computed tomography scan was performed and showed a thick-walled mass associated with the upper portion of the fundus of the uterus, which was thought to be consistent with a large exophytic fibroid with possibly some central necrosis. A small granuloma was noted in the right lobe of the liver, but there were no other abnormal findings. Her symptoms were consistent with exogenous oestrogen production in the presence of a degenerating fibroid, within which malignant change could not be excluded. Laparoscopic assisted vaginal hysterectomy and bilateral salpingooophorectomy with pelvic node dissection was therefore recommended. At operation the uterus contained a large mass which had the appearance of necrotic and hydropic villi (Fig. 1). Frozen section confirmed the presence of chorionic villi. There was no evidence of macroscopic spread from the uterus. Beta human chorionic gonadotropin (βhCG) performed intraoperatively was 96463 IU/L. Histopathology confirmed the presence of a complete hydatidiform mole. Lymph nodes and peritoneal washings were clear of malignant spread. Since the operation, βhCG fell to negative levels over a period of 6 weeks and has remained negative for 12 months.