Causes
In principle, the causes of chronic inflammatory bowel disease are still unknown or largely unexplained. It is assumed that it is a multifactorial event. This means that defective genetic predisposition (disposition) and environmental factors in combination cause a chronic inflammatory bowel disease.
The interaction of these factors apparently leads to a disturbance of the barrier function of the intestine. As a result, bacteria of the normal intestinal flora can enter the mucous membrane of the intestine and trigger a chronic inflammation there. As already mentioned, both Crohn’s disease and ulcerative colitis occur for the first time predominantly in the age of 15-35 years.
However, Crohn’s disease can also appear for the first time in childhood, whereas ulcerative colitis usually occurs after puberty. Several genes have also been identified that are associated with this chronic inflammatory bowel disease. The most important gene mutation (alteration of a gene) lies in the so-called NOD-2 gene.
The NOD-2 gene has the task of recognising bacterial components in the intestine and then activating immune cells to defend against them. A NOD-2 mutation is present in over 50 percent of Crohn’s disease patients. In comparison, this gene mutation occurs rather rarely in ulcerative colitis patients.
An important environmental factor that should be mentioned and which shows different effects in the two most important chronic inflammatory bowel diseases is smoking. Smokers are thus more likely to contract Crohn’s disease. In addition, smoking often causes the disease to progress more severely, which is why Crohn’s disease patients should definitely stop smoking.
In contrast, smoking obviously has a protective effect in ulcerative colitis, as smokers are less likely to develop ulcerative colitis. According to the latest studies, chronic inflammatory bowel diseases are not, as assumed, autoimmune diseases. Psychosomatic incidents have also been excluded as a cause. However, psychological factors (such as stress) can have a negative impact on the course of the chronic inflammatory bowel disease.
Diagnosis
A stool examination belongs to the standard diagnostics of chronic inflammatory bowel disease. The main purpose of stool diagnostics is to rule out gastroenteritis caused by bacteria (gastroenteritis). The stool is therefore tested for pathogenic (disease-causing) bacteria.
In addition, the markers for mucosal inflammation “calprotectin” and “lactoferrin” can be measured. These also serve to differentiate between non-inflammatory causes. Calprotectin, for example, is a protein that occurs in certain white blood cells (defence cells) in our body.
If these are increasingly active because an inflammatory process takes place in the intestine, this indicates an inflammatory bowel disease. If calprotectin or lactoferrin exceeds a certain level, this therefore indicates an inflammatory disease. These parameters are also determined for follow-up.
In order to distinguish between Ulcerative colitis and Crohn’s disease, in some cases of Ulcerative colitis an increased concentration of beta-defensin-2, which is only produced in inflammation, may be observed. In Crohn’s disease patients this level is usually low or absent. However, this value may also be partially absent in patients with ulcerative colitis and is therefore not suitable for reliable differentiation.
In addition to the clinical symptoms such as diarrhoea and pain, laboratory parameters are also available to make a diagnosis. If a chronic inflammatory bowel disease is suspected, the blood should be examined for signs of chronic inflammation, anaemia and malabsorption or malnutrition. Thus, a blood count and the determination of the CRP (C-reactive protein) should be carried out in any case.
Anemia and an increase in immune cells indicate chronic inflammation. In chronic inflammatory bowel disease, the CRP is usually elevated in the acute inflammatory flare, but negative CRP values do not rule out chronic bowel inflammation. If Crohn’s disease is suspected, vitamin B-12 should also be determined.
In Crohn’s disease, vitamin B-12 is often reduced due to poor absorption in the lower part of the small intestine. Furthermore, antibody determination can often help to identify either a chronic inflammatory bowel disease or to distinguish between Crohn’s disease and ulcerative colitis. These include the antibodies ASCA and ANCA. For example, the ASCA antibody is found in 70% of patients with Crohn’s disease and only in 15% of ulcerative colitis patients.
