Related Experiment Video
Updated: Jul 24, 2025
Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
Effect of Helicobacter pylori Eradication on Body Weight: A Multicenter Propensity Score-matched Analysis in Korea
Jong Wook Kim1, Myong Ki Baeg2, Chang Seok Bang3
1Division of Gastroenterology, Department of Internal Medicine, Inje University Ilsan Paik Hospital, Goyang, Gyeonggi-do, Korea.
Background/Aims:
There is growing interest in whether Helicobacter pylori eradication (HPE) can affect body weight.
Methods:
Data from 5 universities between January 2013 and December 2019 were analyzed retrospectively. H. pylori-positive subjects who had body weight measurements taken at least twice at intervals of 3 months or longer were included. Using propensity score (PS)-matched data, changes in body mass index (BMI) and the lipid profile after HPE were compared with the non-HPE group.
Results:
Among 363 eligible patients, 131 HPE patients were PS-matched to 131 non-HPE patients. The median intervals between the measurements were 610 (range, 154-1250) days and 606 (range, 154-1648) days in the HPE and non-HPE groups, respectively. In both groups, the mean BMI increased (from 24.5 kg/m2 to 24.7 kg/m2 in the HPE group, and from 24.4 kg/m2 to 24.5 kg/m2 in the non-HPE group). The 2 groups did not show significantly different changes (P = 0.921). In the lowest baseline BMI quartile, the BMI increased after HPE by 1.23 (standard deviation [SD], 3.72) kg/m2 (P = 0.060), and the non-HPE group showed a decreased BMI at the time of follow-up (by -0.24 [SD, 5.25] kg/m2; P = 0.937) (between-group P = 0.214). Triglyceride levels increased after HPE (mean: 135 [SD, 78] to 153 [SD, 100] mg/dL; between-group P = 0.053).
Conclusion:
The overall BMI change was not significantly different between the HPE and non-HPE groups, but patients with low BMI showed a tendency to gain weight after HPE. Triglyceride levels increased after HPE with marginal significance.
More Related Videos
03:47Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
Published on: November 1, 2024
06:55Inverse Probability of Treatment Weighting Propensity Score using the Military Health System Data Repository and National Death Index
Published on: January 8, 2020
Related Concept Videos
01:16Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
01:26Peptic Ulcer Disease IV: Management
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
01:28Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
01:30Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...