LAUSR

Purpose To identify the correlation of nonalcoholic pancreatic steatosis (NAPS) with nonalcoholic fatty liver disease (NAFLD) in an outpatient group. Based on its metabolic and imaging properties, NAPS has been increasingly recognized in recent years; however, its interaction with NAFLD is still not clear. Patients and Methods In this cross-sectional observational study, 345 consecutive patients without any chronic illness who were referred to the senior radiologist for abdominal ultrasound (US) were included. The US report showed hepatic and pancreatic echogenicity. The patients’ demographic, anthropometric, and laboratory data were collected from medical records. Results Overall, NAPS and NAFLD were seen in 227 (65.8%) and 219 (63.5%) patients, respectively. Normal echogenicity was noted in 74 (21.4%) patients. Forty-four patients (12.8%) had steatotic liver without NAPS, 52 (15.1%) had steatotic pancreas without NAFLD, and 175 (50.7%) had steatosis in both organs. The discordance in steatosis grading between NAPS and NAFLD was 55.1%. Insulin resistance was present in 8.7, 26.7, 19, and 61.3% of patients with no steatosis, only NAFLD, only NAPS, and steatosis in both organs, respectively. Evident NAFLD and NAPS having grade 2 and 3 steatosis were present in 15.3% and 29.0% of the study group, respectively. Cholecystolithiasis was present in 6.8, 13.6, and 28.8% of patients with normal echogenic pancreas, only NAFLD, and only NAPS, respectively (p=0.01). Conclusion Based on the ultrasonographic, clinical, demographic, and anthropometric features of the included patients, we found that NAPS did not fully accompany nonalcoholic fatty liver. Despite severe pancreatic steatosis, more than a quarter of cases had normal liver echogenicity. Insulin resistance frequency was insignificantly higher in NAFLD than NAPS (p=0.694). The significantly higher frequency of cholecystolithiasis in NAPS needs further large-scale studies. The inconsistency of steatosis degree in NAPS and NAFLD in >50% cases may reflect differences in the pathophysiology of these two clinical entities.