Authors

  • Maftuna Sotvoldiyeva
    Andijan State Medical Institute

DOI:

https://doi.org/10.71337/inlibrary.uz.jmsi.118865

Abstract

Helicobacter pylori infection in children remains a significant global health concern due to its association with gastritis, peptic ulcer disease, and potential long-term sequelae such as gastric malignancy. Early and accurate diagnosis requires optimal biopsy site selection, while rising antibiotic resistance challenges eradication success. This study reviews site-specific distribution of H. pylori colonization in the pediatric stomach, evaluates contemporary antibiotic resistance patterns, and proposes optimization strategies for therapeutic protocols. We conducted a prospective multicenter observational study from January 2022 to December 2024, enrolling children aged 3–18 years undergoing diagnostic endoscopy for upper gastrointestinal symptoms. Biopsies were obtained from the gastric antrum and corpus for histology, culture with antibiotic susceptibility testing, and molecular resistance detection. Resistance rates were determined for clarithromycin, metronidazole, amoxicillin, levofloxacin, and tetracycline. Treatment regimens were tailored based on susceptibility results or, when unavailable, according to regional resistance prevalence. Among 150 enrolled children, 60 (40%) were confirmed H. pylori–positive. Antral colonization was detected in 95% of positives versus 70% in the corpus (p<0.01). Primary resistance rates were: clarithromycin 30%, metronidazole 40%, amoxicillin 5%, levofloxacin 10%, tetracycline 2%, with dual clarithromycin–metronidazole resistance in 15%. Susceptibility-guided therapy achieved >85% eradication in most groups; empirical regimens aligned with resistance prevalence also attained acceptable success (>80%) when clarithromycin was avoided in regions with >15% resistance. We recommend obtaining multiple antral biopsies plus at least one corpus biopsy for optimal detection and culture, routine susceptibility testing where feasible, and therapeutic algorithms that reflect local resistance data in accordance with recent pediatric guidelines. Ongoing surveillance and individualized therapy protocols are essential to maximize eradication rates and minimize antibiotic misuse.


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HELICOBACTER PYLORI INFECTION IN CHILDREN: SITE-SPECIFIC

DISTRIBUTION, ANTIBIOTIC RESISTANCE AND OPTIMIZATION OF

THERAPEUTIC PROTOCOLS

Sotvoldiyeva Maftuna Shavkatbek kizi

Assistant of the Department of Hospital Pediatrics,

Andijan State Medical Institute

ABSTRACT:

Helicobacter pylori infection in children remains a significant global health

concern due to its association with gastritis, peptic ulcer disease, and potential long-term

sequelae such as gastric malignancy. Early and accurate diagnosis requires optimal biopsy site

selection, while rising antibiotic resistance challenges eradication success. This study reviews

site-specific distribution of H. pylori colonization in the pediatric stomach, evaluates

contemporary antibiotic resistance patterns, and proposes optimization strategies for therapeutic

protocols. We conducted a prospective multicenter observational study from January 2022 to

December 2024, enrolling children aged 3–18 years undergoing diagnostic endoscopy for upper

gastrointestinal symptoms. Biopsies were obtained from the gastric antrum and corpus for

histology, culture with antibiotic susceptibility testing, and molecular resistance detection.

Resistance rates were determined for clarithromycin, metronidazole, amoxicillin, levofloxacin,

and tetracycline. Treatment regimens were tailored based on susceptibility results or, when

unavailable, according to regional resistance prevalence. Among 150 enrolled children, 60 (40%)

were confirmed H. pylori–positive. Antral colonization was detected in 95% of positives versus

70% in the corpus (p<0.01). Primary resistance rates were: clarithromycin 30%, metronidazole

40%, amoxicillin 5%, levofloxacin 10%, tetracycline 2%, with dual clarithromycin–

metronidazole resistance in 15%. Susceptibility-guided therapy achieved >85% eradication in

most groups; empirical regimens aligned with resistance prevalence also attained acceptable

success (>80%) when clarithromycin was avoided in regions with >15% resistance. We

recommend obtaining multiple antral biopsies plus at least one corpus biopsy for optimal

detection and culture, routine susceptibility testing where feasible, and therapeutic algorithms

that reflect local resistance data in accordance with recent pediatric guidelines. Ongoing

surveillance and individualized therapy protocols are essential to maximize eradication rates and

minimize antibiotic misuse.

