Apart from distinguishing Crohn's from Ulcerative Colitis, there are some rare cases of treatable diseases that need to be ruled out during differential diagnosis for Crohn's:
CASE REPORT: GASTROINTESTINAL TUBERCULOSIS SIMULATING CROHN'S
DISEASE.
Kaushik SP; Bassett ML; McDonald C; Lin BP; Bokey EL; Gastroenterology
Unit, Woden Valley Hospital, ACT, Australia. J Gastroenterol
Hepatol, 1996 Jun, 11:6, 532-4
A male Caucasian presented with abdominal pain and a right iliac fossa
mass. There were no risk factors for Mycobacterium tuberculosis infection.
He was investigated by upper and lower gastrointestinal endoscopy, chest
and small bowel radiology. The latter showed stricturing of the third and
fourth parts of the duodenum, mid-jejunum and terminal ileum. Biopsies
were non-specific and he was thought to have Crohn’s disease. Subsequent
treatment with corticosteroids resulted in improved well being and weight
gain; however, the patient demonstrated disease progression with the development
of complex fistulae and Escherichia coli septicaemia. At surgery the patient
was found to have an ileal inflammatory mass with fistulae to the sigmoid
colon. The terminal ileum, fistulae and a segment of colon were resected.
Treatment with anti-tuberculous drugs ensued and the patient is now asymptomatic
after 15 months of follow-up. This case serves to highlight the difficulty
in making the diagnosis of gastrointestinal tuberculosis, a disease that
may mimic Crohn’s disease, and the need for caution in the use of corticosteroids
in any disease in which tuberculosis enters into the differential diagnosis.
The role of surgery in making the diagnosis and managing the complications,
in conjunction with anti-tuberculous drugs, and the prospect of cure are
exemplified by this case.
STRONGYLOIDES STERCORALIS EOSINOPHILIC GRANULOMATOUS ENTEROCOLITIS.
Gutierrez Y; Bhatia P; Garbadawala ST; Dobson JR; Wallace TM; Carey
TE Address Department of Pathology, University Hospitals of Cleveland,
OH 44106, USA. Am J Surg Pathol, 1996 May, 20:5, 603-12
Six patients suffering from an unusual form of colitis produced by Strongyloides
stercoralis hyperinfection are described. In contrast to the usual Strongyloides
hyperinfection syndrome, in which small intestinal and pulmonary manifestations
are seen in patients with some forms of immunodeficiency, the patients
described here presented with only a characteristic transmural
eosinophilic granulomatous inflammation affecting mostly the colonic
wall and clinically mimicking ulcerative colitis or Crohn’s disease.
This Strongyloides eosinophilic granulomatous enterocolitis apparently
results from a florid inflammatory response by eosinophils, histiocytes,
and giant cells with formation of granulomas that destroy the larvae entering
the colon. This morphologic picture differs from that of the well-described
hyperinfection syndrome, in which the bulk of the larvae pass through the
colonic wall to complete the life cycle, with only a few larvae destroyed
in the colon. The probable pathophysiologic mechanism of this unusual manifestation
of hyperinfection is discussed based on the anatomic and clinical observations
of patients who presented at different stages in the evolution of their
condition and whose length of follow-up varied.
INTESTINAL STRONGYLOIDIASIS. A CASE REPORT AND REVIEW OF THE LITERATURE.
Brasitus TA; Gold RP; Kay RH; Magun AM; Lee WM; Am J Gastroenterol,
1980 Jan, 73:1, 65-9
A patient infected with Strongyloides stercoralis presented with hematemesis
and abdominal pain mimicking peptic ulcer disease. Radiologic evaluation,
however, suggested Crohn’s disease of the proximal small intestine. Aspiration
of intestinal fluid and a small bowel biopsy lead to a diagnosis of invasive
strongyloidiasis. This case is presented and the literature reviewed to
demonstrate the protean manifestation of this parasite which commonly involves
the gastrointestinal tract.
