Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as the most common chronic liver condition in children and adolescents, particularly in association with the global epidemic of pediatric obesity [1]. NAFLD encompasses a spectrum of liver abnormalities ranging from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, and cirrhosis [2]. Pediatric NAFLD is of particular concern, as affected children are at increased risk for progression to advanced liver disease in adulthood and for developing metabolic complications such as type 2 diabetes and cardiovascular disease [3,4].

The prevalence of NAFLD in the general pediatric population is estimated to be between 3% and 10%, but this increases significantly to 40–70% in obese children [5,6]. In India, the rising prevalence of childhood obesity due to urbanization, sedentary lifestyles, and dietary changes has been accompanied by a surge in NAFLD cases [7].

Screening for NAFLD in children is challenging, as the condition is often asymptomatic. Ultrasonography remains the most widely used, non-invasive imaging modality for diagnosis, despite its limitations compared with histology [8]. Several anthropometric (BMI, waist circumference, waist-to-hip ratio) and biochemical parameters (ALT, triglycerides, insulin resistance) have been investigated as potential predictors of NAFLD in children [9–11].

The present study was undertaken to determine the prevalence of NAFLD among obese pediatric patients attending a tertiary care center in Karnataka and to identify significant clinical, anthropometric, and biochemical predictors associated with NAFLD in this population.

MATERIALS AND METHODS

Study Design and Setting

This was a hospital-based, observational case–control study conducted in the Department of Pediatrics, Yadgir Institute of Medical Sciences, Yadgir, Karnataka, from April 1, 2025, to August 31, 2025. The institute is a tertiary care referral center catering to both urban and rural pediatric populations.

Study Population

A total of 50 obese children, aged 6–18 years, were enrolled. Participants were divided into two groups:

• Cases (n = 25): Obese children with ultrasonographic evidence of non-alcoholic fatty liver disease (NAFLD).
• Controls (n = 25): Age- and sex-matched obese children without NAFLD on ultrasonography.

The sample size was determined based on feasibility within the study period and was consistent with comparable pediatric NAFLD studies.

Inclusion Criteria

• Children between 6–18 years.
• Obesity defined as BMI ≥ 95th percentile for age and sex as per WHO growth reference charts.
• Informed consent from parents/guardians and assent from children above 7 years.

Exclusion Criteria

• Children with chronic liver diseases (e.g., viral hepatitis, Wilson’s disease, autoimmune hepatitis).
• History of alcohol consumption or hepatotoxic drug intake.
• Systemic/metabolic disorders known to affect liver function.

Data Collection

A structured proforma was used to collect demographic details, medical history, dietary and physical activity patterns, and family history of metabolic disorders. Physical examination included measurement of weight, height, BMI, waist circumference, hip circumference, waist-to-hip ratio, and blood pressure using standard pediatric protocols.

Laboratory Investigations

After overnight fasting, venous blood samples were collected. The following parameters were analyzed:

• Liver function tests (LFTs): ALT, AST, ALP, total and direct bilirubin, serum albumin.
• Fasting lipid profile: Total cholesterol, triglycerides, HDL-C, LDL-C.
• Glycemic profile: Fasting blood glucose and fasting insulin; insulin resistance assessed using the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR).

Radiological Evaluation

All participants underwent abdominal ultrasonography performed by a single experienced radiologist blinded to clinical and laboratory details. NAFLD was diagnosed based on increased hepatic echogenicity relative to the renal cortex and impaired visualization of intrahepatic vessels. The severity was graded according to standard sonographic criteria (Grade I–III).

Outcome Measures

• Primary outcome: Prevalence of NAFLD in obese pediatric patients.
• Secondary outcomes: Clinical, anthropometric, and biochemical predictors associated with NAFLD.

Statistical Analysis

Data were entered in Microsoft Excel and analyzed using IBM SPSS Statistics for Windows, Version 25.0 (Armonk, NY: IBM Corp.). Continuous variables were expressed as mean ± standard deviation (SD) or median (interquartile range, IQR) depending on distribution. Categorical variables were summarized as frequencies and percentages. Comparisons between cases and controls were made using the Independent sample t-test or Mann–Whitney U test for continuous variables, and the Chi-square test/Fisher’s exact test for categorical variables. Binary logistic regression analysis was performed to identify independent predictors of NAFLD. A p-value <0.05 was considered statistically significant.

RESULTS AND OBSERVATIONS

Prevalence of NAFLD

Among 50 obese children screened, 25 (50%) had ultrasonographic evidence of NAFLD.

Table 1: Age and Sex Distribution of Study Population

Table 2: Anthropometric Parameters

*Significant at p < 0.05

Table 3: Laboratory Parameters

Figure;1 Laboratory Parameters

Table 4: Distribution of NAFLD Grades (Ultrasonography)

Table 5: Metabolic Syndrome Components in Study Groups

Table 6: Correlation of Anthropometric and Biochemical Parameters with NAFLD Severity

Table 7: Predictors of NAFLD (Binary Logistic Regression)

Figure 2 Predictors of NAFLD (Binary Logistic Regression)

DISCUSSION

In the present study, the prevalence of NAFLD among obese children was found to be 50%, which is consistent with reports from both Indian and international studies that document prevalence rates of 40–70% among obese pediatric populations [5,6,12]. This underscores the importance of early screening for NAFLD in all obese children, particularly in high-risk populations.

Anthropometric predictors: Our study demonstrated that BMI, waist circumference, waist-to-hip ratio, and systolic blood pressure were significantly higher in children with NAFLD compared to controls. Waist-to-hip ratio ≥0.9 emerged as a strong independent predictor of NAFLD, in line with studies emphasizing the role of central obesity as a key determinant of hepatic fat accumulation [9,13].

