Alcohol consumption affects the late endocrine consequences of mild traumatic brain injury.

BACKGROUND: Currently there are no widely applied methods which could identify, at the time of head trauma, those mild traumatic brain injury (mTBI) patients who later develop pituitary dysfunction. The effect of alcohol consumption on post-TBI endocrine dysfunction is unclear. METHODS: Five hundred and eight TBI patients, 406 of them with mTBI, were studied. Sixty-one patients (46 males, 15 females) were available for follow-up. Admission serum samples were evaluated for S100B protein and markers of alcohol consumption: ethanol level for day-of-injury intake and carbohydrate deficient transferrin (CDT) level for regular alcohol consumption. Regular alcohol consumption was defined as CDT > 1.5%, including both social and heavy drinkers. Admission and one-year follow-up samples were evaluated for pituitary dysfunction. RESULTS: Newly developed pituitary hormone deficiency was found in 16% of mTBI patients. When cohorts developing and not developing late pituitary dysfunction were compared, 30% and 69% of patients were regular alcohol consumers, respectively (p = 0.02). Neither S100B level nor day-of-injury alcohol consumption was predictive of late pituitary dysfunction. CONCLUSION: The findings of this preliminary study suggest that regular alcohol consumption may protect against the late endocrine consequences of mTBI. Alcohol intake during the weeks preceding mTBI may identify patients at higher risk for late pituitary dysfunction.

Plasminogen Activator Inhibitor Type 1: A Possible Novel Biomarker of Late Pituitary Dysfunction after Mild Traumatic Brain Injury.

More than 80% of traumatic brain injury (TBI) patients suffer from mild TBI (mTBI). However, even mTBI carries the risk of late pituitary dysfunction. A predictive biomarker at the time of injury that could identify patients who subsequently may develop permanent pituitary dysfunction would help to direct patients toward endocrine care. We enrolled 508 TBI patients (406 with mTBI) into our study. Blood samples were collected for identification of predictive biomarkers of late pituitary dysfunction at the time of admission. Follow-up blood samples were collected between 6 and 12 months after the TBI and were evaluated for pituitary function. Of the 406 mTBI patients, 76 were available for follow-up. Pre-existing mild pituitary dysfunction was found for 15 patients based on hormone levels at the time of injury. Of the remaining 61 patients, 10 have shown deficiency in at least one pituitary hormone: 4 had growth hormone deficiency, 3 gonadotropin, 2 thyrotropin, and 1 patient combined gonadotropin and thyrotropin deficiency. Hence, newly developed pituitary hormone deficiency was found in 16% of mTBI patients. Neither the cause of mTBI nor its complications were predictive of late pituitary dysfunction. Of the hemostasis parameters studied, lower plasminogen activator inhibitor type 1 (PAI-1) level at the time of injury was found to be predictive for the development of late pituitary dysfunction; sensitivity, specificity, and positive and negative predictive values were 80%, 67%, 32%, and 94%, respectively. Even mTBI carries a substantial risk of endocrine consequences. Serum PAI-1 level at the time of TBI may serve as a predictive biomarker of late pituitary dysfunction in mTBI patients.