Letter: hereditary role in non‐alcoholic fatty liver disease – authors' reply

We thank Dr Chang and Dr Gau for their interest in our study.1,2 We agree with them on the potential influence of nonalcoholic fatty liver disease (NAFLD)risk associated comorbidities, such as inflammatory diseases and diabetes mellitus (DM), in our analysis. When children's DM was defined according to the American Diabetes Association (fasting glucose ≥126 mg/dl or haemoglobin A1c ≥ 6.5),3 the overall prevalence of children's DM was 0.4% (n = 9). The prevalence of DM was higher in children with parental NAFLD than in those without parental NAFLD (0.6% vs. 0.2%, p = 0.034), and higher in children with NAFLD than in those without NAFLD (4.2% vs. 0.1%, p < 0.001). Unfortunately, the Korean National Health and Nutrition Examination Surveys (KNHANES) do not have any information about psoriasis and inflammatory bowel diseases. In the original analysis, we used children's fasting serum glucose levels (<100 vs. ≥100 mg/ dl) for adjustment. When we used children's DM for adjustment instead of children's fasting serum glucose levels, the overall findings were virtually the same (Table 1). Concerning body mass index (BMI), we used children's BMI for adjustment in the original analysis. The BMI of parents was higher in children with parental NAFLD than without parental NAFLD [26.5 (24.6– 28.3) vs. 23.3 (21.9– 24.8), p < 0.001, for fathers, and 23.9 (21.6– 27.0) vs. 22.1 (20.6– 23.8), p < 0.001, for mothers, respectively]. In a model further adjusted by parental BMI, the overall findings were also similar (Table 1). In addition to children's DM and parental BMI, residual confounders may exist and mediate the observed association between parental NAFLD and children's NAFLD. Hence, further studies are required to see whether NAFLD should be screened for children if they have a family history of NAFLD. Nevertheless, at the present, close attention is warranted for the children's NAFLD when a parent has NAFLD.