Standard therapeutic regimens in H. pylori infection leads to activation of transitory fungal flora in gastric mucus.
Administration of broad-spectrum Antibiotics with antisecretory agents in treatment of H. pylori-associated diseases results in decreased representation of normal intestinal microflora and growth of transitory microflora, whose representatives are yeast-like fungi (Candida). This mayprimarily be caused by disordered microbial biocenosis in stomach, conditioned by eradication of H. pylori. Studies over recent years have yielded reliable information confirming that H. pylori is a source of peptides possessing a potent fungicidal activity. It still remains unclear whether there takes place an activation of fungal flora pre-existing in intestine, or drug-induced disorders of microbiocenosis in stomach.
MATERIALS AND METHODS:
We carried out a histological and bacterioscopic study of biopsy materials obtained from gastric antral mucosa in 679 patients with H. pylori-associated erosive or/and ulcerative gastric lesions, chronic gastritis and gastroesophageal reflux disease (GERD), with erosive or/and ulcerative duodenal lesions before and after eradication therapy.
Prior to treatment, the yeast-like fungi in stomach were revealed in 112 patients (16.5%). Eradication of H. pylori was achieved in 85% of patients, with large growth of elements resembling yeast-like fungi and pseudomycelium being detected in gastric mucosa in 33% of case.
The findings obtained suggest that an increased influx of yeast-like fungi from stomach into the gut may play role in proliferation of intestinal fungal microflora following antihelicobacter therapy. Under the conditions of decreased acidity of gastric juice on the background of antisecretory therapy and the lack of microbial antagonism on behalf of H. pylori in gastric mucus, Candida-genus fungi receive optimal conditions for development and subsequent passage to the intestine.