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Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study
Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study
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Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study
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Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study
Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study

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Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study
Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study
Journal Article

Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study

2023
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Overview
Background It is suspected that microbiome-derived trimethylamine N-oxide (TMAO) may enhance platelet responsiveness and accordingly be thrombophilic. The purpose of this prospective observational study is to evaluate TMAO in patients with subarachnoid hemorrhage (SAH) and compare it with a control group. A secondary aim was to investigate TMAO in the cerebrospinal fluid (CSF) from SAH patients. This should provide a better understanding of the role of TMAO in the pathogenesis of SAH and its thrombotic complications. Methods The study included patients with diagnosed spontaneous SAH recruited after initial treatment on admission and patients with nerve, nerve root, or plexus disorders serving as controls. Blood samples were gathered from all patients at recruitment. Additionally, sampling of SAH patients in the intensive care unit continued daily for 14 days. The CSF was collected out of existing external ventricular drains whenever possible. Results Thirty-four patients diagnosed with SAH, and 108 control patients participated in this study. Plasma TMAO levels at baseline were significantly lower in the SAH group (1.7 μmol/L) compared to the control group (2.9 μmol/L). TMAO was detectable in the CSF (0.4 μmol/L) and significantly lower than in plasma samples of the SAH group at baseline. Plasma and CSF TMAO levels correlated positively. The TMAO levels did not differ significantly during the observation period of 15 days. Conclusions Although we assumed that patients with higher TMAO levels were at higher risk for SAH a priori, plasma TMAO levels were lower in patients with SAH compared with control subjects with nerve, nerve root, or plexus disorders on admission to the hospital. A characteristic pattern of plasma TMAO levels in patients with SAH was not found.