Parameters of blood short-chain peptides and digestive hydrolases in patients with chronic hepatitis B virus infection

The aim of the study was to examine specifics of changes in the level of stomach- and pancreas-released blood hydrolases in chronic viral hepatitis B and analyze the mechanisms underlying such changes. We assessed serum markers of HBV infection, liver enzymes tests as well as gastric and pancreatic hydrolase level. The patients examined were divided into three groups: control (healthy) and two study groups — HBV post-infection and chronic HBV infection. Patients with HBV post-infection had no significant deviations from normal range for blood level of gastric and pancreatic hydrolases. Patients with chronic HBV infection were found to contain increased blood level of amylase and lipase, which may evidence about increasing pancreatic functional activity and development of covert pancreatitis. At the same time, decline in the concentration of serum pepsinogen-1 below 40 μg/l could indicate about prominently decreased secretion of hydrochloric acid and development of atrophic gastritis, and it was found that the major factor contributing to development of such disorders was the short-chain peptide CCK-8, which utilization declines in patients with chronic HBV infection. CCK-8 can play a pivotal role in inhibiting stimulation of gastric acid secretion and controls gastric acid, plasma gastrin and somatostatin secretion. Cholecystokinin has been found to inhibit acid secretion by activating CCK type A receptors as well as via somatostatin-involving mechanism. The secretion of gastric somatostatin-14 increased by fivefold due to CCK-8 alone, but was blocked by the CCK-A receptor blocker loxiglumide. These data show that CCK-8 directly inhibits acid reactions by stimulating the release of gastric somatostatin indirectly through the CCK-A receptor. Thus, it can be assumed that normally CCK-8 is mainly utilized by the liver, which is altered during chronic hepatitis B resulting in elevated blood CCK-8 concentration. As a consequence, it enhances pancreatic secretion resulting in developing pancreatitis that is paralleled with inhibited gastric secretion and emerged atrophic gastritis