In inactive hepatitis B carriers, the histological activity index and NLR were found to be correlated negatively. NLR can be used as a predictor of fibrosis in combination with other noninvasive markers.

Objective: The increase in obesity in children has caused nonalcoholic fatty liver disease to become the most important chronic liver disease in the pediatric age group. In this study, we aimed to evaluate the portal diameter and blood flow velocity in obese children with fatty liver (NAFLD) and to compare them with normal healthy children. Method: 71 obese adolescent patients aged 10-18 years were divided into two groups (NAFLD group and non-NAFLD group) according to the presence of elevated transaminases and the presence of hepatosteatosis on ultrasound. 30 healthy adolescents were included in the study as the control group. Blood samples were taken from each patient for fasting glucose, insulin, transaminases, and thyroid functions. Insulin resistance was calculated using the HOMA index. Portal vein measurements were performed from the main portal vein before bifurcation. Results: The portal vein diameter (8.5 ± 0.9 mm) of the NAFLD group was statistically significantly wide compared to both the control group (7.8 ± 2.0 mm) and the non-NAFLD obese group (7.6 ± 1.1 mm) (p: 0.004) and (p: 0.002). There was no significant difference between the non-NAFLD obese group and the control group (p=0.460, p=0.214). There was no significant difference between the groups in terms of portal vein Vmax, Vmin, RI, S/D. Although there was no difference in portal vein diameter in the obese groups classified according to insulin resistance, Vmax (33.9 ± 10.3 and 28.6 ± 10.6 cm/sec, p= 0.03) and Vmin (24.8 ± 6.2 and 20.5 ± 5.5 cm/sec) were significantly different in the insulin resistance group. Conclusion: In this study, it was determined that portal vein diameter and flow velocities (Vmax and Vmin) increased in obese adolescents with NAFLD. Thus, we suggest that resistance develops in hepatic venous flow due to hepatic portal vein steatosis, especially in obese patients with insulin resistance in adolescence. This finding suggests that when fatty liver continues, portal diameter will increase in adulthood, leading to portal hypertension.