Among our overweight/obese children presenting with hepatomegaly and/or raised ALT, 60% met three or more criteria for MS; 76% of them were obese. Many authors reported the prevalence of MS among obese adolescents to be between 12.4 and 54.2%,[5
] reaching approximately 50% in some populations.[23
] The higher prevalence of MS among our studied group may be explained by the fact that our obese/overweight patients were presenting with at least one hepatic abnormality (clinical hepatomegaly and/or raised ALT). This fact also accounts for the higher percentage of hypertriglyceridemia (81%) seen in our studied patients, in comparison to 26% in obese children as reported by Cruz et al
] Our selection criteria necessitated the presence of at least one hepatic abnormality to justify performing a liver biopsy for the patients.
In the present study, we graded according to the scoring system for NAFLD.[13
] No special criteria were used that distinguish children from adults. The prevalence of MS in children with biopsy-proven NAFLD in the present study was 80%. A high prevalence of risk factors for the MS in patients with NAFLD has been previously described.[24
] Goessling et al
] found that increased ALT was associated with developing MS over 20 years of follow-up. In the present study, almost half of children with NAFLD had increased ALT levels. Our patients with NAFLD had significantly higher ALT as compared to those with normal liver histology (mean ALT 43 ± 6 vs. 28 ± 7; P
Obesity is strictly related to the development of NAFLD. In the present study, 45% of obese/overweight patients had biopsy-proven NAFLD which is similar to values observed by other authors,[29
] but lower than Chan and colleagues who found it in 77% of their studied population.[31
] This difference may be explained by genetic and/or environmental factors, similar to what has been hypothesized for adults.[32
] Moreover, it is to be noted that 100% of our patients with NAFLD were obese. Thus, NAFLD is invariably associated with obesity and not simply overweight, although these results need to be verified and reproduced on a larger number of studied children.
In the present study, 100% of children with NAFLD had an elevated WC. WC is a surrogate marker for visceral fat, and visceral fat appears tightly correlated with hepatic TG content, elevated ALT, liver inflammation, and fibrosis.[34
] In a pediatric study,[37
] every 1 cm increase in WC was associated with a 1.97-fold increased risk of NAFLD in boys and a 2.08-fold increased risk in girls.
In the present study, fasting serum insulin was significantly higher in patients with NAFLD in the present study. IR leads to increased lipolysis and free fatty acid output. The influx of free fatty acid into the liver combined with alternations of the fat metabolism in the liver result in accumulation of TG within the hepatocytes.[38
] Hepatic steatosis alone can have a benign course without histological progression to fibrosis. IR is involved in the development of not only steatosis but also fibrosis by increasing fatty acid β-oxidation and oxidative stress.[40
In the present study, 73% of our NAFLD patients had IR. The high rates of obese, insulin-resistant children with NAFLD meeting the criteria for MS suggest that a large number of these children will go on to develop diabetes.[41
] This belief is supported by a cohort study from Sweden of adults with biopsy-proven NAFLD who had a 9% prevalence of diabetes at baseline. After nearly 14 years of follow-up, the majority (78%) of these patients developed impaired glucose tolerance or diabetes.[42
The study limitation is the lack of data about liver histology from obese/overweight children who do not have hepatic abnormalities (lacking hepatomegaly and having normal ALT). The authors considered obtaining liver biopsy in obese children with no evidence of hepatic abnormalities unjustifiable.
Another limitation is the choice of raised ALT as an inclusion criterion. Among the seven cases with raised ALT, six had histologically proven NAFLD. However, raised ALT in one patient with normal liver biopsy may point to a patchy distribution of fatty infiltration in early NAFLD.
Abdominal ultrasonography showed an increased echogenicity: Grade I in 11 cases with normal liver histology and grade II in another 6 cases with normal liver histology. This may point to the lack of specificity of grades I and II echogenicity of abdominal ultrasound in detecting hepatic steatosis.