6. Ferguson-Smith MA, May HM, O’Hare E, Aitken mellitus. Malignancy, use of steroids, prior gastrectomy, DA. Hereditary persistence of alphafetoprotein: a new prolonged use of antibiotics, and acid-suppressive therapy autosomal dominant trait identified in an antenatal screening programme for spina bifida. J Med Genet. have been identified as other risk factors. Here we describe 1983;20(6):454-8. a young male with upper gastrointestinal bleeding due to 7. Alj Y et al. Hereditary persistence of alpha-fetoprotein is duodenal ulcer, who developed esophageal candidiasis due to both proximal and distal hepatocyte nuclear factor-1 after being treated for Helicobacter pylori (H. pylori) site mutations. Gastroenterology. 2004 Jan;126(1):308-17. infection. 8. Omata M, Cheng AL, Kokudo N, Kudo M, Lee JM, Jia J, Tateishi R, et al. Asia-Pacific clinical practice guidelines on the management of hepatocellular carcinoma: a 2017 Case Report update. Hepatol Int. 2017 Jul;11(4):317-370. 9. Houwert AC, Giltay JC, Lentjes EG, Lock MT Hereditary A 37 year-male presented with complaints of massive persistence of alpha-fetoprotein (HPAFP): review of the hematemesis followed by syncope. literature. Neth J Med.2010 Nov;68(11):354-8. His past history was significant for surgical repair 10. McVey JH, Michaelides K, Hansen LP, Ferguson-Smith M, Tilghman S, Krumlauf R, et al. A G-->A substitution in an of perforated duodenal ulcer about 10 years ago. He HNF I binding site in the human alpha-fetoprotein gene is was non-diabetic, without prior history of liver disease, associated with hereditary persistence of alpha-fetoprotein immunosuppressive therapy, alcohol use, or smoking. (HPAFP). Hum Mol Genet. 1993 Apr;2(4):379-84. 11. Hsu SX, Siegel AB, Berk PD. A 70-year-old woman After resuscitation, he underwent UGI endoscopy with 10 years of markedly elevated alpha-fetoprotein that found an ulcer with a visible vessel (Figure 1), in the measurements. In Seminars disease 2010 Feb (Vol. 30, No. anterior wall of the duodenum. Bleeding was controlled 01, pp. 099-106). with an injection of diluted epinephrine, followed by the 12. Deshpande N, Chavan R, Bale G, Avanthi US, Aslam M, application of two hemoclips (Figure 2). He was treated Ramchandani M, et al. Hereditary Persistence of Alpha- Fetoprotein Is Associated with the -119G>A Polymorphism with esomeprazole infusion, and a re-look endoscopy at in AFP Gene. ACG Case Rep J. 2017 Mar 1;4:e33. 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. Esophageal Candidiasis following Helicobacter pylori Eradication Therapy Ankur Gupta1 Priyanka Jain2 Departments of 1Gastroenterology and 2Pathology, Max Hospital, Mussoorie. Dehradun, Uttarakhand, India.

Corresponding Author: Dr Ankur Gupta Email: [email protected]

Esophageal candidiasis is well known to be associated Figure 1: Upper GI endoscopy: Peptic ulcer on the with immunocompromised states, including acquired anterior wall of duodenum with a visible bleeding immunodeficiency syndrome (AIDS) and diabetes vessel.

Tropical Gastroenterology 35 Vol.40, No.1, January-March 2019 Figure 2: Upper GI endoscopy: Duodenal peptic Figure 3: Upper GI endoscopy: Healed duodenal ulcer with a visible bleeding vessel, post application of peptic ulcer. two hemoclips.

