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Case Report
 
Esophageal Candidiasis following Helicobacter pylori Eradication Therapy
Keywords :
Ankur Gupta1, Priyanka Jain2
Departments of 1Gastroenterology and 2Pathology, Max Hospital, Mussoorie. Dehradun, Uttarakhand, India.


Corresponding Author
:
Dr Ankur Gupta
Email: mail.guptaankur@gmail.com


DOI: http://dx.doi.org/10.7869/tg.523

48uep6bbphidcol2|ID
48uep6bbphidvals|1907
48uep6bbph|2000F98CTab_Articles|Fulltext
Esophageal candidiasis is well known to be associated with immunocompromised states, including acquired immunodeficiency syndrome (AIDS) and diabetes mellitus. Malignancy, use of steroids, prior gastrectomy, prolonged use of antibiotics, and acid-suppressive therapy have been identified as other risk factors. Here we describe a young male with upper gastrointestinal bleeding due to duodenal ulcer, who developed esophageal candidiasis after being treated for Helicobacter pylori (H. pylori) infection.  

Case Report

A 37 year-male presented with complaints of massive hematemesis followed by syncope.
His past history was significant for surgical repair of perforated duodenal ulcer about 10 years ago. He was non-diabetic, without prior history of liver disease, immunosuppressive therapy, alcohol use, or smoking.
After resuscitation, he underwent UGI endoscopy that found an ulcer with a visible vessel (Figure 1), in the anterior wall of the duodenum. Bleeding was controlled with an injection of diluted epinephrine, followed by the application of two hemoclips (Figure 2). He was treated with esomeprazole infusion, and a re-look endoscopy at 48 hours confirmed ulcer healing. Rapid urease test was positive in the biopsy specimen, and he was treated for H. pylori with amoxicillin, clarithromycin, and esomeprazole for two weeks.



Two weeks after discharge, he presented to the out-patient clinic with complaints of dysphagia. UGI endoscopy revealed well healed duodenal ulcer, (Figure 3) and upper and mid esophageal candidiasis (Figure 4). Microscopic examination of the brush cytology confirmed the presence of Candida. HIV serology and evaluation for diabetes were negative.  He was treated with fluconazole and was well on follow up after a month.




Discussion

Our patient developed esophageal candidiasis after being treated with proton pump inhibitors (PPI), followed by H. pylori eradication therapy for two weeks.
Besides acquired immunodeficiency syndrome, diabetes mellitus, malignancy, use of systemic or inhaled steroids are other well-known factors predisposing for candida esophagitis.1
Acid suppression, too, has been considered as a risk factor for the development of candida esophagitis.2 It has been seen that the predisposition is more with the use of PPI than with H2 receptor antagonists. This relates to their respective potency of acid suppression.Depletion of the gastric acid barrier has been thought of as the most prominent reason for the occurrence of esophageal candidiasis in these patients.3 Vermeersch et al. had shown higher rates of fungal colonization in the esophagus of patients receiving acid suppressants.4
Adverse effects associated with PPI have been increasingly recognized lately and include, increased risk of fractures, community-acquired pneumonia, bacterial infections like Salmonella, renal failure, dementia and increased risk of hepatic encephalopathy and spontaneous bacterial peritonitis in patients with liver cirrhosis.5
It is also interesting to note that acid-suppressive therapy may interfere with the activity of antifungal drugs, a relevant aspect when treating these patients.6
To conclude, it is likely that there was a synergistic increase in the risk of esophageal candidiasis with PPI and antibiotics in our patient. Since the use of both PPI and antibiotics is common in both out-patient and in-patient settings, it is essential to recognize and suspect this potential adverse effect, in otherwise immunocompetent patients, and also to use the drugs judiciously.

References
  1. Mimidis K, Papadopoulos V, Margaritis V, Thomopoulos K, Gatopoulou A, Nikolopoulou V, Kartalis G. Predisposing factors and clinical symptoms in HIV-negative patients with Candida oesophagitis: are they always present? Int J Clin Pract. 2005 Feb;59(2):210-3.
  2. Kim KY, Jang JY, Kim JW, Shim JJ, Lee CK, Dong et al. Acid suppression therapy as a risk factor for Candida esophagitis. Dig Dis Sci. 2013 May;58(5):1282-6. 
  3. Daniell HW Acid suppressing therapy as a risk factor for Candida esophagitis. Dis Esophagus. 2016 Jul;29(5):479-83.
  4. Vermeersch B, Rysselaere M, Dekeyser K, Rasquin K, De Vos M, Elewaut A, Barbier F. Fungal colonization of the esophagus. Am J Gastroenterol. 1989 Sep;84(9):1079-83.
  5. Vaezi MF, Yang YX, Howden CW. Complications of Proton Pump Inhibitor Therapy. Gastroenterology. 2017 Jul;153(1):35-48. 
  6. Ning-Ning Liu and Julia R. Köhler. Antagonism of Fluconazole and a Proton Pump Inhibitor against Candida albicans. Antimicrob Agents Chemother. 2016 Feb; 60(2): 1145–1147.