IBD and its Mimics

It is important to differentiate features of IBD from mimics, especially regarding whether they are features of chronicity or not. Those in which there are no histological features of chronicity could be seen in etiologies like infective, transient and antibiotic-related-type colitides. Those which may exhibit features of chronicity include ischemia, radiation and diversion colitides.

It is also important to realise that in the event of having a series of biopsies in a patient with active disease but no features of chronicity, we recommend another series of biopsies in 6-weeks time because most of the infective colitides or other causes of active disease will revert back to normal, whereas IBD in the early stage of evolution may not. It is also important to appreciate that patients with chronic IBD may not have histological features of chronicity; in this instance the pathologist should not exclude such a diagnosis.

Endoscopic biopsy plays an important role in the diagnosis of infective type colitis, because in a high number of cases the causative organism is not found [98]. This is called transient or self-limiting colitis. Diagnosis of infective colitis depends heavily on the absence of features seen in IBD, especially absence of architectural distortion and a diffuse increase in inflammatory cells. Architectural distortion, together with transmural increase in lamina propria cellulari-ty and epithelial changes, are more common in IBD than infective type colitis. On the other hand, preservation of crypt architecture, superficial increase in lamina propria cellularity with neutrophil infiltration is suggestive of infective etiology [54]. Some forms of chronic intestinal infection, e.g. shigellosis, amoebia-sis and yersinia may resemble features seen in IBD [99].

In the first attack of IBD, the distinction from infective-type colitis is difficult and features depend on the timing of diseases [61]. Florid neutrophilic infiltrate is characteristically seen in the first 2 weeks of infective colitis [100, 40]. Even poorly formed microgranulomas can be seen in certain infections like salmonella [101]. The most useful histological features of infective colitis on endoscopic biopsy are the predominance of acute over chronic inflammation, lack of crypt distortion and the occurrence of oedema and neutrophil polymorph infiltration within the lamina propria and the crypt epithelium rather than the lumen [102, 74].

Drugs, especially non-steroidal anti-inflammatory drugs (NSAIDs), have also been known to cause colitis, the features of which can be confused with IBD, and the elderly seem to be at a higher risk [102]. Thus a drug history is mandatory when investigating patients with suspected IBD. Non-steroidal anti-inflammatory drugs (NSAIDs) can cause small-intestinal ulceration together with mucosal inflammation and colonic ulcerations. Other drugs such as methyl-dopa and gold treatment can also be complicated by colitis [103-106]. Colitis associated with diverticular disease of the sigmoid is a well-recognised feature and can be mistaken for features of IBD. Mucosal biopsies from an area of inflammation associated with diverticular disease may show features of crypt distortion, basal plasmacytosis, cryptitis and even crypt abscesses [107]. CD-like changes in the sigmoid of a patient with diverticular disease are an idiosyncratic inflammatory response to the diverticulosis rather than to coexistent CD. Pathologists should be wary of making the diagnosis of sigmoid CD in the context of diverticular disease unless there is CD in other parts of the bowel [108].

Microscopic colitis (collagenous and lymphocytic) are characterised by distinct histological and clinical presentation and should not ideally be confused with changes seen in IBD. However, lymphocytic and collagenous colitis patterns of injury preceded the eventual clinical diagnosis of CD in one study [109].

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