allied
academies
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.jpCANDIDA-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