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Chronic inflammatory bowel diseases (CIBD) are characterised by inflammation in different parts of the gastrointestinal tract and occur in episodes. Symptomatic phases (relapses) alternate with remission phases, in which the disease is inactive. The severity of the symptoms and the duration of the episodes vary from patient to patient. The aetiology of CIBD is still relatively unknown, but it is assumed that genetic susceptibility and certain environmental factors (antibiotic treatment, smoking, “western diet”) may cause the disease. The most frequent forms of CIBD are ulcerative colitis (UC) and Crohn’s disease (CD).
UC belongs to the CIBD with autoimmune reactions against the mucosa and submucosa of the colon or rectum and increased immune reactions against the intestinal flora. The inflammation spreads continuously from the rectum, that is from the anal region upwards.
CD is classified as an autoimmune disease of the intestinal mucosa and is among the CIBD with a high recurrence rate. The chronic granulomatous inflammation, which can affect the whole digestive tract from the oral cavity to the anus, is found in most cases only in the lower small intestine (terminal ileum) and the large intestine (colon), very rarely in the oesophagus and mouth. CD is characterised by discontinuous, segmental involvement of the intestinal mucosa, whereby several sections of the intestine may be affected simultaneously, divided by healthy sections.
In around 10% of cases, a mixed form is observed, which cannot be clearly classified as either of the two diseases (indeterminate colitis).
In both CD and UC, the intestinal barrier of the mucosa and intestinal epithelium is weakened so that pathogenic bacteria from the intestinal lumen can enter the epithelial cells and trigger an inflammatory response.
When the gastrointestinal tract is inflamed, neutrophil granulocytes pass through the intestinal mucosa into the lumen where they release calprotectin, a calcium- and zinc-binding protein that stimulates an immune response and has an antimicrobial effect. The calprotectin released into the intestinal lumen accumulates and is then excreted in the stool. Faecal calprotectin can therefore help to distinguish CIBD from irritable bowel syndrome.
For the differentiation of different CIBD and their differentiation from irritable bowel syndrome, targeted differential diagnostics are of great importance.
CIBD diagnostics are based on the clinical picture of the patient as well as on a combination of laboratory, endoscopic, histological and radiological examinations. The faecal inflammation marker calprotectin is an important parameter in laboratory analyses. In addition to early diagnosis, it enables discrimination of CIBD from functional bowel diseases such as irritable bowel syndrome. The additional detection of CIBD-associated autoantibodies (IgA and IgG) in serum can further secure the diagnosis. EUROIMMUN offers BIOCHIP combinations with different IIFT substrates to detect specific autoantibodies against intestinal goblet cells, exocrine pancreas, anti-neutrophil cytoplasm antibodies (ANCA) as well as antibodies against Saccharomyces cerevisiae (ASCA). In addition, the detection of ASCA can be performed monospecifically by EUROLINE or ELISA.
To discriminate irritable bowel syndrome from CIBD and to further differentiate CIBD from each other, the EUROIMMUN portfolio includes ELISA, EUROLINE and IIFT test systems.