Gastric Subepithelial Mass-like Involvement in Crohn’s Disease: Another Upper Gastrointestinal Manifestation?

Gastric Subepithelial Mass-like Involvement in Crohn’s Disease: Another Upper Gastrointestinal... A 55-year-old woman was referred for investigation of a gastric subepithelial lesion diagnosed incidentally during endoscopy. The patient had a 2-month history of abdominal pain, and a past medical history included hypothyroidism. Upper endoscopy revealed a 3-cm sized subepithelial lesion located in the gastric corpus, with superficial erosions due to biopsies performed during the first endoscopic examination [Figure 1A]. The lesion was firm and not indented when pressed with a biopsy forceps. Endoscopic ultrasound confirmed the presence of a 30-mm to 15-mm sized, ovoid, hypoechoic mass lesion involving the third (submucosa) and fourth (muscularis propria) endosonographic layers with ill-defined borders. Internal structure was not homogeneous, with more hypo- and hyper-echoic areas [Figure 1B]. Histological examination of endoscopic bite-on-bite biopsies showed focal chronic inflammation with abundant eosinophils and granulocytic infiltration. There were collections of epitheloid histiocytes forming ill-defined granulomas without acid-fast bacilli [Figure 1A, inset]. No Helicobacter pylori (Hp) were identified. Figure 1. View largeDownload slide A. Endoscopy showing subepithelial lesion. Inset; histopathological image [haematoxylin and eosin stain, x 100] showing lymphocytic infiltration with eosinophils and collections of epithelioid histiocytes forming ill-defined granulomas [arrowheads]. B. Radial endoscopic ultrasound image showing hypoechoic subepithelial lesion involving the third and fourth [asterisk] layers. Intact first [arrow] and second [double arrows] layers. C. Transabdominal ultrasound image showing subepithelial lesion [Lx] in the gastric corpus (first [arrow], second [double arrows], and fourth [asterisk] layers). D. Endoscopic view after treatment. Figure 1. View largeDownload slide A. Endoscopy showing subepithelial lesion. Inset; histopathological image [haematoxylin and eosin stain, x 100] showing lymphocytic infiltration with eosinophils and collections of epithelioid histiocytes forming ill-defined granulomas [arrowheads]. B. Radial endoscopic ultrasound image showing hypoechoic subepithelial lesion involving the third and fourth [asterisk] layers. Intact first [arrow] and second [double arrows] layers. C. Transabdominal ultrasound image showing subepithelial lesion [Lx] in the gastric corpus (first [arrow], second [double arrows], and fourth [asterisk] layers). D. Endoscopic view after treatment. Although inflammation had attacked the mucosa, the superficial epithelial lining was protected in most parts, compatible with the subepithelial nature of the involvement. It was also possible to identify the subepithelial lesion by abdominal ultrasound [Figure 1C, supplementary video]. Ileocolonoscopy revealed diffuse ileitis with ulcerations, and apthous ulcers with skip hyperaemic areas throughout the colon. Histopathological examination of ileocolonoscopic biopsies was consistent with Crohn’s disease (CD). Mycobacterium tuberculosis polymerase chain reaction assay and culture of mucosal biopsies were negative. Computed tomography of the chest was unremarkable, and a Quantiferon test was negative. Pantoprazole, azathiopurine, and prednisolone treatment was initiated. Four months after the initiation of treatment, no significant change was observed at upper endoscopy or ileocolonoscopy. Azathiopurine treatment ceased because of persistent leukopenia even with dose reduction, and adalimumab (ADA) monotherapy started (160/80 induction 2 weeks apart, then 40 mg subcutaneously every other week). Gastric lesions regressed considerably after remission induction with ADA. After the first year of treatment (trough serum ADA level 7.7 µg/ml), endoscopic evaluation revealed complete healing of the subepithelial lesion, leaving an atrophic mucosa [Figure 1D]. Upper endoscopy has revealed at least one of the specific endoscopic findings in up to 75% of CD patients, according to the recent literature.1 Microscopic findings such as Hp-negative focally active gastritis and/or granulomas have been reported between 30% and 76% of cases.2–4 To the best of the authors’ knowledge, gastric subepithelial mass-like involvement has so far not been identified in CD. This involvement pattern, probably is a rare presentation of the transmural nature of the disease. Also, data regarding the effect of anti-TNF treatment on mucosal healing of upper gastrointestinal lesions are scarce. ADA treatment resulted in complete endoscopic mucosal healing and regression of the submucosal involvement in our case. Subepithelial lesion-like involvement should be considered in the wide armamenterium of upper gastrointestinal CD manifestations. Funding No specific funding has been received for this study. Data have not been generated as part of the routine work of an organisation. Confict of Interest None. Author Contributions CG: data collection, literature search, writing the manuscript, figure preparation. SO: data collection, figure preparation, critical review of the manuscript. Both authors had full access to all the data in the study and had final responsibility for the decision to submit for publication. Supplementary Data Supplementary data are available at ECCO-JCC online. References 1. Kuriyama M, Kato J, Morimoto N, Fujimoto T, Okada H, Yamamoto K. Specific gastroduodenoscopic findings in Crohn’s disease: Comparison with findings in patients with ulcerative colitis and gastroesophageal reflux disease. Dig Liver Dis  2008; 40: 468– 75. Google Scholar CrossRef Search ADS PubMed  2. Oberhuber G, Püspök A, Oesterreicher Cet al.   Focally enhanced gastritis: a frequent type of gastritis in patients with Crohn’s disease. Gastroenterology  1997; 112: 698– 706. Google Scholar CrossRef Search ADS PubMed  3. Sonnenberg A, Melton SD, Genta RM. Frequent occurrence of gastritis and duodenitis in patients with inflammatory bowel disease. Inflamm Bowel Dis  2011; 17: 39– 44. Google Scholar CrossRef Search ADS PubMed  4. Annunziata ML, Caviglia R, Papparella LG, Cicala M. Upper gastrointestinal involvement of Crohn’s disease: a prospective study on the role of upper endoscopy in the diagnostic work-up. Dig Dis Sci  2012; 57: 1618– 23. Google Scholar CrossRef Search ADS PubMed  Copyright © 2017 European Crohn’s and Colitis Organisation (ECCO). Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Crohn's and Colitis Oxford University Press

