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Published on: April 3, 2017
Immune phenotype and serum leptin in children with obesity-related liver disease
Raffaele Iorio1, Angela Sepe, Antonietta Giannattasio
1Department of Pediatrics, University of Naples Federico II, 80131 Naples, Italy. riorio@unina.it
Insights
Obesity-related liver disease in children is linked to higher natural killer (NK) and B cell counts, and IgA levels. Leptin did not correlate with liver disease severity or related markers in these obese children.
Area of Science:
- Pediatric Endocrinology
- Hepatology
- Immunology
Background:
- Pathogenesis of pediatric obesity-related liver disease remains poorly understood.
- Limited data exists on leptin, immune parameters, and liver disease in obese children.
Purpose of the Study:
- To investigate immune cell phenotypes and serum leptin levels in obese children.
- To compare these parameters between children with and without obesity-related liver disease.
Main Methods:
- Two groups of obese children were studied: those with obesity-related liver disease and those with isolated obesity.
- Evaluated serum leptin, immunoglobulins, and peripheral T, B, and natural killer (NK) cells.
Main Results:
- Serum leptin levels were elevated in both groups but showed no significant difference.
- No correlation was found between leptin and aminotransferases, lipids, or lymphocyte subsets.
- Children with obesity-related liver disease had significantly higher peripheral NK and B cell counts and IgA levels compared to controls.
Conclusions:
- Leptin levels did not correlate with hepatic steatosis, aminotransferases, or serum lipids in obese children.
- Elevated peripheral NK and B cells and IgA levels are associated with obesity-related liver disease in children.
- Further research is needed to elucidate the role of these immune findings in disease pathogenesis.
Context:
Little is known about pathogenesis of obesity-related liver disease in childhood. Data on the relationship among leptin, immunological parameters, and liver disease in obese children are lacking.
Objective:
Thus, the objective of this study was to evaluate immune phenotype and leptin serum levels in obese children with and without obesity-related liver disease.
Design:
The study was performed in two groups of consecutive obese children: the first formed by children with obesity-related liver disease, diagnosed in the presence of chronic hypertransaminasemia, liver steatosis at ultrasound, and absence of known etiologies; the second composed of children with isolated obesity. In all patients serum leptin, immunoglobulins, peripheral T, B, and natural killer (NK) cells were evaluated.
Results:
Twenty-three children in the first group and 16 children in the second were considered eligible. Serum leptin was increased in both groups but without any significant difference. No significant correlation was found between leptin and aminotransferases, lipid serum levels, and all tested lymphocyte subpopulations. Patients with obesity-related liver disease showed significantly higher peripheral NK and B cell counts and IgA levels than children with isolated obesity. Furthermore, no correlation was found between severity of liver disease and lymphocyte subpopulations.
Conclusion:
In our study, leptin did not correlate with hepatic steatosis, aminotransferases, and serum lipids. Children with obesity-related liver disease showed significantly higher peripheral NK and B cells and IgA levels. Additional studies are required to define the pathogenetic role of these immunological findings.
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