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equires full-thickness biopsy due to an inability to detect ty�ical histological findings �ith conventional endosco�ic biopsy [6] . Therapy in children is supportive and includes adequate hydration, antisecretory agents (histamine 2 receptor antagonists and proton pump inhibitors) and albumin replacement [3-5] . Treatment of CMV, when detected, is usually associated with remission [7,8] . Interestingly, transforming growth factor α, one of the ligands for the epidermal growth factor receptor (EGF-R), has been implicated in the mechanisms underlying MD [14] : it causes dose-de�endent in vitro proliferation of gastric epithelial cells and reduction of acid secretion, which are hallmarks of the disease [15,16] . Treatment with an experimental monoclonal antibody against EGF-R has been successful in 3 severe MD cases [17,18] . There is also evidence that somatostatin decreases the number of EGF binding sites at the cell surface [19] ; thus, octreotide may modulate EGF-R signalling at several levels [20,21] . These mechanisms and preliminary reports on successful use of octreotide in adults with MD [9-13] prompted us to use this agent in our patient. In conclusion, we describe an uncommon case of pediatric MD with atypical presentation (only anemia) and chronic unremitting course. MD should be considered in all children with thickened gastric folds at endoscopy, even in the absence of typical clinical and laboratory manifestations. EMR is a good alternative to full thickness biopsy for diagnosing disorders associated with gastric wall thickening such as MD. To the best o�� our �no�ledge�� this is the first �ediatric MD case successfully treated with octreotide LAR. Our experience suggests octreotide LAR as treatment for refractory MD before gastrectomy. REFERENCES 1 Lee EL, Feldman M. Gastritis and Gastropathies. In: Feld- Feldman M, Friedman LS, Brandt LJ. �ditors. �ditors. Feldman: Sleisen- Sleisen- ger and Fordtran's Gastrointestinal and Liver Disease. . 8th ed. Philadelphia: : Saunders; ; 200�: 200�: 200�: 200�: 200�: 10�8-1083 10�8-1083 10�8-1083 10�8-1083 10�8-1083 2 Sundt TM, Compton CC, Malt RA. Ménétrier’s disease. A trivalent gastropathy. Ann Surg 1988; 208: �94-701 3 Scharschmidt BF. �he �he natural history o�� o�� hypertrophic gasgastrophy (Menetrier’s disease). Report o�� a case with 1� year ��ollow-up and review o�� 120 cases ��rom the literature. Am J Med 1977; 63: �44-�52 4 Wolfsen HC, Carpenter HA, �alley NJ. Menetrier’s disease: a ��orm o�� hypertrophic gastropathy or gastritis? Gastroenterology 1993; 104: 1310-1319 5 Blackstone MM, Mittal MK. �he edematous toddler: a case o�� pediatric Ménétrier disease. Pediatr Emerg Care 2008; 24: �82-�84 � Gleeson FC, Mangan �F, Levy MJ. �ndoscopic �ndoscopic ultrasound WJG|www.wjgnet.com Di Nardo G et al . Octreotide in pediatric Menetrier's disease and endoscopic mucosal resection ��eatures o�� a non-protein losing ��orm o�� Ménétrier’s disease. Clin Gastroenterol Hepatol 2008; 6: e24-e25 7 Eisenstat DD, Gri��iths AM, Cutz �, Petric M, Drumm B. Acute cytomegalovirus in��ection in a child with Ménétrier’s disease. Gastroenterology 1995; 109: 592-595 8 Xiao SY, Hart J. Marked gastric ��oveolar hyperplasia associated with active cytomegalovirus in��ection. Am J Gastroenterol 2001; 96: 223-22� 9 Yeaton P, Frierson HF. Octreotide reduces enteral protein losses in Ménétrier’s disease. Am J Gastroenterol 1993; 88: 95-98 10 Ojeda E, Ruiz J, Cosme A, Lobo C. [Menetrier disease associated with ulcerative colitis. Response to the treatment with octreotide. Review o�� the diagnostic criteria and etiopathogenesis]. Gastroenterol Hepatol 1997; 20: 175-179 11 Green BT, Branch MS. Menetrier’s disease treated with octreotide long-acting release. Gastrointest Endosc 2004; 60: 1028-1029 12 Gadour MO, Salman AH, �l Samman el �el W, �adros NM. Menetrier’s disease: an excellent response to octreotide. A case report ��rom the Middle �ast. Trop Gastroenterol 2005; 26: 129-131 13 Rothenberg M, Pai R, Stuart K. Success��ul use o�� octreotide to treat Ménétrier’s disease: a rare cause o�� abdominal pain, weight loss, edema, and hypoalbuminemia. Dig Dis Sci 2009; 54: 1403-1407 14 Nalle SC, �urner JR. Menetrier’s disease therapy: rebooting mucosal signaling. Sci Transl Med 2009; 1: 8ps10 15 Dempsey PJ, Goldenring JR, Soroka CJ, Modlin IM, Mc- Clure RW, Lind CD, Ahlquist DA, Pittelkow MR, Lee DC, Sandgren �P. Possible role o�� trans��orming growth ��actor alpha in the pathogenesis o�� Ménétrier’s disease: supportive evidence ��orm humans and transgenic mice. Gastroenterology 1992; 103: 