Gastric Subepithelial Mass-like Involvement in Crohn’s Disease: Another Upper Gastrointestinal Manifestation?

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Publisher
Elsevier Science
Copyright
Copyright © 2017 European Crohn’s and Colitis Organisation (ECCO). Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com
ISSN
1873-9946
eISSN
1876-4479
D.O.I.
10.1093/ecco-jcc/jjx127
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Abstract

A 55-year-old woman was referred for investigation of a gastric subepithelial lesion diagnosed incidentally during endoscopy. The patient had a 2-month history of abdominal pain, and a past medical history included hypothyroidism. Upper endoscopy revealed a 3-cm sized subepithelial lesion located in the gastric corpus, with superficial erosions due to biopsies performed during the first endoscopic examination [Figure 1A]. The lesion was firm and not indented when pressed with a biopsy forceps. Endoscopic ultrasound confirmed the presence of a 30-mm to 15-mm sized, ovoid, hypoechoic mass lesion involving the third (submucosa) and fourth (muscularis propria) endosonographic layers with ill-defined borders. Internal structure was not homogeneous, with more hypo- and hyper-echoic areas [Figure 1B]. Histological examination of endoscopic bite-on-bite biopsies showed focal chronic inflammation with abundant eosinophils and granulocytic infiltration. There were collections of epitheloid histiocytes forming ill-defined granulomas without acid-fast bacilli [Figure 1A, inset]. No Helicobacter pylori (Hp) were identified. Figure 1. View largeDownload slide A. Endoscopy showing subepithelial lesion. Inset; histopathological image [haematoxylin and eosin stain, x 100] showing lymphocytic infiltration with eosinophils and collections of epithelioid histiocytes forming ill-defined granulomas [arrowheads]. B. Radial endoscopic ultrasound image showing hypoechoic subepithelial lesion involving the third and fourth [asterisk] layers. Intact first [arrow] and second [double arrows] layers. C. Transabdominal ultrasound image showing subepithelial lesion [Lx] in the gastric corpus (first [arrow], second [double arrows], and fourth [asterisk] layers). D. Endoscopic view after treatment. Figure 1. View largeDownload slide A. Endoscopy showing subepithelial lesion. Inset; histopathological image [haematoxylin and eosin stain, x 100] showing lymphocytic infiltration with eosinophils and collections of epithelioid histiocytes forming ill-defined granulomas [arrowheads]. B. Radial endoscopic ultrasound image showing hypoechoic subepithelial lesion involving the third and fourth [asterisk] layers. Intact first [arrow] and second [double arrows] layers. C. Transabdominal ultrasound image showing subepithelial lesion [Lx] in the gastric corpus (first [arrow], second [double arrows], and fourth [asterisk] layers). D. Endoscopic view after treatment. Although inflammation had attacked the mucosa, the superficial epithelial lining was protected in most parts, compatible with the subepithelial nature of the involvement. It was also possible to identify the subepithelial lesion by abdominal ultrasound [Figure 1C, supplementary video]. Ileocolonoscopy revealed diffuse ileitis with ulcerations, and apthous ulcers with skip hyperaemic areas throughout the colon. Histopathological examination of ileocolonoscopic biopsies was consistent with Crohn’s disease (CD). Mycobacterium tuberculosis polymerase chain reaction assay and