Features of Liver and Pancreas Pathomorphological Pattern in Case of their Combined Alcohol-Induced Injury

The level of alcohol consumption has significantly increased in recent years. Liver and pancreas are both directly and indirectly affected by its negative impact. Fibrosis-producing cells (stellate cells) are activated in these organs leading to cirrhosis and fibrotic changes in the pancreas. The objective of the research was to study the features of morphologic changes in the liver and pancreas in case of their combined alcohol-induced injury. Multiple clinical anatomicopathological and morphological investigation of liver and pancreas was conducted using autopsied specimen. Alcohol-induced cirrhosis is micronodular manifesting in degenerative changes of hepatocytes, capillarization of the sinusoids and significant stage of fibrosis. Atrophic changes in acini, necrosis of exocrine pancreatic cells, enlargement of stromal and peryductal components by means of neoplasms and proliferation of connective tissue were found in pancreas in cases of the alcohol induced disorder. There were also presented signs of chronic inflammation of the excretory pancreatic ducts wall. Fibrosis was established to be more severe and the number of stellate cells was significantly higher in the case of combined alcohol induced pathology. Areas of hepatocytes necrosis were wider in liver, Mallory bodies in hepatocytes were larger and more numerous. Sclerogenic hyaloid necrosis, severe fibrosis with steatotic injury of hepatocytes in portal areas of the lobule was detected in two-thirds of deceased. Acini of the pancreas were deformated, metaplasia of exocrine pancreas cells, proliferation of epithelial cells in the ducts and accumulation of thick secret in duct’s lumen were observed. Thus, it can be concluded, that morphological changes in the liver and pancreas in case of comorbidity are more severe than in case of separate diseases and therefore combined injury require individualized approach to their correction and further studies.