Biochemical predictors: Children with NAFLD had significantly elevated ALT and AST levels, higher triglycerides, and lower HDL-C compared to controls. ALT >40 U/L was the strongest independent biochemical predictor, consistent with findings by Patton et al. and Nobili et al., who highlighted ALT as a surrogate marker of steatosis and inflammation in pediatric NAFLD [10,14]. Additionally, HOMA-IR ≥4.0 was significantly associated with NAFLD, supporting the central role of insulin resistance in its pathogenesis [11,15].

Severity correlation: Among NAFLD cases, most (56%) had Grade I disease on ultrasonography, while only 12% had Grade III. ALT, waist circumference, triglycerides, and HOMA-IR showed positive correlations with NAFLD severity. These results align with reports by Schwimmer et al. and Lin et al., who described progressive metabolic derangements with worsening grades of NAFLD [12,16].

Metabolic syndrome: NAFLD cases had a higher prevalence of metabolic syndrome components, particularly central obesity, hypertriglyceridemia, and low HDL-C, consistent with the clustering of metabolic risk factors in pediatric NAFLD [17].

Strengths and limitations: A strength of this study is the case–control design with age- and sex-matched groups, allowing clear comparison of predictors. However, limitations include the relatively small sample size, the hospital-based nature of the study which may limit generalizability, and the use of ultrasonography instead of liver biopsy, which remains the gold standard.

Clinical implications: The findings highlight the importance of simple, non-invasive markers—BMI, waist-to-hip ratio, ALT, triglycerides, and HOMA-IR—for identifying obese children at risk for NAFLD. Early screening and lifestyle interventions targeting obesity and metabolic risk factors are crucial to prevent progression to advanced liver disease.

CONCLUSION

The present case–control study conducted at Yadgir Institute of Medical Sciences demonstrated a high prevalence of non-alcoholic fatty liver disease among obese pediatric patients, with obesity, central adiposity, and metabolic abnormalities emerging as significant predictors. Ultrasonography proved to be a reliable, non-invasive diagnostic tool for identifying NAFLD in this age group. The findings highlight the urgent need for early screening and risk stratification in obese children to prevent progression to advanced liver disease in adulthood. Implementation of preventive strategies, including lifestyle modification, dietary counseling, and regular follow-up, is critical for reducing the long-term burden of NAFLD.

REFERENCES

1. Schwimmer JB, Deutsch R, Kahen T, Lavine JE, Stanley C, Behling C. Prevalence of fatty liver in children and adolescents. Pediatrics. 2006;118(4):1388-1393.
2. Vos MB, Abrams SH, Barlow SE, et al. NASPGHAN Clinical Practice Guideline for the diagnosis and treatment of NAFLD in children. J Pediatr Gastroenterol Nutr. 2017;64(2):319-334.
3. Anderson EL, Howe LD, Jones HE, et al. The prevalence of NAFLD in children and adolescents: A systematic review and meta-analysis. PLoS One. 2015;10(10):e0140908.
4. Della Corte C, Mosca A, Vania A, Alterio A, Alisi A, Nobili V. Pediatric NAFLD: Current perspectives. Clin Res Hepatol Gastroenterol. 2014;38(4):407-415.
5. Molleston JP, Schwimmer JB, Yates KP, et al. Histological abnormalities in children with NAFLD. J Hepatol. 2014;60(3):505-512.
6. Nobili V, Alkhouri N, Alisi A, et al. Nonalcoholic fatty liver disease: A challenge for pediatricians. JAMA Pediatr. 2015;169(2):170-176.
7. Kelishadi R, Cook SR, Amra B, Adibi A. Factors associated with fatty liver in children and adolescents: A population-based study. Arch Dis Child. 2009;94(9):722-726.
8. Pacifico L, Martino MD, Catalano C, et al. T1-weighted dual-echo MRI in detecting fatty infiltration of the liver in obese children. Radiology. 2007;242(2):440-447.
9. Lin YC, Chang PF, Hu FC, et al. Waist circumference and BMI in predicting NAFLD in obese children. Obesity (Silver Spring). 2013;21(3):544-551.
10. Patton HM, Lavine JE, Van Natta ML, Schwimmer JB, Kleiner D, Molleston J. Clinical correlates of histopathology in pediatric NAFLD. Gastroenterology. 2008;135(6):1961-1971.
11. Nobili V, Marcellini M, Devito R, et al. NAFLD and metabolic syndrome in obese children. J Hepatol. 2006;44(2):253-259.
12. Schwimmer JB, Pardee PE, Lavine JE, Blumkin AK, Cook S. Cardiovascular risk factors and the metabolic syndrome in pediatric NAFLD. Circulation. 2008;118(3):277-283.
13. Alisi A, Feldstein AE, Villani A, Raponi M, Nobili V. Pediatric NAFLD: A multidisciplinary approach. Nat Rev Gastroenterol Hepatol. 2012;9(3):152-161.
14. Loomba R, Sirlin CB, Schwimmer JB, Lavine JE. Advances in pediatric NAFLD. Hepatology. 2009;50(4):1282-1293.
15. Manco M, Marcellini M, Devito R, et al. Metabolic syndrome and liver histology in pediatric NAFLD. Int J Obes. 2008;32(2):381-387.
16. Lin HZ, Yang SQ, Chuckaree C, Kuhajda F, Ronnet G, Diehl AM. Metformin reverses fatty liver disease in obese, leptin-deficient mice. Nat Med. 2000;6(9):998-1003.
17. Schwimmer JB, Ugalde-Nicalo P, Welsh JA, et al. Effect of a low free sugar diet vs usual diet on NAFLD in adolescent boys. JAMA. 2019;321(3):256-265.