Gastric Perforation Associated with Candidiasis and NSAIDS

Febriana Aquaresta, Arthur Pohan Kawilarang, Pepy Dwi Endraswari

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Invasive candidiasis is an important health-care-associated fungal infection. Candida is often described as an opportunistic pathogen. It is commensal flora in the gastrointestinal tract. Invasive candidiasis can happen usually because of a consequence of increased or abnormal colonization together with a local or generalized defect in host defenses. Candidiasis can occur in patients with HIV, therapy with a broad-spectrum antibiotic, transplant organ, and immunocompromised. Most cases of gastric perforation occur as complications of Peptic Ulcer Disease (PUD), Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) and gastric neoplasms, but candidiasis as a cause of gastric perforation is very rare. This study aims to reveal the correlation between gastric perforation with candidiasis and NSAIDs. It was reported that a 57-year-old East Java Indonesian female presented with severe epigastric pain, generalized peritonitis, fever, nausea also vomiting and had a history of NSAIDs used for five years. The patient was taken to the general surgery of Dr. Sutomo Surabaya Hospital and performed exploratory laparotomy. A gastric perforation was discovered in the antrum. Microbiology culture examination from biopsy gastric tissue revealed an intense fungal growth from sabouraudagar medium and there is no other microorganism that grew in aerobic culture. Candida albicans was identified by VITEK® 2 COMPACT. Histopathological examination from biopsy gastric tissue was performed by Olympus CX-21 microscope, showed invasive Candida albicans consisting of numerous fungal yeasts and pseudohyphae invading and destroying the gastric wall. The patient was subsequently treated with fluconazole anti-fungal and discharge home after nine days postoperative period in good condition. From this result, we suggest using an antifungal treatment for patients who use NSAIDs for long periods to prevent candidiasis.


Candida albicans, fluconazole, gastric perforation, histopathological, NSAIDs, peritonitis

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Kumamoto Carol, “Inflammation and gastrointestinal Candida colonization,” Curr. Opin. Microbiol., vol. 14, no. 4, pp. 386–391, 2011, doi: 10.1016/j. mib.2011.07.015.Inflammation.

R. Mahon, Connie and C. Lehman, Textbook of Diagnostic Microbiology. 2019.

,. Tille, Balley & Scott’s: Diagnostic Microbiology. 2017.

D. Prieto, I. Correia, J. Pla, and E. Román, “Adaptation of Candida albicans to commensalism in the gut,” Future Microbiol., vol. 11, no. 4, pp. 567–583, 2016, doi: 10.2217/fmb.16.1.

N. Gupta, “A rare cause of gastric perforation-Candida infection: A case report and review of the literature,”

J. Clin. Diagnostic Res., vol. 6, no. 9, pp. 1564–1565, 2012, doi: 10.7860/JCDR/2012/4632.2563.

S. Höfs et al., “Candidiasis, a rare cause of gastric perforation: A case report and review of literature,” Ann. Med. Health Sci. Res., vol. 54, no. 4, p. 314, 2015, doi: 10.4103/2141-9248.160187.

G. Pappas, Peter, S. Lionakis, Michail, C. Arendrup, Maiken, L. Zeichner-Ostrosky, and J. Kullberg, Bart, “Invasive candidiasis,” Nat. Rev. Dis. Prim., vol. 4, 2018, doi: 10.1038/nrdp.2018.27.

A. da Silva Dantas et al., “Cell biology of Candida albicans–host interactions,” Curr. Opin. Microbiol., vol. 34, pp. 111–118, 2016, doi: 10.1016/j. mib.2016.08.006.

S. Höfs, S. Mogavero, and B. Hube, “Interaction of Candida albicans with host cells: virulence factors, host defense, escape strategies, and the microbiota,” J. Microbiol., vol. 54, no. 3, pp. 149–169, 2016, doi: 10.1007/s12275-016-5514-0.

T. Yamada, E. Deitch, R. D. Specian, M. A. Perry,

R. B. Sartor, and M. B. Grisham, “Mechanisms of acute and chronic intestinal inflammation induced by indomethacin,” Inflammation, vol. 17, no. 6, pp. 641–662, 1993, doi: 10.1007/BF00920471.

G. C. Nadǎş et al., “Erratum to: The Interplay Between NSAIDs and Candida albicans on the Gastrointestinal Tract of Guinea Pigs (Mycopathologia, (2013), 175, (221-230), 10.1007/s11046-013-9613-8),” Mycopathologia, vol. 176, no. 1–2, pp. 171–173, 2013, doi: 10.1007/s11046-013-9659-7.