CHRONIC MESENTERIC ISCHEMIA—A RARE DIFFERENTIAL DIAGNOSIS OF
CROHN DISEASE
Johanns W; Jakobeit C; Louis W; Greiner L; Medizinische Klinik A, UniversitÂat
Witten-Herdecke, Kliniken der Stadt Wuppertal. Z Gastroenterol, 1994
Aug, 32:8, 444-6
A 59-year-old patient was treated for six years assuming Crohn’s disease.
Recurrent segmental colitis, spontaneous perforation of the jejunum and
chronic weight loss were suggestive of this diagnosis despite a missing
typical histology, even in the resected part of jejunum. Only unspecific
inflammatory changes were found. Typical angina abdominalis occurred late.
Angiography showed a complete occlusion of the coeliacaxis and both mesenteric
arteries. Only the slow progress of occlusion of the visceral arteries
with extensive collateral circulation from iliacal arteries explains the
absence of severe bowel infarction. After aortomesenteric bypass operation
the patient is without any complaint.
YERSINIA ENTEROCOLITICA
U.S. Food & Drug Administration, Center for Food Safety & Applied
Nutrition
Foodborne Pathogenic Microorganisms and Natural Toxins Handbook
Y. enterocolitica, a small rod-shaped, Gram-negative bacterium, is often
isolated from clinical specimens such as wounds, feces, sputum and mesenteric
lymph nodes. However, it is not part of the normal human flora. Strains
of Y. enterocolitica can be found in meats (pork, beef, lamb, etc.), oysters,
fish, and raw milk. The exact cause of the food contamination is unknown.
Yersiniosis is frequently characterized by such symptoms as gastroenteritis
with diarrhea and/or vomiting; however, fever and abdominal pain are the
hallmark symptoms. Diagnosis of yersiniosis begins with isolation of the
organism from the human host's feces, blood, or vomit, and sometimes at
the time of appendectomy.Confirmation occurs with the isolation, as well
as biochemical and serological identification, of Y. enterocolitica from
both the human host and the ingested foodstuff. Diarrhea is reported to
occur in about 80% of cases; abdominal pain and fever are the most reliable
symptoms.Yersiniosis has been misdiagnosed as Crohn's disease (regional
enteritis) as well as appendicitis( since one of the main symptoms
of infections is abdominal pain of the lower right quadrant ).
Finally, here is the e-mail from a patient that I received and that prompted me to start this page:
"It's not just virus and bacteria, it's also parasites that can cause an ongoing inflammatory process. Of particular importance is amebiasis and strongyloidiasis. My experience is as follows: I had worms (Strongyloides stercoralis) discovered by an infectious disease doctor using a serology test. My GI doctor called it ulcerative colitis for 14 years and used prednisone. I lost my colon because another GI doctor, a teacher of gastro and PhD, didn't believe the serology and my medical history showing sores on rear at the time of the original diagnosis. I was refused the continuation of TPN and forced into the colectomy. After the surgery the GI doctor admitted that she had made a mistake, that I should have had a temporary ileostomy for gut healing. She said "my infectious disease training was practically non-existent, I learned more from you than in my training." There are lots of details like I ate steak tartare, foreign travel, etc that would put me a risk. Also had Campylobacter, Chilomastic mesnili, a preliminary finding of giardia and an overgrowth of E.coli and entercoccus at the time of the original differential diagnosis. After the surgery she suggested that I call Johns Hopkins Travelers Disease Clinic to ask the question "Could acute and chronic dysentery imitate the clinical course of ulcerative coitis and Crohn disease?" I didn't know before the surgery that I was seeing the wrong kind of doctor. How do I get the information out about my case and the information about food-borne infectious colitis? I am concerned for the 2 million UC/Crohn disease patients who may never have had a complete, rigorous differential diagnosis by an appropriately trained and experienced doctor."