Candida Colonization of the Esophagus and Gastric Mucosa; a Comparison of Patients Taking Proton Pump Inhibitors and Those Taking Histamine Receptor Antagonist Drugs Publisher



Mottaghi B¹ ; Emami MH² ; Riahi P² ; Fahim A² ; Rahimi H² ; Mohammadi R^{1, 3} Show Affiliations
Source: Gastroenterology and Hepatology from Bed to Bench Published:2021

Abstract

Aim: Investigation of Candida colonization of the esophagus and gastric mucosa in patients taking proton pump inhibitors in comparison with those taking histamine-2 receptor antagonists. Background: Candida species are normal flora of alimentary tract that can cause infection of the esophagus and gastro-intestinal tract in immunocompromised patients. Consumption of proton pump inhibitors and histamine-2 receptor antagonists has been shown to alter the gastric pH, which may predispose the esophagus and stomach to floral transmission and colonization Methods: Two hundred and forty-five clinical specimens were obtained from 91 patients who underwent endoscopy from September 2019 to February 2020. Direct microscopy with KOH 10% and subculture on sabouraud dextrose agar containing chloramphenicol was used as primary screening. PCR with ITS primers was performed to amplify the ITS1-5.8SrDNA-ITS2 region, and the MspI restriction enzyme was used for RFLP to identify clinical isolates. Results: Seventy cultures out of 245 specimens were positive for Candida colonization (28.5%). Colonization of Candida species in gastric acid and gastric tissue biopsies of patients who took PPIs and H2 blockers was significantly higher than in those in the control group (p= 0.001). The use of ranitidine, pantoprazole, and omeprazole increased the risk of gastric candidiasis by 10.60, 9.20, and 12.99 times, respectively (p< 0.05). Conclusion: The use of PPIs and H2 blockers, ageing, and consumption of vegetables were main risk factors for gastric colonization in the present survey; other variables, such as Candida species, cigarette smoking, and alcohol consumption, were not implicated in the development of gastroesophageal lesions. Further investigations are necessary to understand how these predisposing factors change the host's defense mechanisms and increase colonization of fungi at mucosal surfaces. © 2021 RIGLD.