Gastric ulcer associated with Candida, although formerly thought to affect only weakened people, has been reported to occur in seemingly healthy people. While nothing but unspecific endoscopic features have been documented, the disease sometimes exhibits an apparently typical finding designated by the author as a candidarium. Helicobacter pylori (H. pylori)-negative, apparently immunocompetent patient without prior ulcers or history of lesions who have not been given non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, antineoplastics The natural history of the disease has been unclear, however the ulcer has been shown not only to occur but also to recur in a different location with a different form in a non-diabetic, Helicobacter pylori (H. pylori) In relation to candidiasis, immune deficiency has been recently identified, which may explain the cause of intractable gastric ulcer associated with Candida. Candida albicans has recently been shown in the oropharyngeal area to secrete a previously unknown cytolytic peptide pore-forming toxin (PFT), candidalysin, into an epithelial pocket that penetrates and triggers the mitogen-activated protein kinase (MAPK)/MAPK phosphatase 1 (MKP1)/c-Fos pathway, causing damage and immune cytokines to be published. Although the PFT directly injures the tissue with weakened cytokines, exerting an effect also on the neighboring cells, it induces immune counterparts to cause polymorphonuclear leukocytes (PMN) to ultimately end inflammation, resulting in the restitution or eradication of the fungus to the commensal state. As it can not be argued that such a phenomenon exists in the gastric mucosa, a potentially strong probability has emerged that Candida-induced ulcer is possibly the so-called Candida-associated gastric ulcer. A scientifically conclusive possibility has arisen that the so-called Candida-associated gastric ulcer is a Candida-induced ulcer due to recent developments in microbiology, molecular biology, and immunology. The disease has entered a point in which the etiology should be re-examined and the disease itself should be re-examined in the light of not only the character of the pathogens but also the immunological status of the hosts. The disease should therefore be re-examined in the light of recent immunological, microbiological and molecular biological findings.
Author(s) Details
Kenji Sasaki
Department of Internal Medicine,
Midtown Medicare Clinic, Japan.
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