Towards a new paradigm of microscopic colitis: Incomplete and variant forms

Abstract

Microscopic colitis (MC) is a chronic inflammatory bowel disease that has emerged in the last three decades as a leading cause of chronic watery diarrhoea. MC classically includes two main subtypes: lymphocytic colitis (LC) and collagenous colitis (CC). Other types of histopathological changes in the colonic mucosa have been described in patients with chronic diarrhoea, without fulfilling the conventional histopathological criteria for MC diagnosis. Whereas those unclassified alterations remained orphan for a long time, the use of the term incomplete MC (MCi) is nowadays universally accepted. However, it is still unresolved whether CC, LC and MCi should be considered as one clinical entity or if they represent three related conditions. In contrast to classical MC, the real epidemiological impact of MCi remains unknown, because only few epidemiological studies and case reports have been described. MCi presents clinical characteristics indistinguishable from complete MC with a good response to budesonide and cholestiramine. Although a number of medical treatments have been assayed in MC patients, currently, there is no causal treatment approach for MC and MCi, and only empirical strategies have been performed. Further studies are needed in order to identify their etiopathogenic mechanisms, and to better classify and treat MC.

Keywords: Collagenous colitis; Incomplete microscopic colitis; Lymphocytic colitis; Microscopic colitis.

Figure 1

Photomicrographs of a colonic specimen from a lymphocytic colitis patient showing inflammatory hypercellularity in the lamina propria of colonic mucosa and clear presence of a greater number of intraepithelial lymphocyte cells. A: Hematoxylin-eosin staining, magnification × 200; B: More evident with the CD3 staining, magnification × 200.

Figure 2

Photomicrographs of a colonic specimen from a collagenous colitis patient showing detachment of superficial epithelium. Hematoxylin-eosin staining, magnification × 100 (A) and thick subepithelial collagen band, Gomori’s Trichrome staining (B and C, magnification × 100, × 400, respectively).

Figure 3

Photomicrographs of a colonic specimen from an incomplete lymphocytic colitis patient. Hematoxylin-eosin staining, magnification × 100 (A) with a mild increase in intraepithelial lymphocytes cells (B, CD3, magnification × 200) and a regular collagen band (C, Gomori’s Trichrome staining, magnification × 400).

Figure 4

Photomicrographs of a colonic specimen from an incomplete collagenous colitis patient. Hematoxylin-eosin staining, magnification × 100 (A) with slight enhancement of subepithelial collagen band (B, Gomori’s Trichrome staining, magnification × 200) without increased intraepithelial lymphocyte cells infiltration (C, CD3 inmunostaining, magnification × 200).

Figure 5

Photomicrographs of a colonic specimen from a cryptal lymphocytic colitis patient. Hematoxylin-eosin staining, magnification × 100 (A) showing only the presence of cryptal lymphocytosis (B, CD3, magnification × 200) and lack of intraepithelial lymphocytosis (C, CD3, magnification × 200).

Figure 6

Photomicrographs of a colonic specimen from a healthy donor. Hematoxylin-eosin staining, magnification × 100 (A) showing low number (usually less than 5) of intraepithelial lymphocyte cells, which can be easily identified by CD3 immunohistochemistry marker (B, magnification × 100). The subepithelial collagen band is tiny and regular (C, Gomori’s Trichrome staining, magnification × 10 and inset, Gomori’s Trichrome staining, magnification × 400).