Fig. 7
Hypothalamic-pituitary-ovarian axis in group B. a, mechanisms of ovarian suppression by the Gn-RH analog in women of reproductive age. The Gn-RH analog causes the down-regulation of Gn-RH receptors in pituitary cells, which then induces a decrease of gonadotropin secretion and the subsequent low production of estrogen in the ovary. Under these low-estrogen conditions, Gn-RH secretion in the hypothalamus may be accelerated. b and c, possible explanation for the delayed resumption of menses in women during TAM administration after combined Gn-RH analog treatment. b, the delayed resumption of menses during TAM administration after combined Gn-RH analog treatment suggests transient suppressing effects of TAM on Gn-RH secretion in the hypothalamus (see pathway [I]). TAM acts on the hypothalamus as an estrogenic modulator under the low-estrogen conditions during Gn-RH analog treatment, suppressing high secretion of Gn-RH in the hypothalamus. c, the suppressing effects of TAM persist for over half a year even after cessation of the Gn-RH analog. When the balance between the hypothalamus-suppressing effect [I] and negative feedback-inhibitory effect (see pathway [II]) become converted, normal follicular growth and menses gradually restart and then OHS will occur