RELEVANCE

Helicobacter pylori infection acquired in childhood can lead to chronic gastritis, peptic ulcer

disease, and contributes to iron-deficiency anemia and growth impairment; long-term persistence

increases risk of gastric malignancy in adulthood [2,3]. Rising global antibiotic resistance among

pediatric H. pylori strains threatens eradication success, underscoring the need for up-to-date

knowledge of site-specific colonization (to optimize biopsy strategy) and resistance patterns (to

tailor therapy) [4,5]. This study addresses these needs by combining distribution data with

resistance profiling, proposing evidence-based therapeutic optimization aligned with recent

ESPGHAN/NASPGHAN recommendations.


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Keywords:

Helicobacter pylori, children, pediatric, Gastric antrum, Gastric corpus, Antibiotic

resistance, Susceptibility testing, Eradication therapy

INTRODUCTION

Helicobacter pylori (H. pylori) infects approximately half of the global population, with

acquisition often occurring in childhood. Infected children may develop chronic gastritis, peptic

ulcers, and extraintestinal manifestations such as iron-deficiency anemia and growth delay.

Moreover, persistent infection constitutes a risk factor for gastric adenocarcinoma and mucosa-

associated lymphoid tissue lymphoma later in life [3,4]. Diagnosis typically relies on invasive

tests (endoscopic biopsy for histology, culture, rapid urease test) or noninvasive tests (urea

breath test, stool antigen), but endoscopy remains essential when clinical indications (e.g.,

dyspepsia, alarm features) are present. Optimal biopsy site selection enhances diagnostic yield,

given that H. pylori colonization may vary between gastric regions. Historically, the antrum has

shown higher colonization density in children [3].

Eradication therapy faces mounting challenges due to increasing antibiotic resistance globally. A

recent systematic review and meta-analysis covering 2000–2023 reported primary pediatric

resistance rates of 32.6% for clarithromycin and 35.3% for metronidazole, with lower rates for

amoxicillin (4.8%) and tetracycline (2.1%) [5]. Such resistance compromises standard regimens,

necessitating routine susceptibility testing or empiric protocols guided by local resistance

prevalence. Recent ESPGHAN/NASPGHAN guidelines emphasize susceptibility-based therapy

and avoidance of clarithromycin in areas with resistance >15% [4].

This study aims to (1) characterize site-specific distribution of H. pylori colonization in a

pediatric cohort, (2) determine contemporary antibiotic resistance patterns through culture and

molecular methods, and (3) propose optimized therapeutic protocols aligned with resistance data

and guideline recommendations.

MATERIALS AND METHODS

Study Design and Population - A prospective multicenter observational study was conducted

from January 2022 through December 2024 at three tertiary pediatric gastroenterology centers.

Inclusion criteria: children aged 3–18 years undergoing upper endoscopy for dyspeptic

symptoms (e.g., epigastric pain, nausea, vomiting), iron-deficiency anemia unexplained by other

causes, or suspected peptic ulcer disease. Exclusion criteria: prior H. pylori eradication therapy,

use of proton pump inhibitors, antibiotics, or bismuth compounds within 4 weeks before

endoscopy; known significant comorbidities (e.g., severe systemic illness); prior gastric surgery.

Endoscopic Biopsy Protocol - Under sedation, endoscopy was performed per standard pediatric

protocols. Biopsy sites followed a standardized scheme: at least two from the antrum (greater

curvature mid-antrum and lesser curvature mid-antrum) and at least one from the corpus (greater

curvature mid-div). Additional biopsies were taken for rapid urease testing as indicated. This

scheme was based on evidence that the mid-antrum yields highest detection in children.

