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    • br Results Patients with AISC were significantly younger tha

    2018-11-13


    Results Patients with AISC were significantly younger than those with PSC and IBD (Table 1). Immunosuppressants and ursodeoxycholic PalMitoyl Tripeptide-1 were commonly used in the liver patients, but not in the IBD groups, but otherwise the demographic details of patients with AISC and PSC at the time of study did not differ significantly.
    Discussion This study shows that patients with AISC have a colitis that is indistinguishable from that seen in patients of PSC, which, by convention, represents UC (Saich and Chapman, 2008; Loftus et al., 2005). Certain clinical and histopathology aspects of the disease conform to what is already described, however, we have also demonstrated that over a third of patients with AISC have small bowel findings similar to that seen in CD. Thus, placing these colitides under the umbrella of UC may need revision. In this report, all patients with AISC and PSC had initially been diagnosed with liver disease prior to the diagnosis of colitis. The colonoscopic and histopathologic features of the colitis associated with AISC and PSC conforms to that already described (Saich and Chapman, 2008; Loftus et al., 2005). As colonoscopies were carried out at varying times and prior to this study it is not possible to correlate the functional (calprotectin) and morphological (colonic biopsies) inflammatory activity in these patients. Most studies show a good correlation between levels of faecal calprotectin and intestinal inflammation in patients with UC (Roseth et al., 1999; Schoepfer et al., 2009; Sipponen et al., 2008a) and somewhat more variable, albeit significant, in CD (Sipponen et al., 2008b; D\'Incà et al., 2007; Costa et al., 2003; Vieira et al., 2009). The histopathology features in the colitis associated with AISC and PSC are less severe than in classical IBD, yet, these patients have comparable levels of intestinal inflammation as assessed by faecal calprotectin. This apparent discrepancy may be due to the fact that the inflammation was predominantly right sided in AISC and PSC and thus not associated with the common symptoms of proctitis, evident in patients with classic ulcerative colitis, and they may hence have been ‘undertreated’. Furthermore histology represents a static picture whereas faecal calprotectin levels represent the total flux of neutrophils entering the bowel over time. The speed by which neutrophils pass through the colonic mucosa differs from disease to disease depending on the site of the principal neutrophil chemoattractant (Teahon and Bjarnason, 1993), and if particularly rapid may not be so evident on biopsy. A most significant finding is that of approximately one third of the patients with AISC having mucosal breaks on capsule enteroscopy. A possible confounding factor, however, is that these patients were frequently on immunosuppressive agents that have been implicated in small bowel damage (Gabe et al., 1998; Bjarnason et al., 2004; 2006), although if this was the case then this should have been equally evident in PSC as they were receiving the same drugs. Capsule enteroscopy images of mucosal breaks (erosions and ulcers) are not pathognomonic for any disease and have numerous causes including use of NSAIDs, cocaine, certain chemotherapeutic agents and are also described in patients with HIV, CD, Behçet\'s syndrome, spondyloarthropathy and radiation enteropathy (Bjarnason et al., 2006; Oette et al., 2009). Most of these can be and were excluded as a cause for the small bowel findings in AISC. Mucosal breaks are not seen in small bowel bacterial overgrowth, but bacterial overgrowth and or immunosuppressant drugs could be responsible for the mild small intestinal inflammatory changes seen in some patients with AISC and PSC. The combination of colitis and small bowel mucosal breaks in the patients with AISC might represent CD. However, it is unusual to see histopathological changes consistent with UC in Crohn\'s disease of the small bowel. There is a case report of 4 patients with well established pan-ulcerative colitis that had problematic diffuse upper small bowel inflammation (Valdez et al., 2000) but this inflammation seems to be somewhat different in location to the damage we observed at capsule enterosocpy and it is otherwise firmly accepted that patients with ulcerative have the disease confined to the large bowel. Small bowel CD frequently progresses to structuring requiring surgery, something which is not in evidence clinically (Gregorio et al., 2001) nor as evidenced by the capsule enteroscopy results in AISC.