Collagenous colitis was first described more than three decades previously in middle-age to elderly women experiencing watery diarrhea (1
). Since then, the epidemiology and clinical features of this entity have been detailed, the pathogenesis and histopathological features noted, and its outcome, complications and treatment described (3
). Most often, the colonic mucosa is variably described by the endoscopist as normal or minimally altered; however, these changes are not specific. Some clinicians have reported submucosal dissection and colonic ‘fracturing’ after instrumentation or air insufflation during endoscopy, believed to be caused by a compromised colonic wall from collagen deposition (4
), but it is not known whether these unusual endoscopic findings are specific for collagenous colitis per se. Pathological changes may be distributed uniformally throughout the colon, but in some cases, changes are patchy or discontinuous (6
Detection of collagenous colitis with giant cells is rare, largely limited to the histopathological literature (7
). In these reports, endoscopic findings were either normal or nonspecifically abnormal, with erythematous or ‘edematous’ mucosa. Biopsies of the sessile, carpet-like lesion showed the unanticipated pathological changes of an atypical form of collagenous colitis with giant cells. No adenomatous (dysplastic) epithelium was present. In retrospect, despite its extensive nature, the macroscopic lesion observed would not require colonoscopic or surgical removal. Indeed, even pharmacological treatment aimed at resolution of her symptoms was not necessary. The endoscopic findings noted here, however, add to previous endoscopic changes reported in collagenous colitis and extend the differential diagnosis of non-neoplastic sessile polypoid lesions.
The precise cause of the histopathological finding detected in this particular patient remains elusive. Infectious causes were excluded and, clearly, the clinical findings were not consistent with an entity such as Crohn’s disease. The location of these giant cells within the mucosa was primarily in the subepithelial region, believed by others (7
) to reflect fusion of subepithelial macrophages. It is intriguing that this is precisely the same subepithelial site as the collagen deposits in collagenous colitis. Further studies are needed to determine the possibly important role, if any, of these subepithelial multinucleated giant cells in the immunopathogenesis of the subepithelial collagen band deposits in collagenous colitis.