Influence of Pancreatic Steatosis on the Structural Changes of the Liver and Pancreas in Children with Overweight and Obesity

Abstract

Introduction: The ectopic fat accumulation in the liver, known as nonalcoholic fatty liver disease (NAFLD), is associated with insulin resistance, dyslipidemia, and high risk of diabetes and cardiovascular diseases. Nonalcoholic fatty pancreas disease (NAFPD) is defined as obesity-associated accumulation of fat in the pancreas without signs of secondary causes of steatosis. The pathophysiology of NAFPD and NAFLD is closely related. But the causal relationship between NAFLD and NAFPD has not been well established yet. The aim of the study is to investigate the relationship between liver and pancreatic steatosis (PS); to establish the influence of the PS on the structural changes of the liver and pancreas. Materials and Methods: A total of 117 children aged 6-17 years (mean 11.67 ± 2.81 years; 68 boys, 49 girls) were included. Patients were divided into 5 groups: group 1-37 children with combined liver and pancreatic steatosis, 2 group-30 children with isolated steatosis of the pancreas, 3 group-6 children with isolated liver steatosis, 4 group-28 children with obesity / overweight without liver and pancreatic steatosis, 5 group-16 children with normal weight. Pancreatic steatosis was established on the basis of ultrasound examination of the pancreas. Diagnosis of non-alcoholic fatty liver disease was established in the presence of signs of liver steatosis according to transient elastography with CAP function (Fibroscan 502 Touch). We also performed a quantitative estimation of the ultrasound attenuation coefficient (UAC) conducted on UltimaPAExpert apparatus ("Radmir", Ukraine). To determine the stiffness of the pancreatic parenchyma, shear wave elastography using UltimaPAExpert (Radmir, Ukraine) was performed. Results: It was found that children with combined steatosis showed higher levels of UAC and CAP compared to children with normal weight (p<0,05). The maximum degree of liver steatosis according to the CAP was observed in the group with combined steatosis (p<0.05). It should be noted that children with combined liver steatosis had higher liver and pancreatic stiffness values in comparison with children having isolated pancreatic steatosis (p<0,05). This fact can be explained by more intensive fibrotic changes in the liver and pancreas in case of combined steatosis but also inflammatory changes in this organs can influence on stiffness parameters. In the correlation analysis, there was a positive correlation between UAC and СAP. Also we found positive correlation between pancreatic and liver stiffness according to SWE. Conclusion: Our findings along with literature data show that pancreatic steatosis precedes the appearance of liver steatosis. We assume that pancreatic steatosis as well as liver steatosis is accompanied with rise of parenchyma stiffness of these organs. Patients who had signs of liver steatosis and pancreatic steatosis had the most adverse structural changes in the form of increased stiffness of the parenchyma of the liver and pancreas.