Endocrine Abstracts

Introduction: Cancer treatment including oophorectomy, radiotherapy and chemotherapy with gonadotoxic agents may induce premature ovarian failure. Early diagnosis and treatment of ovarian failure avoids cardiovascular disorders, osteoporosis and compromised sexual health due to estrogen deficiency and also ensures growth and pubertal development in children.

Aim: Raise awareness for early assessment and management of premature ovarian failure after cancer treatment.

Methods: A retrospective longitudinal study was performed by analysis of medical records of patients with premature ovarian failure due to cancer treatment followed at our centre. Demographics, primary tumour clinicopathological data, cancer treatment details, clinical and biochemical features of hypogonadism, puberty induction requirement and hypogonadism treatment were analysed.

Results: Twenty-one women with previously diagnosed ovarian failure due to cancer treatment were included. Median age at cancer diagnosis was 8 years (minimum: 6 months, maximum: 39 years); at last follow-up median age was 17 years (minimum: 9 years, maximum: 44 years) and one was deceased. Hematological and solid malignancies were documented as primary tumours, the former being more frequent: acute lymphocytic leukemia (n=6), acute myeloid leukemia (n=2), non-Hodgkin lymphoma (n=2) and chronic myeloid lymphoma (n=2). All patients underwent chemotherapy, four were also submitted to abdominal or pelvic radiotherapy and one underwent additional unilateral oophorectomy due to small cell carcinoma of the ovary. The mean dose of radiotherapy used was 39.5 Gy±10.3 (SD). Eighteen cases underwent chemotherapy in context of conditioning regimens for hematopoietic stem cell transplant. Gonadotoxic drugs were used in 19 patients, the most common agents were cyclophosphamide (n=15), busulfan (n=13), cisplatin (n=3), melphalan (n=2) and carboplatin (n=2). Primary or secondary amenorrhea had been described in 11 and 7 cases respectively. Mean FSH at diagnosis of premature ovarian failure after cancer treatment was 74.7±8.5 (SD) mUI/ml. At last follow-up, 3 patients had completed puberty induction and 5 patients were under therapy for puberty induction with estrogen patch. Vigilance of spontaneous pubertal development was described in 3 girls under 14 years with gonadotrophin levels suggestive of primary ovarian insufficiency. Regarding maintenance hormone therapy, 2 patients were treated with estrogen patch and oral progestin, 2 were treated with oral estradiol/progesterone replacement therapy regimens, and 7 were under oral combined contraceptive pill.

Conclusion: Assessment of ovarian function must be performed after cancer treatments with potential risk of inducing ovarian insufficiency. Sex hormones replacement strategies vary according to pubertal development and prevent estrogen deficiency effects.