Schneider Harald Jörn, Kreitschmann-Andermahr Ilonka, Ghigo Ezio, Stalla Günter Karl, Agha Amar
Neuroendocrinology Group, Max Planck Institute of Psychiatry, Munich, Germany.
JAMA. 2007 Sep 26;298(12):1429-38. doi: 10.1001/jama.298.12.1429.
Neuroendocrine dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage may occur with a much higher prevalence than previously suspected. This sequela is a potentially serious but treatable complication of brain injury.
To review research on hypothalamopituitary dysfunction as an underdiagnosed consequence of traumatic brain injury and subarachnoid hemorrhage, the natural history of this complication, and the potential clinical and public health implications of posttraumatic hypopituitarism.
The MEDLINE database was searched for articles published between 2000 and 2007 using any combination of the terms traumatic brain injury or subarachnoid hemorrhage with pituitary, hypopituitarism, growth hormone deficiency, hypogonadism, hypocortisolism, hypothyroidism, or diabetes insipidus. The reference lists of articles identified by this search strategy were also searched. All articles reporting original data on endocrine outcomes after traumatic brain injury or aneurysmal subarachnoid hemorrhage in peer-reviewed journals with regard to prevalence, pathogenesis, risk factors, outcomes, and clinical course were selected. We pooled data and calculated prevalence rates and 95% confidence intervals (CIs).
We identified 19 studies including 1137 patients. The pooled prevalences of hypopituitarism in the chronic phase after traumatic brain injury and aneurysmal subarachnoid hemorrhage were 27.5% (95% confidence interval [CI], 22.8%-28.9%) and 47% (95% CI, 37.4%-56.8%), respectively. The pooled prevalence of hypopituitarism was greater in patients with severe compared with those with mild or moderate traumatic brain injury. Early neuroendocrine abnormalities were transient in some patients while, less commonly, hypopituitarism evolved over time in others. Patients with posttraumatic hypopituitarism showed an impaired quality of life and an adverse metabolic profile.
Hypopituitarism is a common complication of both traumatic brain injury and aneurysmal subarachnoid hemorrhage and might contribute to morbidity and poor recovery after brain injury.
创伤性脑损伤和动脉瘤性蛛网膜下腔出血后的神经内分泌功能障碍发生率可能比之前怀疑的要高得多。这种后遗症是脑损伤潜在的严重但可治疗的并发症。
综述关于下丘脑垂体功能障碍作为创伤性脑损伤和蛛网膜下腔出血未被充分诊断的后果、该并发症的自然病程以及创伤后垂体功能减退潜在的临床和公共卫生影响的研究。
在MEDLINE数据库中检索2000年至2007年发表的文章,使用创伤性脑损伤或蛛网膜下腔出血与垂体、垂体功能减退、生长激素缺乏、性腺功能减退、皮质醇缺乏、甲状腺功能减退或尿崩症的任意组合词。还检索了通过该检索策略确定的文章的参考文献列表。选择所有在同行评审期刊上报告创伤性脑损伤或动脉瘤性蛛网膜下腔出血后内分泌结果的原始数据的文章,内容涉及患病率、发病机制、危险因素、结果和临床病程。我们汇总数据并计算患病率和95%置信区间(CI)。
我们确定了19项研究,包括1137名患者。创伤性脑损伤和动脉瘤性蛛网膜下腔出血后慢性期垂体功能减退的汇总患病率分别为27.5%(95%置信区间[CI],22.8%-28.9%)和47%(95%CI,37.4%-56.8%)。与轻度或中度创伤性脑损伤患者相比,重度创伤性脑损伤患者垂体功能减退的汇总患病率更高。一些患者早期神经内分泌异常是短暂的,而在其他患者中,垂体功能减退较少见地会随时间发展。创伤后垂体功能减退患者的生活质量受损且代谢状况不良。
垂体功能减退是创伤性脑损伤和动脉瘤性蛛网膜下腔出血的常见并发症,可能导致脑损伤后的发病率和恢复不良。