De Sanctis Vincenzo, Soliman Ashraf T, Elsedfy Heba, Soliman Nada A, Elalaily Rania, El Kholy Mohamed
Pediatr Endocrinol Rev. 2015 Sep;13(1):458-64.
The intent of the current manuscript is to review the cases of central precocious puberty (CPP) in early childhood following traumatic brain injury (TBI). SEARCH OF THE LITERATURE: The MEDLINE database was accessed through PubMed in April 2015. Results were not restricted to the date and language of the articles. For the first search we utilized MeSH terms "precocious puberty" in conjunction with "traumatic brain injury" and with "endocrine consequences". Reference lists were reviewed and relevant papers were also consulted to find additional studies and data. In selected cases the corresponding author was contacted by email.
In our systematic review, only a few case reports or small case series have highlighted a link between TBI and hypothalamic-pituitary hormone abnormalities. Fourteen reported children were females and 8 were males. The majority of patients reported had severe TBI, assessed by Glasgow Coma Scale or structural injury (skull fractures, intracranial hemorrhage or cerebral injury) reported on computerized tomography or magnetic resonance imaging scans. The pathogenic mechanism of precocious puberty has not yet been determined. An increased pressure on the hypothalamic-pituitary area with loss of normal childhood hypothalamic inhibition of pituitary gonadotropins could be one of the factors responsible for CPP after TBI.
The current review highlights the importance of close clinical follow-up to evaluate the rate of linear growth and pubertal development after TBI. Although, precocious puberty appears to be rare after TBI, prevalence should ideally be assessed by longitudinal follow-up of a large population. Therefore, further multicenter and multidisciplinary studies are required to explore in detail the true incidence and the possible mechanisms of CPP after TBI. Because precocious puberty can be detected on clinical assessment during childhood, a pragmatic approach would be for family physicians to monitor growth and development in children after TBI. Inasmuch as precocity is mediated through the hypothalamic-pituitary pathways, use of LH-RH analogue therapy should be effective in arresting pubertal progression.
本手稿旨在回顾创伤性脑损伤（TBI）后儿童期中枢性性早熟（CPP）的病例。
2015年4月通过PubMed访问MEDLINE数据库。检索结果不受文章日期和语言限制。首次检索时，我们使用了医学主题词“性早熟”，并结合“创伤性脑损伤”和“内分泌后果”。对参考文献列表进行了审查，并查阅了相关论文以寻找更多研究和数据。在某些选定病例中，通过电子邮件与通讯作者取得了联系。
在我们的系统综述中，只有少数病例报告或小型病例系列强调了TBI与下丘脑 - 垂体激素异常之间的联系。报告的14名儿童为女性，8名儿童为男性。报告的大多数患者患有严重的TBI，通过格拉斯哥昏迷量表评估或根据计算机断层扫描或磁共振成像扫描报告的结构性损伤（颅骨骨折、颅内出血或脑损伤）来判断。性早熟的发病机制尚未确定。下丘脑 - 垂体区域压力增加，同时儿童期下丘脑对垂体促性腺激素的正常抑制作用丧失，可能是TBI后发生CPP的因素之一。
本综述强调了密切临床随访对于评估TBI后线性生长速度和青春期发育的重要性。虽然TBI后性早熟似乎很少见，但理想情况下应通过对大量人群的纵向随访来评估其患病率。因此，需要进一步开展多中心、多学科研究，以详细探讨TBI后CPP的真实发病率和可能机制。由于性早熟可在儿童期临床评估中被发现，务实的做法是家庭医生监测TBI后儿童的生长发育情况。鉴于性早熟是通过下丘脑 - 垂体途径介导的，使用促性腺激素释放激素（LH - RH）类似物疗法应能有效阻止青春期进展。
