Guaraldi Federica, Grottoli Silvia, Arvat Emanuela, Ghigo Ezio
Division of Endocrinology, Diabetes and Metabolism, Department of Medical Sciences, University of Turin, Corso Dogliotti 14, Turin 10126, Italy.
Division of Oncological Endocrinology, Department of Medical Sciences, University of Turin, Corso Bramante 88, Turin 10126, Italy.
J Clin Med. 2015 May 19;4(5):1025-35. doi: 10.3390/jcm4051025.
Traumatic brain injury (TBI) is a leading cause of secondary hypopituitarism in children and adults, and is responsible for impaired quality of life, disabilities and compromised development. Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Although the exact pathophysiology is unknown, several mechanisms have been hypothesized, including hypothalamic-pituitary autoimmunity (HP-A). The aim of this study was to systematically review literature on the association between HP-A and TBI-induced hypopituitarism. Major pitfalls related to the HP-A investigation were also discussed.
The PubMed database was searched with a string developed for this purpose, without temporal or language limits, for original articles assessing the association of HP-A and TBI-induced hypopituitarism.
Three articles from the same group met the inclusion criteria. Anti-pituitary and anti-hypothalamic antibodies were detected using indirect immunofluorescence in a significant number of patients with acute and chronic TBI. Elevated antibody titer was associated with an increased risk of persistent hypopituitarism, especially somatotroph and gonadotroph deficiency, while no correlations were found with clinical parameters.
HPA seems to contribute to TBI-induced pituitary damage, although major methodological issues need to be overcome and larger studies are warranted to confirm these preliminary data.
创伤性脑损伤（TBI）是儿童和成人继发性垂体功能减退的主要原因，会导致生活质量下降、残疾和发育受损。垂体功能改变可在创伤事件后的任何时间发生，表现形式多样且随时间演变，因此需要进行适当筛查以早期发现和治疗。尽管确切的病理生理学尚不清楚，但已提出了几种机制，包括下丘脑 - 垂体自身免疫（HP - A）。本研究的目的是系统回顾关于HP - A与TBI诱导的垂体功能减退之间关联的文献。还讨论了与HP - A研究相关的主要缺陷。
使用为此目的制定的检索词在PubMed数据库中进行检索，无时间或语言限制，以查找评估HP - A与TBI诱导的垂体功能减退之间关联的原始文章。
同一组的三篇文章符合纳入标准。在大量急性和慢性TBI患者中，使用间接免疫荧光法检测到抗垂体和抗下丘脑抗体。抗体滴度升高与持续性垂体功能减退的风险增加相关，尤其是生长激素分泌细胞和促性腺激素分泌细胞缺乏，而与临床参数无相关性。
尽管需要克服主要的方法学问题，并且需要更大规模的研究来证实这些初步数据，但HPA似乎促成了TBI诱导的垂体损伤。