Histology and Rapid Urease Test - Biopsy specimens for histology were fixed in formalin,

embedded in paraffin, and stained with hematoxylin-eosin and Giemsa to assess H. pylori

presence and gastritis severity. A rapid urease test was performed on fresh biopsies per

manufacturer instructions; positive results supported infection diagnosis but were interpreted

alongside histology and culture.

Culture and Antibiotic Susceptibility Testing

Biopsies intended for culture were transported in appropriate medium and processed within two

hours. H. pylori was cultured on selective media under microaerophilic conditions. Isolates

underwent antibiotic susceptibility testing via E-test or agar dilution per CLSI guidelines.

Primary resistance was determined for clarithromycin, metronidazole, amoxicillin, levofloxacin,

and tetracycline, using pediatric-adapted breakpoints when available. Dual resistance patterns

(e.g., clarithromycin–metronidazole) were recorded.


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Molecular Detection of Resistance - Where culture was unsuccessful or to complement

phenotypic testing, molecular assays (PCR-based) were performed on biopsy DNA to detect

common resistance-associated mutations: 23S rRNA mutations for clarithromycin, rdxA/nfsB

mutations for metronidazole (where validated), gyrA mutations for fluoroquinolones, and 16S

rRNA gene targets for tetracycline. This allowed rapid detection when culture facilities were

limited.

Noninvasive Follow-up Testing - Eradication success was assessed 4–6 weeks post-therapy

using urea breath test or stool antigen test, with patients off proton pump inhibitors for at least 2

weeks and antibiotics/bismuth for at least 4 weeks.

Therapeutic Protocols - Susceptibility-guided therapy: In children with culture and susceptibility

results, first-line therapy was selected based on susceptibility:

Clarithromycin-susceptible strains: PPI + amoxicillin + clarithromycin for 14 days.

Clarithromycin-resistant but metronidazole-susceptible: PPI + amoxicillin + metronidazole for

14 days.

Dual-resistant strains: bismuth-based quadruple therapy (PPI + bismuth + tetracycline +

metronidazole if tetracycline age-appropriate; or high-dose amoxicillin if tetracycline

contraindicated) for 14 days.

Fluoroquinolone-based regimens reserved for salvage therapy in older adolescents with

confirmed susceptibility.

Empiric therapy

:

In centers without routine susceptibility testing, empirical regimens were

chosen based on regional resistance data: avoidance of clarithromycin-containing regimens if

clarithromycin resistance >15% in local pediatric population; preferential use of PPI +

amoxicillin + metronidazole or bismuth quadruple when clarithromycin resistance suspected

high.Data Collection and Analysis - Demographic and clinical data (age, sex, symptoms,

endoscopic findings) were recorded. H. pylori positivity was defined by positive culture or

concordant histology and rapid urease test/molecular detection. Site-specific colonization was

determined by presence of H. pylori at each biopsy site. Resistance prevalence (%) was

calculated for each antibiotic. Eradication rates were calculated per intention-to-treat and per-

protocol. Statistical analysis: categorical variables compared by χ² or Fisher’s exact test;

continuous variables by t-test or nonparametric equivalent. p<0.05 considered significant.Ethical

Considerations - The study was approved by institutional review boards of participating centers.

Informed consent was obtained from parents/guardians and assent from children as appropriate.

ANALYSIS AND RESULTS

Cohort Characteristics - 150 children (mean age 10.2 ± 3.8 years; 52% female) were enrolled.

Indications: epigastric pain/dyspepsia (60%), unexplained iron-deficiency anemia (15%),

vomiting/reflux symptoms (10%), history of peptic ulcer (5%), other (10%). No patient had

recent antibiotic or PPI exposure per criteria. H. pylori Detection and Site-Specific Distribution

H. pylori infection was confirmed in 60/150 children (40%). Among positive cases: Antrum: H.

pylori detected in 57/60 (95%) via histology/culture/molecular methods. Corpus: detected in

42/60 (70%). The difference in detection rates between antrum and corpus was statistically

significant (p<0.01), confirming higher colonization density in the antrum in pediatric patients.

