Endocrine Abstracts

Introduction/background: Hypothalamic Amenorrhea (HA), or stress-induced anovulation, is one of the most common causes of secondary amenorrhea (1,2) and accounts for the reproductive dysfunction seen in under nutrition, excessive exercise, sever emotional stress and chronic disease. From a teleological standpoint, in the face of nutritional or physical stress, it is adaptive for an organism to allocate energy resources for its own survival rather than the costly process of reproduction and therefore HA is a physiologic response to environmental, physical or emotional stressors. In this case we report a 37y.o otherwise healthy mother, whose longstanding postpartum secondary amenorrhea resolved post gonadotropin releasing hormone(GnRH) stimulation test done for diagnostic purposes.

Aims: To test gonadotropic cell ability of secreting LH and FSH under the stimulating action of GnRH.

Materials and methods: A standard GnRH test was used, after all other underlying conditions likely causing primary or secondary amenorrhea were excluded via biochemical parameters and imaging methods (Pituitary MRI, abdo-pelvic U/S scan). Furthermore, the patient was on no medication.

Results: Pre GnRH administration, 08:30am blood tests were performed, indicating euthyroidism (TSH:0,94mU/L), normoprolactinaemia (PRL:121mU/L), normocortisolaemia (Cort:595 nmol/L) and normoandrogenism (Testo:0,4 nmol/L, DHEAS:5,7 nmol/L). MRI of the pituitary and adrenal-ovarian U/S scans previously performed, were also unremarkable. Pre GnRH administration, gonadotropins were (LH:<1IU/L, FSH:3IU/L) while 30 min after, (LH:10 and FSH:9IU/L) and 60 min after (LH:14IU/L and FSH:18IU/L) indicating a reverse response pattern, non characteristic of a female adult. A few days after the test, her menstruations returned and remained regular since then, after an absence of four years.

Conclusion: To the extent of our knowledge, there are very few recorded cases of spontaneous resolution of a hypothalamic amenorrhea after a GnRH test. This necessitates for further research in this disorder’s complex pathophysiological mechanisms in order to allow for early diagnosis and better patient outcomes.

References: 1. Lindsay et al. JCEM 2015.

2. Reindollar et al. Am J Obstet Gynecol. 1986.