1950-19�3 1� Takagi H, Jhappan C, Sharp R, Merlino G. Hypertrophic gastropathy resembling Ménétrier’s disease in transgenic mice overexpressing trans��orming growth ��actor alpha in the stomach. J Clin Invest 1992; 90: 11�1-11�7 17 Burdick JS, Chung �, �anner G, Sun M, Paciga J�, Cheng JQ, Washington K, Goldenring JR, Co��ey RJ. �reatment o�� Ménétrier’s disease with a monoclonal antibody against the epidermal growth ��actor receptor. N Engl J Med 2000; 343: 1�97-1701 18 Settle SH, Washington K, Lind C, Itzkowitz S, Fiske WH, Burdick JS, Jerome WG, Ray M, Weinstein W, Co��ey RJ. Chronic treatment o�� Ménétrier’s disease with �rbitux: clinical efficacy and insight into pathophysiology. Clin Gastroenterol Hepatol 2005; 3: �54-�59 19 Pinski J, Halmos G, Schally AV. Somatostatin analog RC-1�0 and bombesin/gastrin-releasing peptide antagonist RC-3095 inhibit the growth o�� androgen-independent DU-145 human prostate cancer line in nude mice. Cancer Lett 1993; 71: 189-19� 20 Lahlou H, Guillermet J, Hortala M, Vernejoul F, Pyronnet S, Bousquet C, Susini C. Molecular signaling o�� somatostatin receptors. Ann N Y Acad Sci 2004; 1014: 121-131 21 Watt HL, Kharmate GD, Kumar U. Somatostatin receptors 1 and 5 heterodimerize with epidermal growth ��actor receptor: agonist-dependent modulation o�� the downstream MAPK signalling pathway in breast cancer cells. Cell Signal 2009; 21: 428-439 S- Editor Shi ZF L- Editor O’Neill M E- Editor Xiong L 2729 June 7, 2012|Volume 18|Issue 21|
Online Submissions: http://www.wjgnet.com/1007-9327office wjg@wjgnet.com doi:10.3748/wjg.v18.i21.2730 World J Gastroenterol 2012 June 7; 18(21): 2730-2734 ISSN 1007-9327 (print) ISSN 2219-2840 (online) © 2012 Baishideng. All rights reserved. Infliximab stopped severe gastrointestinal bleeding in Crohn's disease CASE REPORT Satimai Aniwan, Surasak Eakpongpaisit, Boonlert Imraporn, Surachai Amornsawadwatana, Rungsun Rerknimitr Satimai Aniwan, Boonlert Imraporn, Surachai Amornsawadwatana, Rungsun Rerknimitr, Division of Gastroenterology, Department of Medicine, King Chulalongkorn Memorial Hosptial, Bangkok 10330, Thailand Surasak Eakpongpaisit, Institute of Liver and Gastrointestinal Diseases, Samitivej Hospital, Bangkok 10330, Thailand Author contributions: Aniwan S and Reknimitr R carried out the studies, performed data analyses and drafted the manuscript; Eakpongpaisit S, Imraporn B and Amornsawadwatana S collected data and carried out the sample analyses; all authors read and approved the final manuscript. Correspondence to: Rungsun Reknimitr, MD, Division of Gastroenterology, Department of Medicine, King Chulalongkorn Memorial Hosptial, Bangkok 10330, Thailand. rungsun@pol.net Telephone: +66-2-2564356 Fax: +66-2-2527839 Received: November 7, 2011 Revised: February 20, 2012 Accepted: February 26, 2012 Published online: June 7, 2012 Abstract To report the result of rapid ulcer healing by infliximab in Crohn’s patients with severe enterocolic bleeding. During 2005 and 2010, inflammatory bowel disease database of King Chulalongkorn Memorial and Samitivej hospitals were reviewed. There were seven Crohn’s disease (CD) patients (4 women and 3 men; mean age 52 ± 10.4 years; range: 1186 years). Two of the seven patients developed severe gastrointestinal bleeding (GIB) as a flare up of CD whereas the other five patients presented with GIB as their first symptom for CD. Their mean hemoglobin level dropped from 12 ± 1.3 g/ dL to 8.7 ± 1.3 g/dL in a 3d period. Median packed red blood cells units needed for resuscitation was 4 units. Because of uncontrolled bleeding, surgical resection was considered. However, due to the poor surgical candidacy of these patients (n = 3) and /or possible development of short bowel syndrome (n = 6), surgery was not pursued. Likewise angiographic embolization was not considered in any due to the risk of large infarction. All WJG|www.wjgnet.com severe GIBs successfully stopped by one or two doses of intravenous infliximab. Our data suggests that infliximab is an alternative therapy for CD with severe GIB when surgery has limitation or patient is a high risk. © 2012 Baishideng. All rights reserved. Key words: Crohn’s disease; Gastrointestinal bleeding; Complications; Infliximab; Biologic agents Peer reviewer: Andrew M Veitch, MD, MRCP, Department of Gastroenetrology, Royal Wolverhampton Hospitals NHS Trust, New Cross Hospital, Wednedfield Road, Wolverhampton TF11 8HG, United Kingdom Aniwan S, Eakpongpaisit S, Imraporn B, Amornsawadwatana S, Rerknimitr R. Infliximab stopped severe gastrointestinal bleeding in Crohn’s disease. World J Gastroenterol 2012; 18(21): 2730-2734 Available from: URL: