It has been shown that there is a decrease in the barrier function of the intestines and an increase in bacterial translocation at the onset of AP.6,7 It has been determined that bacterial translocation develops with the deterioration of intestinal barrier function due to AP, leading to systemic inflammation and sepsis.8 It has been proven that damage to tight and adherens junctions by various factors plays a role in the development of intestinal barrier dysfunction in AP.9 From this point of view, we aimed to show whether there was a change in serum zonulin levels in patients with AP. This evidence concerns the gene HP and alkaline phosphatase measurement.