The Little Beast That Pretended to Be a Severe Crohn's Disease

Abstract

Question: A 49-yearold woman attended our unit with progressive abdominal pain that progressively worsened over a period of several months, accompanied by chronic diarrhea with 3-4 stools per day, without rectal bleeding. She had no personal or family history of digestive disease and she had travelled to Vietnam and to India 3 and 10 years ago, respectively. Blood testing revealed moderate biological inflammatory syndrome (C-reactive protein levels ranging from 10 to 15 mg/L). Bacterologic stool examinations, Clostridium difficile testing and parasitological stool examinations were all negative for 3 days in a row. A first ileocolonoscopy was carried out and revealed diffuse involvement of the right and the transverse colon, with multiple ulcers surrounded by sections of healthy mucosa, which was compatible with Crohn's disease (Figure A). Pathologic analysis of the colonic mucosa found ulcerations, neutrophil infiltrates with features of cryptitis, and distortion of the crypts. However, no epithelial or gigantocellular granulomas were observed. Magnetic resonance enterography revealed parietal thickening in the ascending colon, with several nodes of the ileocecal pedicle, and no ileal involvement (Figure B). In light of the possibility of Crohn's disease, corticosteroid therapy was initiated, and it led to a clinical response. Thereafter, the patient developed corticodependency that required the administration of a combination therapy comprising azathioprine and infliximab. The infliximab was optimized at week 10 (10 mg/kg) and then administered every 4 weeks (3 infusions). Despite optimization of the infliximab therapy (therapeutic trough levels [6 mg/mL], no antiinfliximab antibody), clinical remission was not achieved. A second ileocolonoscopy was performed, which provided the same findings as the first colonoscopy. Because there was a clear risk of a primary failure, we decided to switch to vedolizumab. This treatment also failed; however, despite optimization (300 mg every 4 weeks). We consequently introduced ustekinumab (6 mg/kg and then 90 mg every 8 weeks), but corticosteroid therapy was required to induce clinical and biological (C-reactive protein <1 mg/L vs 17 mg/L) responses. The patient then became corticoresistant. After experiencing failures with these treatments and prior to inclusion in a clinical research protocol (filgotinib), she underwent a complete endoscopic checkup. The ileocolonoscopy revealed moderate pancolitis with multiple millimetric ulcerations, without ileal involvement. New biopsies were performed (Figure C). What missed diagnosis was finally revealed by this new pathologic examination? Look on page 1484 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.

CD74 Signaling Links Inflammation to Intestinal Epithelial Cell Regeneration and Promotes Mucosal Healing

“…[16][17][18][19][20][21] Amebic colitis shares similar pathology to IBD, explaining why it often is misdiagnosed as IBD. 22,23 In addition, similar to the IBD and chemically induced colitis, increased CD74 expression also was observed in amebic colitis (Figure 3A and B). During homeostasis, epithelial cells of the large intestine selfrenew every 2-3 days.…”

An atypical cause of right lower abdominal pain: amoebiasis, a family cluster

“…Histopathologic examination of biopsies obtained during colonoscopy reveal the presence of trophozoites or cysts and typical flask-shaped ulcers (3). Since the endoscopic findings may resemble those seen in IBD, differential diagnosis can be difficult (4,5). Distinguishing amoebiasis from IBD is, however, important since the administration of corticosteroids in patients with amoebiasis may result in fulminant disease (12).…”

“…The onset is subacute and patients can present with abdominal pain, bloody or watery and mucus containing diarrhea. A different presentation is chronic intestinal amoebiasis in which patients have periodic complaints for years, mimicking inflammatory bowel disease (IBD) (4,5). Complications of intestinal disease are strictures, rectovaginal fistula, ameboma, perianal skin ulceration, bowel obstruction, toxic megacolon, perforation, peritonitis and death (3,6).…”

Colitis caused by Entamoeba histolytica identified by real-time-PCR and fluorescence in situ hybridization from formalin-fixed, paraffin-embedded tissue

“…Furthermore, the disease is rare in Western industrialized countries, while it is still occasionally imported from tropical sites of endemicity [7]. Therefore, it is likely to be overlooked or, even more dangerous, confused with immunological diseases like the chronic inflammatory diseases (CID) Crohn's disease or ulcerative colitis [6,[8][9][10][11][12][13][14][15][16][17][18][19][20] or even Behçet's disease [21] and carcinoma [22] requiring completely different therapeutic approaches. Enteric tuberculosis, pseudomembranous colitis and even proctitis-associated sexually transmitted infections have been described as potential infectious differential diagnoses as well [23][24][25].…”