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Association of Helicobacter pylori infection with insulin resistance, tumor necrosis factor-alpha, and dyslipidemia in obese children with metabolic syndrome
Ahmed Nabil Gamil Mohammed, Walid Mohammed Aboassy, Ahmed A Elhagary, Aldosoky Abd Elaziz Alsaid, Ashraf Mohamed Alkabeer, Mahmoud M Khafagi, Abd Elmoaty Arafat Abd Elmoaty, Aya Nabil Gamil, Hager Adel Zaky, Ayat Mostafa Mohamed Ahmed, Mohamed S Hemeda, Noura M Ibrahim Elbakry
Noura M Ibrahim Elbakry, Ahmed Nabil Gamil Mohammed, Department of Pediatric, Faculty of Medicine, Minia University, Minia 2422998, Egypt
Mohamed S Hemeda, Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Port Said University, Port Said 44654, Egypt
Ayat Mostafa Mohamed Ahmed, Department of Clinical Pathology and Chemistry, Faculty of Medicine, Minia University, Minia 2422998, Egypt
Hager Adel Zaky, Department of Public Health, Faculty of Medicine, Faculty of Medicine, Minia University, Minia 2422998, Egypt
Aya Nabil Gamil, Department of Microbiology and Immunology, Minia University, Minia 45638, Egypt
Abd Elmoaty Arafat Abd Elmoaty, Mahmoud M Khafagi, Department of Hepatology and Infectious Diseases, Faculty of Medicine, Al-Azhar University, Assiut 44654, Egypt
Ashraf Mohamed Alkabeer, Aldosoky Abd Elaziz Alsaid, Ahmed A Elhagary, Department of Internal Medicine, Al-Azhar University, Assiut 2422998, Egypt
Walid Mohammed Aboassy, Pediatric Faculty of Medicine Port Said University, Port Said 42526, Egypt
Author contributions: Elbakry NMI, Hemeda MS, Aboassy WM, and Ahmed AMM conceptualized and designed the study; Elbakry NMI, Mohammed ANG, and Gamil AN recruited participants and collected the data; Ahmed AMM, Zaky HA, and Gamil AN performed the laboratory investigations and analytical procedures; Abd Elmoaty AAA, Khafagi MM, Alkabeer AM, Alsaid AAE, and Elhagary AA contributed to clinical assessment and data interpretation; Hemeda MS and Zaky HA performed the statistical analysis and critically revised the manuscript; Mohammed ANG drafted the initial manuscript; all authors reviewed the final version of the manuscript, approved it for publication, and agreed to be accountable for all aspects of the work.
Institutional review board statement: The study protocol was reviewed and approved by the Institutional Review Board of the Faculty of Medicine, Minia University (MUFMIRB) (Approval No. 92-23/6/2023; June 12, 2023).
Informed consent statement: Written informed consent was obtained from the parents or legal guardians of all participants, and assent was obtained from children whenever applicable, in accordance with the Declaration of Helsinki.
Conflict-of-interest statement: All the authors declare that they have no conflict of interest related to this study.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Data sharing statement: The datasets generated and/or analyzed during the current study are available from the corresponding author on reasonable request.
Corresponding author: Mohamed S Hemeda MD, Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Port Said University, Port Said 44654, Egypt.
mohamudsadawy@med.psu.edu.eg
Received: April 7, 2026
Revised: April 20, 2026
Accepted: May 6, 2026
Published online: September 9, 2026
Processing time: 117 Days and 14.9 Hours
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.
Core Tip: In obese children and adolescents with a metabolic syndrome phenotype, Helicobacter pylori (H. pylori) positivity was associated with higher homeostasis model assessment of insulin resistance, higher tumor necrosis factor-alpha, a more atherogenic lipid profile, elevated liver enzymes, hepatomegaly, and higher rates of elevated blood pressure. Several associations remained significant after adjustment for age, sex, and standardized body mass index value. These findings suggest that H. pylori positivity may mark a greater inflammatory and metabolic burden in high-risk pediatric obesity, while causality still requires confirmation in prospective studies.
