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GASTROENTEROLOGY

International Conference on

J u n e 2 5 - 2 6 , 2 0 1 8 | D u b l i n , I r e l a n d

Journal of Gastronenterology and Digestive Diseases

|

Volume 3

Page 23

Note:

C

andida-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), candida lysin, into a pocket in the

epithelium which penetrates 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 Candida-

induced ulcer. Therefore, the disease should be reinvestigated in the light of

the recent immunological, microbiological, and molecular biological findings.

Biography

Kenji Sasaki received his MD in 1973 and PhD in

1977 from Tohoku University. He is a Board Cer-

tified Fellow and Preceptor of the Japan Gastro-

enterological Endoscopy Society, Board Certified

Gastroenterologist of the Japanese Society of

Gastroenterology, Board Certified Member of the

Japanese Society of Internal Medicine and Edito-

rial Board Member of CRIM. He has given presen-

tations at international medical congresses and

published papers on gastroenterology in interna-

tional journals. Acclaimed by Prof Tarnawski at

DDW 2012, he published his article Candida-as-

sociated gastric ulcer relapsing in a different po-

sition in a different appearance in

World J Gastro-

enterol

. He served as a reviewer for CRIM, JMM,

JPP and J Gastrointestinal Dig Syst.

kydosarnymai@aria.ocn.ne.jp

CANDIDA-ASSOCIATED GASTRIC

ULCER UNTIL YESTERDAY, TODAY,

AND FROM TOMORROW- IN QUEST

OF THE ETIOLOGY

Kenji Sasaki

Home Medical Care Supporting Clinic, Japan

Kenji Sasaki, J Gastroenterol Dig Dis 2018, Volume 3