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6 t h A n n u a l E u r o p e a n C o n f e r e n c e o n
Gastroenterology
Journal of Clinical Gastroenterology and Hepatology
ISSN 2575-7733
J u n e 1 9 - 2 0 , 2 0 1 8
P a r i s , F r a n c e
Euro Gastro 2018
Page 20
Kenji Sasaki, J Clin Gastroenterol Hepatol 2018, Volume: 2
DOI: 10.21767/2575-7733-C1-001
Candida-associated gastric ulcer, though formerly thought to affect only
debilitated persons, has been reported to occur in apparently healthy
individuals. Though had been reported to demonstrate nothing but nonspecific
endoscopic features, the disease occasionally exhibits an apparently typical
finding designated a candidarium. The natural history of the disease had been
unknown and the fungus had been reported to be no longer detected once
the ulcers were healed and no recurrence of the disease had been described.
However, the ulcer is shown to not only occur but also recur in a different site with
a different shape in a non-diabetic, Helicobacter pylori-negative patient without
antecedent ulcers, who has not been given non-steroidal anti-inflammatory drugs
(NSAIDs), antibiotics, or antineoplastic agents, which implies that, contrary to the
prevailing opinion, Candida is no innocuous bystander but an etiologic perpetrator.
Immune deficiency has recently been reported in relation to candidiasis, which
is considered to explain the cause of intractable or recurrent Candida-associated
gastric ulcer. In the oropharyngeal field, Candida albicans has recently been
shown to secrete a hitherto unknown cytolytic peptide pore-forming toxin (PFT),
candidalysin, into a pocket in the epithelium which penetrates into and to activate
mitogen-activated protein kinase (MAPK)/MAPK phosphatase 1 (MKP1)/c-Fos
pathway, triggering release of damage as well as immune cytokines. While the
PFT, exerting an effect even on the adjacent cells, directly injures the tissue with
damage cytokines, immune counterpart activates polymorphonuclear leukocytes
(PMN) to eventually terminate inflammation, which results in restoring the fungus
to the commensal state or eradicating it. Since it cannot be negated that such a
phenomenon occurs in the gastric mucosa, a theoretically strong possibility has
come up that the so-called Candida-associated gastric ulcer is actually Candida-
induced ulcer. Therefore, the disease should be reinvestigated in the light of the
recent immunological, microbiological, and molecular biological findings.
Biography
Kenji Sasaki has completed his MD and as an Immunologist,
he completed his PhD at Tohoku University School of Medicine.
He was trained at Miyagi Cancer Center. He is a Board Certified
Fellow and Preceptor of Japan Gastroenterological Endoscopy
Society, Board Certified Gastroenterologist of Japanese Society
of Gastroenterology, Board Certified Member of the Japanese
Society of Internal Medicine and Editorial Board Member of
CRIM. He has published several papers on Gastroenterology
in international journals and served as a Reviewer for
Journal of Medical Microbiology, Journal of Pharmacology
& Pharmacotherapeutics and Journal of Gastrointestinal &
Digestive System.
Candida-associated Gastric Ulcer until
Yesterday, Today and from Tomorrow
Kenji Sasaki
Midtown Medicare Clinic, Japan