culture of mucosal biopsies were negative. Computed tomography of the chest was unremarkable, and a Quantiferon test was negative. Pantoprazole, azathiopurine, and prednisolone treatment was initiated. Four months after the initiation of treatment, no significant change was observed at upper endoscopy or ileocolonoscopy. Azathiopurine treatment ceased because of persistent leukopenia even with dose reduction, and adalimumab (ADA) monotherapy started (160/80 induction 2 weeks apart, then 40 mg subcutaneously every other week). Gastric lesions regressed considerably after remission induction with ADA. After the first year of treatment (trough serum ADA level 7.7 µg/ml), endoscopic evaluation revealed complete healing of the subepithelial lesion, leaving an atrophic mucosa [Figure 1D]. Upper endoscopy has revealed at least one of the specific endoscopic findings in up to 75% of CD patients, according to the recent literature.1 Microscopic findings such as Hp-negative focally active gastritis and/or granulomas have been reported between 30% and 76% of cases.2–4 To the best of the authors’ knowledge, gastric subepithelial mass-like involvement has so far not been identified in CD. This involvement pattern, probably is a rare presentation of the transmural nature of the disease. Also, data regarding the effect of anti-TNF treatment on mucosal healing of upper gastrointestinal lesions are scarce. ADA treatment resulted in complete endoscopic mucosal healing and regression of the submucosal involvement in our case. Subepithelial lesion-like involvement should be considered in the wide armamenterium of upper gastrointestinal CD manifestations. Funding No specific funding has been received for this study. Data have not been generated as part of the routine work of an organisation. Confict of Interest None. Author Contributions CG: data collection, literature search, writing the manuscript, figure preparation. SO: data collection, figure preparation, critical review of the manuscript. Both authors had full access to all the data in the study and had final responsibility for the decision to submit for publication. Supplementary Data Supplementary data are available at ECCO-JCC online. References 1. Kuriyama M, Kato J, Morimoto N, Fujimoto T, Okada H, Yamamoto K. Specific gastroduodenoscopic findings in Crohn’s disease: Comparison with findings in patients with ulcerative colitis and gastroesophageal reflux disease. Dig Liver Dis  2008; 40: 468– 75. Google Scholar CrossRef Search ADS PubMed  2. Oberhuber G, Püspök A, Oesterreicher Cet al.   Focally enhanced gastritis: a frequent type of gastritis in patients with Crohn’s disease. Gastroenterology  1997; 112: 698– 706. Google Scholar CrossRef Search ADS PubMed  3. Sonnenberg A, Melton SD, Genta RM. Frequent occurrence of gastritis and duodenitis in patients with inflammatory bowel disease. Inflamm Bowel Dis  2011; 17: 39– 44. Google Scholar CrossRef Search ADS PubMed  4. Annunziata ML, Caviglia R, Papparella LG, Cicala M. Upper gastrointestinal involvement of Crohn’s disease: a prospective study on the role of upper endoscopy in the diagnostic work-up. Dig Dis Sci  2012; 57: 1618– 23. Google Scholar CrossRef Search ADS PubMed  Copyright © 2017 European Crohn’s and Colitis Organisation (ECCO). Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com

Journal

Journal of Crohn's and ColitisOxford University Press

Published: Feb 1, 2018

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