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Differential Diagnosis of Inflammatory Bowel Disease
Geeta Malkan-Billa
 

Inflammatory bowel disease encompasses two distinct diseases: ulcerative colitis and Crohn’s disease. Given the chronic nature of these illnesses along with long term requirement of immunomodulatory or immunosuppressive therapy for their management it is important to differentiate them from other gastrointestinal diseases.

Crohn’s disease is a disorder of uncertain aetiology that is characterized by transmural mucosal inflammation. The transmural inflammation often leads to fibrosis and to obstructive clinical presentations which are not typically seen in ulcerative colitis; sinus tracts that burrow through and penetrate the serosa, giving rise to microperforations and fistulae, may also be seen. Crohn’s disease may involve the entire gastrointestinal tract from mouth to perianal area.

There is an extensive differential diagnosis associated with Crohn’s disease that varies with the site of involvement and the chronicity of the clinical presentation. In many patients, for example, the early symptoms of Crohn’s disease are mild and nonspecific. A diagnosis of lactose intolerance or irritable bowel syndrome is often made initially in this setting with subsequent studies revealing the underlying diagnosis of Crohn’s disease.

When Crohn’s disease involves the colon, it must be distinguished from ulcerative colitis since both the medical and surgical therapies of these disorders can differ. Several findings are suggestive of Crohn’s disease in this setting:

  • Involvement of the small bowel (which excludes ulcerative colitis)
  • Sparing of the rectum
  • Absence of gross bleeding
  • Presence of bothersome perianal disease
  • Focality of gross and microscopic lesions, the presence of granulomas, or the occurrence of fistulae.

In the 10 to 15 per cent of patients with inflammatory bowel disease involving only the colon, Crohn’s disease cannot be distinguished from ulcerative colitis and a diagnosis of indeterminant colitis is made.

In patients presenting acutely with the new onset of symptoms, infections including Shigella, Salmonella, Campylobacter, E coli 0157:H, and amebiasis should be excluded. Clostridium difficile infection should be suspected in patients recently treated with antibiotics and, in immunocompromised patients, cytomegalovirus infection can mimic Crohn’s disease. One fresh stool sample for these agents should be obtained in most patients; in addition, tissue endoscopic biopsies should be analyzed in immunocompromised patients.

Because of the segmental nature of Crohn’s disease, appendicitis, diverticulitis, diverticular colitis, ischemic colitis, and a perforating or obstructing carcinoma can all mimic the clinical presentation of Crohn’s disease.

In patients with primarily small bowel involvement, Yersinia can cause an acute ileitis indistinguishable clinically from acute Crohn’s ileitis. Both tuberculosis and amoebiasis can mimic Crohn’s disease of the ileum and caecum, while lymphoma, chronic ischaemia, endometriosis, and carcinoid can all give a radiologic and clinical picture easily confused with Crohn’s disease of the small bowel.

Ulcerative colitis is characterized by recurring episodes of inflammation limited to the mucosal layer of the colon. It almost invariably involves the rectum and may extend in a proximal and continuous fashion to involve other portions of the colon.

The clinical presentation is not specific to ulcerative colitis, and may be seen in a number of other entities including Crohn’s disease, radiation colitis, ischaemic colitis, a variety of infectious processes (Table 1), and colitis related to medications. It is particularly important at initial presentation and during major exacerbations to rule out an infectious disease, such as Salmonella, Shigella, Campylobacter, Aeromonas, Escherichia coli 0157:H7 and sexually transmitted diseases in patients with proctitis. In addition, previous antibiotic therapy may cause Clostridium difficile colitis. This disorder can mimic ulcerative colitis although gross rectal bleeding is not common.

Other disorders that need to be considered vary with the clinical setting, which may be suggested by histologic findings. In the immunocompromised patient, both cytomegalovirus and Kaposi’s sarcoma can mimic ulcerative colitis.

Certain drugs can cause similar symptoms, particularly the nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs can also exacerbate underlying IBD, although some patients appear to be able to tolerate them.

Other drugs that may cause a clinical picture resembling inflammatory bowel disease include retinoic acid, gold, and possibly oral contraceptives. The literature is sufficiently confused with regard to the effects of oral contraceptives; stopping the pill in every woman who develops inflammatory bowel disease is not justified.

Table 1 : Infections mimies of ulcerative colitis

Penicillin-induced segmental haemorrhagic colitis is a rare cause of bloody diarrhoea. Symptoms typically develop within three days of administration of penicillin with resolution in approximately two days after discontinuing the offending agent. The pathogenesis is not well understood. The mucosa is characteristically thickened asymmetrically, most commonly involving the ascending and transverse colon.

Collagenous and microscopic colitis relatively are rare entities, which also present with chronic diarrhoea, and are differentiated on the basis of normal endoscopic findings along with typical histological findings.

A good clinical history, stool examination, endoscopy along with biopsies and radiological tests as required in most cases will lead to accurate diagnosis.

Consultant Gastroenterologist and Hepatologist, Bombay Hospital, Mumbai 400 020.

 
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