[Effects of HPGA suppression on predicted adult height in girls with central precocious puberty].

OBJECTIVE: To study the relationship between the suppression of the hypothalamic-pituitary-gonadal axis (HPGA) and the predicted adult height (PAH) in girls with central precocious puberty (CPP) during the treatment with gonadotropin-releasing hormone analogue (GnRHa), in order to provide guidance for individualized GnRHa dose adjustment in clinical practice. METHODS: The clinical data of 75 CPP girls were collected, and then height, bone age (BA), uterine and ovarian volumes, and peak luteinizing hormone (LH), peak follicle-stimulating hormone (FSH), and estradiol (E2) levels were recorded at different time points of GnRHa treatment. PAH at each time point was calculated. PAH improvement (ΔPAH=PAH-target height) and its relationship with the degree of HPGA suppression were analyzed. Threshold effect analysis was applied to determine the best HPGA suppression range forΔPAH. RESULTS: After GnRHa treatment, PAHs were improved markedly compared with the data in the early stage of treatment. ΔPAH showed a negative correlation with ΔBA. At 24 months of treatment, ΔPAH was also negatively correlated with LH. Uterine volume controlled between 2.3 and 3.0 mL, LH level controlled below 0.8 IU/L, and FSH controlled below 2.4 IU/L could slow down the growth of BA and improve PAH. CONCLUSIONS: GnRHa treatment can improve the PAH of CPP girls. Selection of an appropriate therapeutic dose for GnRHa to control uterine volume, LH and FSH levels within certain ranges can slow down the growth of BA and improve PAH.

Lateral ventricle injection of orexin-A ameliorates central precocious puberty in rat via inhibiting the expression of MEG3.

BACKGROUND: Central precocious puberty (CPP) is characterized as increasing gonadotropin-releasing hormone (GnRH) release. Orexin-A has also been shown to affect GnRH release. However, there are few reports about the effect of orexin A on the treatment of CPP. METHODS: After establishing the precocious puberty model, the rats were divided into four groups: normal control, precocious puberty rats, precocious puberty rats treated with normal saline and precocious puberty rats treated with orexin-A. The vaginal opening time, second estrus cycle, ovarian index and uterus index of rats in each group were detected. qRT-PCR was performed to examine the expression of MEG3 and kisspeptin in rats. HT22 cells were transfected with pcDNA-MEG3 to detect the expression of Kisspeptin. RESULTS: In this study, we found that orexin-A not only delayed the day of vaginal opening and regular estrus cycle days but also decreased the ovarian index and uterus index in rats with CPP. In addition, orexin-A reversed the up-regulation of MEG3 and kisspeptin in rats with CPP. In HT22 cells, the mRNA and protein level of kisspeptin were enhanced by pcDNA-MEG3. CONCLUSION: Our results suggest that orexin-A ameliorates central precocious puberty in rat and MEG3 might be involved in this effect, suggesting that MEG3 might be a novel target in treating central precocious puberty.