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. Figure 4: Upper GI endoscopy: Numerous, curdy white plaques covering esophageal mucosa suggestive Besides acquired immunodeficiency syndrome, of esophageal candidiasis. Brush cytology confirmed diabetes mellitus, malignancy, use of systemic or inhaled the presence of yeast. steroids are other well-known factors predisposing for candida esophagitis.1 Acid suppression, too, has been considered as a most prominent reason for the occurrence of esophageal 3 risk factor for the development of candida esophagitis.2 candidiasis in these patients. Vermeersch et al. had shown It has been seen that the predisposition is more with the higher rates of fungal colonization in the esophagus of 4 use of PPI than with H2 receptor antagonists. This relates patients receiving acid suppressants. to their respective potency of acid suppression.Depletion Adverse effects associated with PPI have been of the gastric acid barrier has been thought of as the increasingly recognized lately and include, increased risk

Tropical Gastroenterology 36 Vol.40, No.1, January-March 2019 of fractures, community-acquired pneumonia, bacterial Ruptured Pseudocyst with infections like Salmonella, renal failure, dementia and increased risk of hepatic encephalopathy and spontaneous Peritonitis in the setting of bacterial peritonitis in patients with liver cirrhosis.5 Disconnected Pancreatic Duct: A It is also interesting to note that acid-suppressive Surgical Challenge therapy may interfere with the activity of antifungal drugs, a relevant aspect when treating these patients.6 Dhruv Jain1 To conclude, it is likely that there was a synergistic Rajesh Panwar1 increase in the risk of esophageal candidiasis with PPI Kumble Seetharama Madhusudhan2 and antibiotics in our patient. Since the use of both PPI Sujoy Pal1 and antibiotics is common in both out-patient and in- Pramod Kumar Garg3 patient settings, it is essential to recognize and suspect this potential adverse effect, in otherwise immunocompetent 1Department of GI Surgery & Liver Transplantation, 2 3 patients, and also to use the drugs judiciously. Department of Radiodiagnosis, Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, India. References Corresponding Author: Dr Rajesh Panwar 1. Mimidis K, Papadopoulos V, Margaritis V, Thomopoulos K, Email: [email protected] 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. The surgical treatment for disconnected pancreatic duct 2. Kim KY, Jang JY, Kim JW, Shim JJ, Lee CK, Dong is difficult, even in the elective setting. Here we describe et al. Acid suppression therapy as a risk factor for Candida a case of DPDS wherein emergency surgery was required. esophagitis. Dig Dis Sci. 2013 May;58(5):1282-6. This report aims to highlight the clinical and technical 3. Daniell HW Acid suppressing therapy as a risk factor nuances of this tricky situation. for Candida esophagitis. Dis Esophagus. 2016 Jul;29(5): 479-83. Case Report 4. Vermeersch B, Rysselaere M, Dekeyser K, Rasquin K, De Vos M, Elewaut A, Barbier F. Fungal colonization of the An 18 year-old male was referred to our hospital after esophagus. Am J Gastroenterol. 1989 Sep;84(9):1079-83. having undergone an emergency laparotomy for blunt 5. Vaezi MF, Yang YX, Howden CW. Complications of abdominal trauma two months prior, at another hospital, Proton Pump Inhibitor Therapy. Gastroenterology. 2017 Jul;153(1):35-48. with the details of the procedure and operative findings 6. Ning-Ning Liu and Julia R. Köhler. Antagonism of being unavailable. He was emaciated (Weight:35 Kg, 2 Fluconazole and a Proton Pump Inhibitor against Candida BMI:14.4kg/m ) and had a high output fistula (600 ml/day) albicans. Antimicrob Agents Chemother. 2016 Feb; 60(2): from the midline wound. The patient was evaluated under 1145–1147. the department of gastroenterology, where he was found to be having disconnected pancreatic duct syndrome (DPDS). An Endoscopic Retrograde Pancreatography (ERP) with trans-papillary pancreatic duct stenting was performed. ERP showed leakage of contrast at the level of the neck of pancreas, and the distal duct was not opacified (Figure 1). The fistula output remained high even after transpapillary stenting. As the patient was malnourished

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