Accepted Manuscript Not all Helicobacter are Pylori Andrew C. Berry, B.S., Rahman Nakshabendi, M.D., Aaron C. Baltz, M.D.
PII: DOI: Reference:
S1542-3565(15)00105-6 10.1016/j.cgh.2015.01.019 YJCGH 54149
To appear in: Clinical Gastroenterology and Hepatology Accepted Date: 21 January 2015 Please cite this article as: Berry AC, Nakshabendi R, Baltz AC, Not all Helicobacter are Pylori, Clinical Gastroenterology and Hepatology (2015), doi: 10.1016/j.cgh.2015.01.019. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. All studies published in Clinical Gastroenterology and Hepatology are embargoed until 3PM ET of the day they are published as corrected proofs on-line. Studies cannot be publicized as accepted manuscripts or uncorrected proofs.
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Not all Helicobacter are Pylori Andrew C. Berry, B.S.,1 Rahman Nakshabendi, M.D.,1 Aaron C. Baltz, M.D.2 1
Department of Medicine, University of Florida College of Medicine-Jacksonville GI Associates, Wauwatosa, WI
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Corresponding Author: Andrew C. Berry, B.S. Department of Medicine, University of Florida College of Medicine-Jacksonville 653-1 West 8th Street, L18 Jacksonville, FL 32209 Phone: 1-414-617-8877 Email:
[email protected] No conflicts of interest by any of the authors.
A 16-year-old male presented with a 5-month history of intermittent post-prandial vomiting. He did not have any weight loss or abdominal pain. He had a 9-month history of similar symptoms as well as non-specific abdominal pain at the age of 6 years old and
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had an esophagogastroduodenoscopy (EGD) and colonoscopy. The EGD at the age of 6 years old revealed nodular gastric mucosa and an Helicobacter pylori test by urease stain was negative. The colonoscopy was unremarkable. He was symptom-free in the 9 years
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between presentations. The patient did have exposure to a pet mutt dog, predominantly lab mix. An EGD revealed mild gastritis manifested by a mosaic pattern (EGD, Figure A)
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and biopsies from the proximal antrum revealed Helicobacter heilmannii (Hematoxylin and Eosin stain, Figure B; Warthin-Starry (silver) stain, Figure C). The patient had an amoxicillin allergy so was treated for 2 weeks with pantoprazole, clarithromycin, and metronidazole. He was kept on pantoprazole for another 6 weeks after treatment. Repeat EGD and biopsies, 3 months after treatment and 4 weeks after stopping pantoprazole,
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confirmed eradication of H. heilmannii. Symptoms completely resolved after treatment with the 2 week course of antimicrobial therapy.
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The frequency of H. heilmannii infections in children with dyspeptic symptoms is
between 0.2-0.5%.1 It has been shown to have zoonotic origin and pass from domestic
animals to children in nearly 60% of cases, as is most likely in this case.1 Most infected
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patients are symptomatic and present with dyspepsia, reflux, or epigastric pain. It
typically presents with chronic nodular antrum gastritis plus interstitial infiltrates, which
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is indistinguishable from that of H. pylori gastritis. H. heilmannii is diagnosed on morphology of biopsy specimen of gastric mucosa, positive rapid urease test, and PCR. It can be differentiated from H. pylori based on microscopy, negative culture, and absence of H. pylori antigen in the stool. If ample organisms, hematoxylin and eosin stains are
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sufficient for diagnosis. However, if a paucity of organisms, immunohistochemical stains may help confirm its corkscrew-shaped appearance, larger size, and greater distance from the surface epithelium compared to H. pylori.2 An association of H. heilmannii with
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gastric cancer and MALT lymphoma has also been shown.3 Thus, eradication is vital and sensitive to antibiotics used for H. pylori, such as pantoprazole, amoxicillin,
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clarithoromycin or metronidazole.4,5 Although the treatment for H. pylori and H. heilmannii is the same, a histological diagnosis is necessary in cases negative for H. pylori, as H. heilmannii may be culprit and must be treated.
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References: 1. Iwanczak F., Gosciniak G., Iwanczak B. Helicobacter heilmannii w patologii chorob zoladka i dwunastnicy u dzieci. Gastroenterol Pol. 1998;5:229-233.
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2. Singhal A.V., Sepulveda A.R. Helicobacter heilmannii gastritis: a case study with review of literature. Am J Surg Pathol. 2005 Nov;29(11):1537-1539.
gastric cancer. Lancet. 1995;346:511–512.
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3. Morgner A., Bayerdorffer E., Meining A., et al. Helicobacter heilmannii and
4. Goddard A.F., Logan R.P., Atherton J.C., et al. Healing of duodenal ulcer after
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eradication of Helicobacter heilmannii. Lancet. 1997;349:1815–1816.
5. Hilzenrat N, Lamoureux E, Weintrub I, et al. Helicobacter heilmannii like spiral bacteria in gastric mucosal biopsies: prevalence and clinical significance. Arch
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Pathol Lab Med. 1995;119:1149–1153.
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