ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P1136 | DOI: 10.1530/endoabs.63.P1136

Kisspeptin in regulation of menstrual function in patients with resistant hyperprolactinemia

Svetlana Vorotnikova, Ekaterina Pigarova, Larisa Dzeranova & Natal’ya Fedorova


Endocrinology research centre, Moscow, Russian Federation.


Introduction: Patients with resistant prolactinomas have reduced fertility todue to chronic anovulation and hypoplasia of uterus and ovaries. SERM tamoxifen demonstrates a recovery of menstrual function and ovulation and reverses the hypoplasia of the uterus. The mechanism of its action in case of hyperprolactinemia is not clear yet.

Aim: To study the role of kisspeptin in restoration of reproductive function in patients with prolactinomas treated by tamoxifen.

Materials and patients: This pilot study included 2 women of reproductive age (30 and 27 years old) with resistant prolactinomas treated by maximal doses of cabergoline 4.5 mg per week. Patients had amenorrhea for 6 and 8 months. Tamoxifen was administered as adjuvant therapy in dose of 10 mg per day for 3 months. Hormonal and pelvic ultrasonic parameters were evaluated before and after complex treatment.

Results: Before addition of tamoxifen, prolactin level was 2658 U/l and 3001 U/l, LH and FSH levels were normal. At ultrasonography, patients presented symptoms of anovulative menstrual cycle. There were no any differences between kisspeptin levels before and after tamoxifen treatment and its levels varied from 0.041 to 0.053 in first patient and from 0.069 to 0.077 in second, P=0.18. Normal menstrual cycle was recovered in 1 month after start of tamoxifen in both women. Prolactin levels decreased by 4.4% and 6.5%. Dynamics of ultrasound picture at 3 months revealed significant improvement of the state of reproductive organs with signs of ovulation, presence of corpus luteum and dominant follicle.

Conclusion: Tamoxifen recovers menstrual function without changes of kisspeptin and normalization of prolactin levels which may be explained by direct activation of estrogen receptors and positive affects at the levels of ovaries and endometrium without recovering of the hypothalamic regulation.

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