Brief Clinical ObservationCollagenous pouchitis
Introduction
Collagenous colitis (CC) is a condition characterised by watery diarrhoea, endoscopically normal colonic mucosa, diffuse histologic colitis with surface epithelial injury, and a distinctive thickening of the subepithelial collagen table at histologic examination. In the normal intestine, collagen type IV, laminin, and fibronectin produced by epithelial cells constitute the normal components of the basal lamina propria [1]. Thickening of basal lamina in CC may be caused by the deposition of type I and III collagens which is produced by fibroblasts [2].
Microscopic colitis, including CC, accounts for 4–13% of patients investigated for chronic diarrhoea [3]. In Europe, CC has an incidence of 0.6–2.3 cases per 100,000 person-years and a prevalence of 10–15.7 cases per 100,000 persons [4], [5]. In the US, the incidence of CC was 6.2 cases per 100,000 person-years as reported in a population-based study in Olmsted County, MN, from 1998 to 2001. In contrast, the incidence of lymphocytic colitis and CC were 6.4 cases per 100,000 person-years and 3.9 cases per 100,000 person-years, respectively, from the same population from 1994 to 1997 [6]. The findings suggest that CC, as well as lymphocytic colitis, has become increasingly recognised.
The aetiology and pathogenesis of CC and the deposition of a subepithelial collagen table are unknown but are thought to be due to a response to chronic injury. Several categories of medicines have been reported to be associated with CC, including non-steroidal anti-inflammatory drugs (NSAIDS) [7], [8], [9], antibiotics [8], lansoprazole [10], ticlopidine [11], and cimetidine [12]. There are several lines of evidence which suggest that CC may be associated with infections or inflammation and an abnormal immune response to luminal antigens [13], [14]. An infectious aetiology was speculated based on findings that acute onset of disease occurred in up to 40% of patients with CC [15]; some of the patients responded to antibiotic therapy [16]; diversion of faecal stream after ileostomy or colostomy placement alleviated symptoms and reduced the thickness of the subepithelial collagen table [14]; the presence of faecal cytotoxins in patients with CC was neutralised by cholestyramine [16]; and there was chronic mucosal inflammation in CC as evidenced by mucosal histology and the presence of faecal leucocytosis [17]. The presence of pseudomembrane in colon biopsy specimens in some patients with CC would also support infection or toxin-related aetiology [14]. The subepithelial collagen deposition along the GI tract was reported in patients with infection from Helicobacter pylori [19], HIV [20], Yersinia enterocolitica [21], [22], and Clostridium difficile infection [23]. Besides the faecal diversion models [14], there is no human model which could duplicate the clinical and histopathologic pattern of CC.
While the majority of patients with CC respond to medical therapy, some may develop a clinically refractory course, which then requires surgical intervention. Reported surgical treatment modalities include subtotal colectomy [24], hemicolectomy [25], and ileostomy or colostomy [14]. There have been case reports of ileal pouch-anal anastomosis (IPAA) following total proctocolectomy [14], [26], [27]. The role of IPAA in the treatment of refractory CC has not been established. However, faecal stasis, bacterial overload, and colonic metaplasia in IPAA would render such a surgery a unique model by which one could study the aetiology and pathogenesis of CC.
Section snippets
Case report
A 58-year-old Caucasian female presented with IPAA dysfunction and diarrhoea. She had suffered from chronic diarrhoea for years and was diagnosed with irritable bowel syndrome at age 20. At age 44, she was diagnosed as having CC with histologic features diffusely involving the colon and rectum. Upper endoscopies and small bowel biopsies showed no evidence of coeliac disease or collagenous enteritis. She was treated with a variety of medicines, including bismuth subsalicylate,
Discussion
The aetiology and pathogenesis of CC are not known. Previous studies have suggested that CC may be associated with infections or inflammation and abnormal immune response to luminal antigens [13], [14], [16], [17], [18], [19], [20], [21], [22], [23]. In this case with CC, we sequentially evaluated the colon and small bowel histology before, during, and after the proctocolectomy and IPAA. The histologic changes of CC were only found in biopsy and resection specimens of the colon and rectum, thus
Conflict of interest statement
None declared.
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2018, Human PathologyCitation Excerpt :Familial cases of microscopic colitis also have been described, suggesting a genetic predisposition in a subset of patients with this condition [26,27]. Thickened subepithelial collagenous deposits and IELs have been previously described in unusual settings, such as in pouches and afferent limbs status post-IPAA [14,19]. The authors postulated that these histologic changes may represent a response to altered bacterial flora and fecal stasis.
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2013, Journal of Crohn's and ColitisCitation Excerpt :Routine pouchoscopy after clinical remission is not required [EL5, RG D] The clinical history and biopsies help discriminate between pouchitis, ischaemia, Crohn's disease (CD) and other rare forms of pouch dysfunction such as collagenous pouchitis, Clostridium difficile or cytomegalovirus pouchitis.28–30 Secondary pouchitis, caused by pelvic sepsis, usually causes focal inflammation and should be considered.