Ultrasound Findings of Liver and Pancreas in Children with Type 1 Diabetes Mellitus: A Case-Control Study

نویسندگان
doi
10.5812/ijradiol-145439
چکیده

Background: Type 1 diabetes mellitus (T1D), characterized by chronic hyperglycemia and insulin dependence, is caused by the autoimmune destruction of β-cells in the pancreas. Diabetes mellitus can potentially lead to excessive accumulation of fat in the liver, resulting in fatty liver. Changes in pancreatic tissue during the course of the disease can lead to decreased insulin secretion and increased insulin resistance. Objectives: This study aimed to investigate the size and fat content of the liver and pancreas in children with T1D using ultrasound and to explore their relationship with clinical and laboratory indicators. Results: The two groups had significant differences in aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), bilirubin, and HbA1c levels, with higher values observed in diabetic subjects. There was no statistical difference between the two groups in terms of liver size. The frequency of fatty liver was higher in patients with T1D (65.1% in diabetic subjects versus 23.3% in non-diabetic subjects). The size of the body and tail of the pancreas in the case group was significantly lower than in the control group (10.33 ± 2.87 vs. 12.30 ± 2.1, P = 0.004 for the body, 9.47 ± 2.4 vs. 10.86 ± 2.2, P = 0.007 for the tail). Fatty pancreas was more prevalent in T1D compared to the control group (P = 0.03). The size and grade of fatty pancreas did not significantly correlate with the presence of autoantibodies. Liver size and body mass index were positively correlated (P = 0.03). Conclusion: Patients with T1D are more susceptible to nonalcoholic fatty liver disease (NAFLD). Pancreatic morphological alterations, including increased echogenicity and a decrease in the size of the pancreas (particularly at the body and tail), can be detected in ultrasound studies of children with T1D. Furthermore, no significant association was found between T1D autoantibodies and pancreatic morphological changes, suggesting that autoantibodies cannot be used to predict future pancreatic morphological alterations.