Candidal infection of benign gastric ulcer

Neeman, A; Kadish, U

doi:10.1016/0016-5085(84)90227-0

Cited by 5 publications

(9 citation statements)

References 2 publications

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“…It was concluded that the older age was the only risk factor for fungal infection, and gender, cigarette smoking and tea or coffee consumption were not implicated in the development of gastric ulcer (Wu et al, 1995 ). It appears that immunosuppression due to aging could facilitate fungal invasion of the gastric ulcer (Neeman et al, 1981 ; Loffeld et al, 1988 ). Reports also indicate that hypochlorhydria provides favorable conditions for the growth of fungi (Goenka et al, 1996 ; Martinsen et al, 2005 ) and bacteria (Thorens et al, 1996 ) in the stomach.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Helicobacter pylori Infection, Aging, and Consumption of Proton Pump Inhibitor on Fungal Colonization in the Stomach of Dyspeptic Patients

et al. 2016

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Background: The importance of coinfection of Helicobacter pylori (H.pylori) and Candida albicans (C. albicans) in the development of gastric diseases is not known. In this study, the frequency of concurrent infection of H. pylori and C. albicans in dyspeptic patients was assessed while considering age, gender, and PPI consumption of patients.Methods: Gastric biopsies were taken from 74 yeast-positive dyspeptic patients and gastric disease, age, gender, and proton pump inhibitor (PPI) consumption of subjects were recorded. One antral biopsy was used for rapid urease test (RUT) and one for H. pylori and yeast cultivation and smear preparation. Bacterial isolates were identified according to spiral morphology and the biochemical characteristics. Yeast isolates were identified on Chromagar and by the Nested-PCR amplification of C. albicans-specific topoisomerase II gene. Twenty-seven biopsy smears were Gram-stained and examined by the light microscope for observing H. pylori and yeast cells. Conclusion:The older age and PPI consumption could favor fungal colonization in the human stomach. The occurrence of a considerable number of H. pylori-positive or H. pylori-negative patients with gastritis or peptic ulcer shows that co-infection of Candida and H. pylori or infection of yeast alone could be associated with dyspeptic diseases. The occurrence of yeast cells in gastric biopsies with different Gram's reactions indicates that fungi might change their cell wall components for establishing a persistent colonization in the stomach.

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Section: Discussionmentioning

confidence: 99%

The Effect of Helicobacter pylori Infection, Aging, and Consumption of Proton Pump Inhibitor on Fungal Colonization in the Stomach of Dyspeptic Patients

et al. 2016

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“…Whereas the disease has been reported to have low healing rate [6,11], some cases of the disease have been reported to have spontaneously healed [12]. In my case, the original lesion was found to have spontaneously healed and the recurrent one was in no way intractable [13].…”

Section: Candida-associated Gastric Ulcer Todaymentioning

confidence: 66%

“…Candida-associated gastric ulcer is regarded as the above mentioned ulcerated-typed gastric candidiasis, the diagnostic criterion of which is demonstration of infiltration of the tissue or ulcer slough by the hyphae [5,8,10]. It is also seen in apparently healthy individuals [5][6][7][8][9] with quite widely different frequency according to the researchers [8][9][10][11][12] ranging from 0.12% to 36% of gastric ulcer. The species in the genus reported to be associated with gastric ulcer are albicans, tropicalis, parapsilosis, krusei, and pseudotropicalis in decreasing order of frequency [10].…”

Section: Candida-associated Gastric Ulcer Until Yesterdaymentioning

confidence: 99%

“…Whereas some cases of the ulcer have been reported to have spontaneously healed [12], it has been reported to have low healing rate [6,11]. The rate of decrease in ulcer diameter, an indication of lesion healing, was slower in patients whose stomachs were significantly colonized by the fungus as compared with patients who were not [17].…”

Section: Candida-associated Gastric Ulcer Until Yesterdaymentioning

confidence: 99%

“…The fungus had been reported to be no longer detected once the ulcers were healed even without antifungal treatment and no recurrence had been described [9,11]. Though the clinical significance of it has not yet been elucidated, ----so that the appellation of the disease is modified by an ambiguous adjectival past participle "associated"----it was not regarded as directly etiologic in development of ulcer but was considered to possibly aggravate or perpetuate ulceration [5,6,8].…”

Section: Candida-associated Gastric Ulcer Until Yesterdaymentioning

confidence: 99%

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Candida-Associated Gastric Ulcer Revisited

Sasaki¹

2021

jbacteriolmycol

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Candida-associated gastric ulcer occurs not only in debilitated but healthy individuals. Though had been reported to demonstrate nothing but nonspecific endoscopic features, it occasionally exhibits a typical finding I designated a candidarium. The natural history of the disease had not been clarified and the recurrence had not been described. However, I demonstrated that the ulcer not only occurs but also recurs in a different site with a different shape in a non-diabetic, H. pylori-negative patient, who has not taken NSAIDs, antibiotics, antineoplastic agents, or systemic corticosteroids, advocating that, contrary to the prevailing opinion, Candida is no innocuous bystander but an etiologic perpetrator. It has recently been shown to secrete a cytolytic PFT, candidalysin, into a pocket in the epithelium after penetrating into it to activate MAPK/MKP1/ c-Fos pathway, triggering release of damage as well as immune cytokines in OPC and VVC. While candidalysin, exerting an effect even on the adjacent oropharyngeal cells, directly injures the tissue with damage cytokines, immune counterparts activate PMNs to eventually terminate inflammation. Though the epithelial response to the fungus is different from organ to organ, it invades into and induces necrotic cellular damage to the IECs through the toxin to translocate: the action of candidalysin is proven not only on the squamous but on the columnar epithelium. Since, by analogy with intestinal candidiasis, it is never difficult to speculate that the PFT inflicts such damage to the gastric mucosa, a theoretically strong possibility has come up that Candida-associated gastric ulcer is actually Candida-induced.

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