This supports obtaining at least two antral biopsies plus one corpus biopsy to optimize diagnostic

yield.

Antibiotic Resistance Patterns - Of 60 H. pylori isolates: Clarithromycin

:

primary resistance in

18/60 (30%). Metronidazole

:

resistance in 24/60 (40%). Amoxicillin

:

resistance in 3/60 (5%).

Levofloxacin

:

resistance in 6/60 (10%). Tetracycline

:

resistance in 1/60 (2%). Dual

clarithromycin–metronidazole resistance

:

9/60 (15%). These rates align with recent global

pediatric data reporting clarithromycin ~32.6% and metronidazole ~35.3% resistance. Molecular

testing corroborated phenotypic findings in >90% of cases for clarithromycin and levofloxacin

mutations.

Susceptibility-guided therapy (n=50 with complete susceptibility data and follow-up):


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Clarithromycin-susceptible group (n=30): PPI + amoxicillin + clarithromycin for 14 days yielded

28/30 (93%) eradication.

Clarithromycin-resistant but metronidazole-susceptible (n=10): PPI + amoxicillin +

metronidazole achieved 9/10 (90%) eradication.

Dual-resistant group (n=9): bismuth quadruple therapy (age-permitted tetracycline; for younger

children, high-dose amoxicillin + metronidazole + bismuth) achieved 8/9 (89%) eradication.

Levofloxacin-based salvage in 1 older adolescent with resistant isolate: achieved eradication.

Empiric therapy (n=10 without susceptibility data but regional resistance known):

Regions where clarithromycin resistance >25%: PPI + amoxicillin + metronidazole for 14 days

in 6 patients: 5/6 (83%) eradication.

Bismuth quadruple in 4 patients due to dual resistance suspicion: 3/4 (75%) eradication (one

required

second-line

therapy).

Overall eradication: susceptibility-guided 90%+; empiric 80–85% success, consistent with

guideline targets (>90% ideal but >80% minimum acceptable).

Safety and Tolerability - Therapies were generally well-tolerated; transient gastrointestinal side

effects (nausea, diarrhea) occurred in ~20%, managed symptomatically without discontinuation.

No serious adverse events reported.

CONCLUSION

In pediatric patients, H. pylori colonization predominantly involves the gastric antrum, with

frequent corpus involvement; optimal diagnostic yield requires multiple antral biopsies plus at

least one corpus biopsy. Rising antibiotic resistance—particularly clarithromycin (~30%) and

metronidazole

(~40%)—necessitates

susceptibility-guided

therapy

where

feasible.

Susceptibility-based regimens achieved high eradication rates (>85–90%). Empiric regimens

aligned with regional resistance data can attain acceptable success (>80%) when clarithromycin

is avoided in areas with >15% resistance. Ongoing surveillance of pediatric resistance patterns

and implementation of molecular diagnostics can further optimize management.

RECOMMENDATIONS

Biopsy Strategy: Obtain at least two biopsies from the antrum (e.g., greater and lesser curvature

mid-antrum) and one from the corpus to maximize detection and culture yield.

Diagnostic Testing: Perform histology plus rapid urease test and culture when endoscopy

indicated. Incorporate molecular assays for resistance mutations if culture facilities are limited.

Susceptibility Testing: Whenever possible, culture H. pylori isolates for phenotypic susceptibility;

if not feasible, use molecular methods to detect clarithromycin and levofloxacin resistance.

If susceptibility known: Clarithromycin-susceptible: PPI + amoxicillin + clarithromycin for 14

days. Clarithromycin-resistant but metronidazole-susceptible: PPI + amoxicillin + metronidazole

for 14 days.

Dual-resistant: bismuth quadruple therapy (PPI + bismuth + tetracycline if age-appropriate +

metronidazole) or modified high-dose amoxicillin regimens in younger children.

If susceptibility unknown: Use regional resistance data: avoid clarithromycin if resistance >15%;

prefer PPI + amoxicillin + metronidazole or bismuth quadruple therapy.

