Effect of traumatic brain injury severity on intestinal barrier and gastrointestinal function

Traumatic brain injury (TBI) is a significant global public health challenge, with an estimated mortality rate of 13 per 100,000 people in China.Bedsides the immediate neurological consequences, [1] TBI is associated with longterm sequelae and an elevated risk of neurodegenerative conditions such as dementia, Parkinson's disease, and epilepsy.Moreover, TBI can induce systemic effects, including acute gastrointestinal injury (AGI), contributing to poor patient outcomes. [2]he bidirectional brain-gut axis plays a crucial role in TBI-related AGI.TBI activates the hypothalamus-pituitaryadrenal (HPA) axis and autonomic nervous system (ANS), leading to an imbalance in sympathetic and parasympathetic signaling.This disruption damages the gastrointestinal (GI) tract, alters the intestinal microbiota, and increases the proliferation of pathogenic bacteria, exacerbating GI injury and worsening patient prognosis. [3,4]urrent research highlights that bacterial overgrowth leads to increased D-lactic acid production, which enters the bloodstream through a compromised intestinal mucosal barrier.Concurrently, damage to intestinal epithelial cells elevates diamine oxidase (DAO) levels, which is an enzyme involved in the metabolism of histamine and is commonly used as a biomarker for assessing GI integrity and function. [5]he focus of this study was to explore the correlation between serological markers of intestinal dysfunction (endotoxins, D-lactic acid, and DAO) and the severity of TBI.By analyzing these markers, we aimed to provide insights into the early diagnosis and treatment of AGI in TBI patients, which might improve the prognosis.