Association of Helicobacter pylori infection with insulin resistance, tumor necrosis factor-alpha, and dyslipidemia in obese children with metabolic syndrome.
In 70 children and adolescents with obesity and a metabolic-syndrome phenotype, H. pylori stool-antigen positivity was associated with greater insulin resistance, elevated TNF-α, adverse lipid measures, and greater hepatic and clinical metabolic burden.
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In 70 children and adolescents with obesity and a metabolic-syndrome phenotype, H. pylori stool-antigen positivity was associated with greater insulin resistance, elevated TNF-α, adverse lipid measures, and greater hepatic and clinical metabolic burden.
Research significance
The evidence supports an association between H. pylori positivity and worse pediatric metabolic parameters; it is only an inference—not tested here—that diagnosing or eradicating H. pylori could improve insulin resistance, inflammation, or dyslipidemia, and no pediatric-oncology therapeutic effect is demonstrated.
Source abstract
BACKGROUND: Previous studies have suggested a link between Helicobacter pylori (H. pylori) and metabolic complications outside the gastrointestinal tract, but the relationship with pediatric obesity remains unclear. We aim to study the correlation between H. pylori infection and components of insulin resistance (IR), inflammation [tumor necrosis factor-alpha (TNF-α)], and cardiometabolic parameters in obese children/adolescents with a metabolic syndrome (MetS) phenotype. AIM: To elucidate the association between H. pylori infection and metabolic disturbances in children with obesity and MetS, focusing on homeostasis model assessment of IR (HOMA-IR), inflammatory markers (TNF-α), and the lipid profile. METHODS: The study recruited 70 obese children/adolescents with MetS phenotype from the pediatric units of Minia University Hospital from September 2023 to October 2024. H. pylori stool antigen quantitative enzyme-linked immunosorbent assay was used to classify participants into H. pylori-negative (n = 35) and H. pylori-positive (n = 35). Assessment of fasting glucose, glycated hemoglobin (HbA1c), fasting insulin, lipid profile, liver enzymes, TNF-α, adiponectin, and leptin, as well as other parameters, was done. IR was calculated in detail using the HOMA-IR formula (fasting insulin × fasting glucose/405). Various statistical analyses, including intergroup comparisons, correlation analyses, and receiver operating characteristic curve analyses, were also performed. RESULTS: Groups were similar in age, sex, and standardized body mass index (BMI) value. Elevated blood pressure (65.7% vs 31.4%, P = 0.004) and hepatomegaly (62.9% vs 28.6%, P = 0.004) were more common in H. pylori-positive participants. The infected group had higher alanine aminotransferase and aspartate aminotransferase (AST) levels (both P < 0.001). It had higher triglycerides and low-density lipoprotein cholesterol and lower high-density lipoprotein cholesterol (HDL) levels, indicating a more unfavorable lipid profile (all P < 0.001) and more impaired glycemic/IR indices: Fasting glucose (158.5 ± 40.1 mg/dL vs 109.5 ± 22.7 mg/dL, P < 0.001), HbA1c (8.5 ± 2.2 vs 7.4 ± 1.7, P = 0.019), fasting insulin (9.4 ± 3.6 μIU/mL vs 3.9 ± 1.0 μIU/mL, P < 0.001), and HOMA-IR (3.61 ± 1.45 vs 1.06 ± 0.36, P < 0.001). TNF-α was elevated in the infected group (median 7.13 vs 6.23, P = 0.011). In H. pylori-positive participants, HOMA-IR had a strong positive correlation with standardized BMI value (r = 0.889, P < 0.001) and TNF-α (r = 0.896, P < 0.001). HOMA-IR > 1.67 had excellent sensitivity and specificity for detecting H. pylori positivity [area under the curve (AUC): 0.954; sensitivity 88.6%, specificity 97.1%], and TNF-α had moderate sensitivity (AUC: 0.677). CONCLUSION: H. pylori positivity was linked to elevated IR, TNF-α, atherogenic dyslipidemia, and a greater hepatic/clinical metabolic burden in the MetS phenotype of obesity in children and adolescents. More longitudinal studies that will help control socioeconomic and lifestyle confounding are warranted.