LIVER DAMAGE IN CHRONIC HELICOBACTERIOSIS AND COMORBID CHRONIC PANCREATITIS

Abstract

The study aimed to determine the state of the pancreatic-hepatobiliary system by biochemical and sonographic data in patients with gastric and/or duodenal ulcer associated with chronic helicobacter pylori and comorbid chronic pancreatitis.

Materials and methods. We examined 56 gastroenterological patients (20 men and 36 women) with gastric ulcer and/or duodenal ulcer caused by chronic helicobacter pylori and 26 relatively healthy individuals who formed the control group. All patients underwent an objective examination, laboratory (biochemical) blood tests, esophagofibrogastroduodenoscopy with biopsy, urease test for Helicobacter pylori (Hp) infection, ultrasound examination of the hepatobiliary system and pancreas.

Results. All patients in the main group, in addition to gastric ulcer and/or duodenal ulcer, suffered from chronic pancreatitis (n=56) and had various comorbidities chronic stone-free cholecystitis (n=27), post-cholecystectomy syndrome (n=3), arterial hypertension (n=17), coronary heart disease (n=7), chronic lung disease (n=3), and chronic kidney disease (n=8). The analysis of Hp infection by the degree of contamination and topogoraphic zones revealed the highest degree of bacterial contamination with active forms of Hp in the gastric mucosa along the small curvature (p <0,05); the average degree of bacterial contamination with inactive forms of Hp was more frequently observed in the body of the stomach along the small curvature compared to the antrum and other parts of the stomach (p >0,05).

The vast majority of patients in the main group had ultrasound signs of hepatobiliary pathology: thickening of the gallbladder wall (9.6%), changes in the structure of the pancreas (100%), diffuse changes in the liver parenchyma (82.1%), and gallbladder calculi (12.5%). Most often, patients with peptic ulcer disease were diagnosed with thickening of the gallbladder wall and its deformation.

Conclusions. The results of our study demonstrate ultrasound changes in the liver parenchyma in patients with gastric and peptic ulcer associated with chronic helicobacter pylori and comorbid chronic pancreatitis, which is in line with the literature. The concomitant liver damage in this cohort of patients occurs under the mask of cytolytic and cholestatic syndromes of mild severity. The list of comprehensive examinations of patients with gastric ulcer and/or duodenal ulcer associated with chronic helicobacter pylori and comorbid chronic pancreatitis should be expanded by adding ultrasound examination of the hepatobiliary system.