http://www.wjgnet.com/1007-9327/full/v18/ i21/2730.htm DOI: http://dx.doi.org/10.3748/wjg.v18.i21.2730 INTRODUCTION Although severe gastrointestinal bleeding (GIB) is an uncommon complication of inflammatory bowel disease (IBD), severe GIB occurs in 0.1% of ulcerative colitis [1] and 1.2%1.3% of Crohn’s disease (CD) [1,2] . This in turn sometimes progresses to a potential lifethreatening condition. Approximately one third of CD patients developed GIB as a flare up and another one fourth of CD patients presented with GIB as an initial symptom [3] . Bleeding sources were mostly found in the colon (50%85%) and the small bowel (15%50%). Unfortunately, one third of CD related GIBs were severe and surgery was required because of refractory bleeding especially after failed conventional medical and endoscopic treatment [1,3] . Therefore treatment for severe hemorrhage in IBD remains a challenge. Recently, there has been only a handful of case reports of severe CD related GIB controlled with tumor 2730 June 7, 2012|Volume 18|Issue 21|
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World Journal of Gastroenterology W
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Phillip S Oates, Perth Ross C Smith
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Deepak N Amarapurkar, Mumbai Abhiji
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Trine Olsen, Tromsø Eyvind J Pauls
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Conor P Delaney, Cleveland Sharon D
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S Contents EDITORIAL FIELD OF VISIO
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Contents ACKNOWLEDGMENTS APPENDIX A
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Cereda S et al . Adjuvant treatment
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DM, Sterling RK, Shiffman M, Topaz
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Selinger CP et al . Pregnancy relat
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Ilan Y. Bacterial translocation in
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Ettreiki C et al . Iron prevents co
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A Macroscopir damage scores (AU) 7.
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A Total flora 12.5 B Log copy numbe
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Ettreiki C et al . Iron prevents co
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Online Submissions: http://www.wjgn
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A Fold changes over untreated cells
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A Migration Invasion B Migration In
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A miR-95 B Li WG et al �� Glarg
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Key words: Colorectal cancer; Niger
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A HT29 cells 100 C SW116 cells 40 P
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A B Ecadherin Vimentin GAPDH Zhou H
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Zhou HM et al �� Nigericin and
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Terzin V et al . Serum IgG4 in auto
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Terzin V et al . Serum IgG4 in auto
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Min YW et al . Sub-centimeter-sized
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Park CH et al . Family history and
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Page 103 and 104: Yang YJ et al . H. pylori eradicati
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Page 107 and 108: Chen JG et al . Colorectal cancer s
Page 109 and 110: Chen JG et al . Colorectal cancer s
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Page 120: primary liver cancer and one of the
Page 123 and 124: A A 490 Li YH et al . GABRQ in HCC
Page 125 and 126: Li YH et al . GABRQ in HCC prostate
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Page 133 and 134: Shen Y et al . PTEN and cetuximab e
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Page 137 and 138: Relative expression 10 8 6 4 2 0 1.
Page 139 and 140: E Methylation (%) F Methylation (%)
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Page 143: Di Nardo G et al . Octreotide in pe
Page 147 and 148: A B Aniwan S et al . Infliximab for
Page 149 and 150: Aniwan S et al . Infliximab for CD
Page 151 and 152: Nishizawa T et al . Dual therapy fo
Page 153 and 154: Nishizawa T et al . Dual therapy fo
Page 157 and 158: Instructions to authors ISSN and EI
Page 159 and 160: Instructions to authors AIM (no mor
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