O. Ekenna and R. J. Sherertz, “Factors affecting colonization and dissemination of Candida albicans from the gastrointestinal tract of mice,” Infect. Immun., vol. 55, no. 7, pp. 1558–1563, 1987.

M. A. S. Alem and L. J. Douglas, “Effects of Aspirin and Other Nonsteroidal Anti-Inflammatory Drugs on Biofilms and Planktonic Cells of Candida albicans,” Antimicrob. Agents Chemother., vol. 48, no. 1, pp. 41–47, 2004, doi: 10.1128/AAC.48.1.41-47.2004.

M. Ilahi, J. Khan, Q. Inayat, and T. S. Abidi, “Histological changes in parts of foregut of rat after indomethacin administration.,” J. Ayub Med. Coll. Abbottabad, vol. 18, no. 3, pp. 29–34, 2006.

P. L. Beck et al., “Mechanisms of NSAID-induced gastrointestinal injury defined using mutant mice,” Gastroenterology, vol. 119, no. 3, pp. 699–705, 2000, doi: 10.1053/gast.2000.16497.

M. C. Noverr, S. M. Phare, G. B. Toews, M. J. Coffey, and G. B. Huffnagle, “albicans Produce Immunomodulatory Prostaglandins,” Infect. Immun., vol. 69, no. 5, pp. 2957–2963, 2001, doi: 10.1128/ IAI.69.5.2957.

A. H. P. Loh et al., “Multiple indomethacin-induced colonic perforations in an adolescent,” Singapore Med. J., vol. 52, no. 4, pp. 82–84, 2011.

R. D. Newberry, J. S. McDonough, W. F. Stenson, and R. G. Lorenz, “ Spontaneous and Continuous Cyclooxygenase-2-Dependent Prostaglandin E 2 Production by Stromal Cells in the Murine Small Intestine Lamina Propria: Directing the Tone of the Intestinal Immune Response ,” J. Immunol., vol. 166, no. 7, pp. 4465–4472,2001,doi: 10.4049/ jimmunol.166.7.4465.

[J. L. F. Kock, O. M. Sebolai, C. H. Pohl, P. W. J. Van Wyk, and E. J. Lodolo, “Oxylipin studies expose aspirin as antifungal,” FEMS Yeast Res., vol. 7, no. 8, pp. 1207–1217, 2007, doi: 10.1111/j.1567- 1364.2007.00273.x.

J. Kock et al., “Development of a Yeast Bio-Assay to Screen Anti-Mitochondrial Drugs,” Curr. Drug Discov. Technol., vol. 6, no. 3, pp. 186–191,2009,doi: 10.2174/157016309789054960.

J. L. F. Kock, C. J. Strauss, C. H. Pohl, and S. Nigam, “The distribution of 3-hydroxy oxylipins in fungi,” Prostaglandins Other Lipid Mediat., vol. 71, no. 3–4, pp. 85–96, 2003, doi: 10.1016/S1098- 8823(03)00046-7.

C. Montagnoli et al., “ B7/CD28-Dependent CD4 + CD25 + Regulatory T Cells Are Essential Components of the Memory-Protective Immunity to Candida albicans ,” J. Immunol., vol. 169, no. 11, pp. 6298– 6308, 2002, doi: 10.4049/jimmunol.169.11.6298.

Tanaka, S. Hase, T. Miyazawa, and K. Takeuchi, “Up-regulation of cyclooxygenase-2 by inhibition of cyclooxygenase-1: A key to nonsteroidal anti- inflammatory drug-induced intestinal damage,” J. Pharmacol. Exp. Ther., vol. 300, no. 3, pp. 754–761, 2002, doi: 10.1124/jpet.300.3.754.

B. J. R. Whittle, “Gastrointestinal effects of nonsteroidal anti-inflammatory drugs,” Fundam. Clin. Pharmacol., vol. 17, no. 3, pp. 301–313, 2003, doi: 10.1046/j.1472- 8206.2003.00135.x.

L. Maiden, “Capsule endoscopic diagnosis of nonsteroidal antiinflammatory drug-induced enteropathy,” J. Gastroenterol., vol. 44, no. SUPPL. 19, pp. 64–71, 2009, doi: 10.1007/s00535-008-2248-8.

A. Vazquez-Torres, J. Jones-Carson, T. Warner, and E. Balish, “Nitric oxide enhances resistance of scid mice to mucosal candidiasis,” J. Infect. Dis., vol. 172, no. 1, pp. 192–198, 1995, doi: 10.1093/infdis/172.1.192.

T. Nakamura et al., “Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats,” J. Gastroenterol. Hepatol., vol. 22, no. 5, pp. 749–756, 2007, doi: 10.1111/j.1440- 1746.2006.04353.x.


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Universitas Airlangga

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