Acute pancreatitis (AP) is an inflammatory gastroenterological disease, during which about 4% of all patients develop disturbance in consciousness. Besides this sypmtom among the severe AP cases 10 % show serious neurological involvement manifesting in pancreatic encephalopathy. Earlier research from our laboratory showed blood-brain barrier (BBB) permeability elevation in a rat non-invasive AP model. Now our goal was to identify potential BBB injury in pancreatitis patients. For this study we used serum from mild, moderate and severe AP patients to identify BBB opening by measuring neuron specific enolase (NSE) and S100B presence in the blood. Cultured brain endothelial cells were also treated with 20% human sera. Functional tests: permeability, transendothelial electrical resistance, ROS/NO production were analyzed. Morphological investigations: interendothelial junctions, adhesion molecules, mitochondrial network visualization were done. Surface glycocalyx integrity analysis: lectin staining, zeta potential and streaming potential measurements were performed. We found elevated NSE and S100B levels in the serum of patients with mild, moderate and severe AP. Serum treatment decreased the brain endothelial cell layer resistance and elevated permeability. Key interendothelial junctional and adhesion molecule expression and morphology were affected. ROS production was increased and mitochondrial network was also damaged. Our results show, that treatment with the AP patient sera influences many important BBB properties such as barrier integrity, level of oxidative stress and junctional morphology. The fact that BBB leakage markers were found in the blood of patients from all AP severity groups draws the attention to the serious neurological side effects of the disease.