Laboratory screening and activity markers
Laboratory evaluation of patients with suspected inflammatory bowel disease begins with basic inflammatory markers. Complete blood count and blood chemistry frequently reveal accelerated ESR, elevated C-reactive protein (CRP) and fibrinogen levels, as well as leukocytosis, thrombocytosis, and signs of anemia.
A key non-invasive marker is fecal calprotectin. This is a neutrophil-derived protein whose concentration in stool directly correlates with the activity of the inflammatory process in the intestinal mucosa. Its progressive increase serves as a strong rationale for a follow-up endoscopic examination.
For the differential diagnosis between Crohn's disease and ulcerative colitis, immunological markers are used:
- ASCA (anti-Saccharomyces cerevisiae antibodies) — their elevation is specific to Crohn's disease, whereas in ulcerative colitis titers remain within the normal range.
- ANCA (antineutrophil cytoplasmic antibodies) — are more frequently detected in ulcerative colitis, but have lower diagnostic specificity.
Endoscopic and imaging visualization
The gold standard for IBD verification is colonoscopy, during which examination of the terminal ileum is strictly mandatory. Routine annual endoscopy is not indicated. Repeat procedures are required only when clinically indicated (clinical deterioration, suspected complications, rising CRP and fecal calprotectin levels), as well as part of routine colorectal cancer screening.
To assess deep lesions and complications, diagnostic imaging is used:
- MRI and/or CT with intravenous contrast of the abdomen and pelvis.
These methods make it possible to determine the extent of the process and identify such severe complications as inter-intestinal fistulas, strictures, perforations, and inflammatory infiltrates. An important supplement to imaging, especially in Crohn's disease, is digital rectal examination, which is necessary to assess perianal manifestations and fistulous tracts.
Histological picture: how to distinguish CD from UC?
Morphological examination of GI biopsies is an absolute mandatory step. Histological features are divided into non-specific (found in both forms of IBD) and specific.
Non-specific changes:
- Disruption of normal crypt architecture (changes in their shape and number).
- Formation of crypt abscesses (accumulation of neutrophil leukocytes in the lumen).
- Pronounced polymorphonuclear infiltration of the lamina propria.
Specific marker of Crohn's disease: Detection of a non-caseating epithelioid cell granuloma, which is often accompanied by peripheral Langhans multinucleated giant cells. Clinical nuance: granulomas are rarely detected on standard biopsy. This is because the pathological process in Crohn's disease involves the deep (submucosal) layers of the intestinal wall, which standard endoscopic biopsy forceps physically cannot reach.
In the differential diagnosis of perianal lesions, histology also plays a decisive role: caseous masses and acid-fast bacteria point to tuberculosis, granulomas with central suppurative necrosis point to actinomycosis, and the presence exclusively of epithelioid and giant cells confirms Crohn's disease.
Differential diagnosis and IBD mimics
Systemic manifestations of inflammatory bowel disease require the exclusion of a vast spectrum of pathologies. If a patient lacks the pathognomonic symptom of systemic lupus erythematosus — the malar rash («butterfly» rash) — an isolated polysyndromic process forces the physician to conduct a broad diagnostic workup.
Excludes:
- Rheumatological diseases: juvenile idiopathic arthritis, juvenile dermatomyositis, systemic vasculitides (Henoch-Schönlein purpura, polyarteritis nodosa).
- Infections: yersiniosis, syphilis, tuberculosis, viral hepatitis B and C with extrahepatic manifestations, borreliosis.
- Hematology and oncology: lymphomas, autoimmune hemolytic anemias.
Special attention should be paid to chronic diarrhea syndrome accompanied by severe intoxication, wasting, and hemocolitis against the background of profound leukopenia and anemia. If endoscopy fails to confirm IBD, and therapy with glucocorticosteroids and sulfasalazine yields no effect (ex juvantibus), a thorough epidemiological history must be collected (e.g., travel to endemic regions of Africa, blood transfusions). In such cases, intestinal symptoms may be a manifestation of opportunistic infections (cytomegalovirus, cryptosporidia, atypical mycobacteria) against the background of severe immunodeficiency, particularly HIV infection (AIDS stage).
To avoid confusing antibodies: ASCA — Crohn's disease (CD), while ANCA more frequently indicates ulcerative colitis.
Class and exam questions
Are granulomas in Crohn's disease often not found in biopsy specimens?
Granulomas are localized predominantly in the deep submucosal layer of the intestinal wall. Standard endoscopic biopsy forceps capture only the superficial layers without reaching the zone of specific inflammation.
What are the criteria for a definitive diagnosis of Crohn's disease?
The diagnosis is considered reliable if any 3 features from the general diagnostic list are present, or if a granuloma is detected in combination with 1 other feature. The diagnosis must be confirmed by a combination of methods: endoscopy + morphology and/or endoscopy + imaging.
Can HIV infection mimic inflammatory bowel disease?
Yes. Opportunistic infections in AIDS (CMV colitis, cryptosporidiosis) cause chronic diarrhea, hemocolitis, and wasting, mimicking IBD. Distinctive features include profound leukopenia, an epidemiological history, and lack of response to glucocorticosteroid therapy.
What else to study on this topic
- Features of extraintestinal manifestations of inflammatory bowel disease
- Differential diagnosis of perianal fistulas
- Opportunistic gastrointestinal lesions in severe immunodeficiency
- Indications for MR enterography in suspected intestinal strictures
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