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Clarithromycin Resistance and Treatment Outcomes in <i>Helicobacter pylori</i> Infections: Molecular Genetic Study From Uzbekistan

J. A. IsmailovaRepublican Specialized Scientific and Practical Center for Therapy and Medical Rehabilitation , Tashkent , UzbekistanAbrorjon YusupbekovRepublican Specialized Scientific and Practical Center of Oncology and Radiology , Tashkent , UzbekistanAbrorjon AbdurakhimovCenter for Advanced Technologies , Tashkent , UzbekistanKhojiakbar NazarovRepublican Specialized Scientific and Practical Center for Therapy and Medical Rehabilitation , Tashkent , Uzbekistan
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Background Antibiotic resistance of Helicobacter pylori ( H. pylori ), especially to clarithromycin, is a major cause of eradication failure worldwide. Data on the molecular mechanisms of clarithromycin resistance and their clinical impact in Central Asia remain limited. Methods This prospective study included 194 patients with H. pylori ‐associated gastrointestinal diseases, with a positive pathogenic status of CagA, in Uzbekistan. Clarithromycin resistance was assessed using multiplex PCR targeting mutations in the 23S rRNA gene (A2142 G/C and A2143G). Patients received first‐ or second‐line eradication therapy depending on their clarithromycin resistance status. The efficacy of eradication therapy was assessed 4–6 weeks after completion of treatment using real‐time PCR targeting the ureC gene, which allowed for objective confirmation of the presence or absence of H. pylori infection. Relative risk (RR), odds ratio (OR), and 95% confidence intervals (CIs) were calculated. Results Clarithromycin resistance was detected in 41.2% of isolates and was significantly associated with disease severity, reaching 65.2% in patients with gastric cancer (OR 6.5; 95% CI 1.9–24.7; p &lt; 0.001). First‐line therapy based on clarithromycin ensured eradication of 93.8% of nonresistant strains but was ineffective in 6.2% of cases. Second‐line therapy without clarithromycin was effective in 96.2% of resistant cases. Conclusion Molecular detection of H. pylori resistance to clarithromycin is crucial for selecting optimal eradication therapy. Resistance increases with disease severity and significantly impacts treatment outcomes, confirming the need for personalized genotype‐based treatment strategies.

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