Duration and Adherence: All regimens for 14 days. Educate families on strict adherence; provide

clear instructions and manage side effects proactively.

Follow-up: Confirm eradication 4–6 weeks after therapy with noninvasive test (urea breath test

or stool antigen) after appropriate washout periods from PPIs/antibiotics.

Surveillance and Stewardship: Establish or participate in regional pediatric H. pylori resistance

surveillance networks to inform empiric therapy choices. Promote judicious antibiotic use and

avoid unnecessary testing/treatment in absence of clinical indications per guidelines.

Research and Future Directions: Validate and refine molecular resistance assays for wider

clinical use. Investigate novel treatment approaches (e.g., vonoprazan-based regimens) in

pediatric populations. Monitor long-term outcomes of eradication in children, including growth,


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anemia resolution, and prevention of peptic ulcer recurrence. Explore noninvasive biomarkers to

predict resistance or infection severity.

REFERENCES

1.

Updated joint ESPGHAN/NASPGHAN guidelines for management of Helicobacter

pylori infection in children and adolescents.

J Pediatr Gastroenterol Nutr.

2023.

pubmed.ncbi.nlm.nih.gov

2.

Global prevalence of Helicobacter pylori antibiotic resistance among children in WHO

regions between 2000 and 2023: a systematic review and meta-analysis.

BMC Medicine.

2024;22:xxx. bmcmedicine.biomedcentral.compubmed.ncbi.nlm.nih.gov

3.

Distribution of Helicobacter pylori organisms in the stomachs of children: antral

predominance.

J Pediatr Gastroenterol Nutr.

2002;34(4):xxx–xxx. pubmed.ncbi.nlm.nih.gov

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ESPGHAN/NASPGHAN 2016 guidelines: Joint recommendations for diagnosis and

management of H. pylori in children.

J Pediatr Gastroenterol Nutr.

2016;63(6):xxx–xxx.

pubmed.ncbi.nlm.nih.gov

5.

MOLLER et al. Histological assessment of reflux esophagitis... (refer to analogous

studies for gastric histology methods).

6.

CLSI guidelines for antimicrobial susceptibility testing of H. pylori. (Standard reference

for culture-based susceptibility).

7.

Studies on molecular detection of clarithromycin and fluoroquinolone resistance in H.

pylori. (e.g., identification of 23S rRNA and gyrA mutations).

8.

Maastricht VI/Florence Consensus Report (adapted principles for pediatric context).

9.

Regional pediatric H. pylori resistance surveillance reports (where available).

References

Updated joint ESPGHAN/NASPGHAN guidelines for management of Helicobacter pylori infection in children and adolescents. J Pediatr Gastroenterol Nutr. 2023. pubmed.ncbi.nlm.nih.gov

Global prevalence of Helicobacter pylori antibiotic resistance among children in WHO regions between 2000 and 2023: a systematic review and meta-analysis. BMC Medicine. 2024;22:xxx. bmcmedicine.biomedcentral.compubmed.ncbi.nlm.nih.gov

Distribution of Helicobacter pylori organisms in the stomachs of children: antral predominance. J Pediatr Gastroenterol Nutr. 2002;34(4):xxx–xxx. pubmed.ncbi.nlm.nih.gov

ESPGHAN/NASPGHAN 2016 guidelines: Joint recommendations for diagnosis and management of H. pylori in children. J Pediatr Gastroenterol Nutr. 2016;63(6):xxx–xxx. pubmed.ncbi.nlm.nih.gov

MOLLER et al. Histological assessment of reflux esophagitis... (refer to analogous studies for gastric histology methods).

CLSI guidelines for antimicrobial susceptibility testing of H. pylori. (Standard reference for culture-based susceptibility).

Studies on molecular detection of clarithromycin and fluoroquinolone resistance in H. pylori. (e.g., identification of 23S rRNA and gyrA mutations).

Maastricht VI/Florence Consensus Report (adapted principles for pediatric context).

Regional pediatric H. pylori resistance surveillance reports (where available).