Abstract

Traumatic brain injury (TBI) can cause damage to peripheral organ systems, such as digestive organ system, and alterations of gut microbiota in addition to brain injury. Our previous study found that TBI induced gastrointestinal dysfunction accompanied by alterations of bile acid metabolism. Bile acid and its receptors have been reported to play important roles in various neurological diseases. To further examine the changes of bile acid metabolism in TBI patients, we performed a retrospective clinical analysis. In this study, 177 patients were included, and the results showed that TBI patients had more frequent antibiotic use compared with a control group. Regression analysis identified TBI as an independent factor for reduction of serum bile acid level (B = −1.762, p = 0.006), even with antibiotic use taken into a regression model. Sub-group regression analysis of TBI patients showed that antibiotic use was negatively associated with bile acid level, while creatinine and triglyceride were positively associated with bile acid level. In conclusion, these data indicated that TBI could greatly reduce serum bile acid. This study provided preliminary but novel clinical evidence of TBI interfering with bile acid metabolism, and further studies with large sample sizes are needed to validate these findings in the future.

Highlights

  • Traumatic brain injury (TBI) is a worldwide major cause of death and disability and leads to heavy medical burden to the society [1]

  • The results indicated that TBI was the only independent factor that had statistically significant influence on serum bile acid level in our study cohort (B = −1.762, 95% CI: −3.020 to −0.505, p = 0.006)

  • We illustrated that TBI might interfere with bile acid metabolism and, as a result, reduce the serum bile acid level

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Summary

Introduction

Traumatic brain injury (TBI) is a worldwide major cause of death and disability and leads to heavy medical burden to the society [1]. One of the most affected peripheral systems is the digestive system, which will suffer various pathological changes and present with different kinds of abnormalities [5, 6]. More than 50% of TBI patients suffer from gastrointestinal symptoms, and the rate of severe complications such as gastrointestinal hemorrhage varies from 5 to 12% in different studies [7,8,9]. This high incidence of gastrointestinal complications has drawn the attention of researchers to relevant physiological or pathological progresses

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