全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Alteraciones neuroendocrinas del síndrome de poliquistosis ovárica en la adolescencia

Keywords: polycystic ovary syndrome, lh, fsh, androgen.

Full-Text   Cite this paper   Add to My Lib

Abstract:

polycystic ovary syndrome (pcos) is the most common endocrine disorder among women in reproductive age, frequently begins during adolescence causing menstrual irregularity and hirsutism. although described up more than seventy years ago, the primary pathophysiologic mechanisms underlying this disorder remain unknown.there is not a single etiologic factor that fully accounts for the spectrum of abnormalities in the pcos. this review addresses current knowledge about the neuroendocrine abnormalities as a major component of the syndrome. from this perspective, adolescents with pcos exhibit an accelerated frequency and/or higher amplitude of lh pulses, augmentation of secretory burst mass, and a more disorderly lh release (higher apen) than eumenorrheic adolescents. several lines of evidence suggest that the mechanisms underlying the defects in lh secretion in pcos include an increased frequency of gnrh secretion. these patients also show elevated in vitro lh bioactivity and a preponderance of basic lh isoforms, which correlate positively with elevated serum of 17-hydroxyprogesterone, androstenedione (a), and testosterone (t) concentrations. heightened gnrh drive of gonadotropin secretion and steroid-permissive milieu appear to jointly promote elevated secretion of basic lh isoforms. non obese adolescents with pcos secrete gh at a higher rate and with more orderly patterns (resembling a male profile) than controls. indeed, gh appears to act as a co-gonadotropin. when synchronicity of paired hormone profiles was appraised by two independent, but complementary, statistical tools (cross-entropy and cross correlation), concomitant uncoupling of the pairwise synchrony of lh - androgens was demonstrated in girls with pcos. asynchrony of lh-a and lh-t pairs further localizes a pathway defect to lh-dependent feedforward control of ovarian androgen secretion. these abnormalities are also consistent with altered androgen negative feed-back regulation of gnrh/lh output. these data

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133