Inflammatory bowel diseases IBD consist mainly of two forms: Both diseases are chronic with the characteristic relapses and remissions. The diagnosis of UC and CD together with accurate differentiation between them and other inflammatory diseases of the colon relies on a combination of clinical, radiological, endoscopic and histological features 1. The pathogenesis of IBD is complex and not completely elucidated. It involves at least three interacting elements: These factors govern the life-long crosstalk between host and intestinal flora.
A popular theory regarding the pathogenesis of IBD contends that the initiation and perpetuation of the intestine inflammation are the results of an abnormal host response to the endogenous microflora. Thus, it seems to be rational to modify host bacteria in the hope that this would downregulate the pathological immune response.
Moreover, it was shown that Lactobacillus and bifidobacteria counts are significantly reduced in faeces of patients with IBD compared to controls, suggesting that normalization of gut flora is a logical means of treatment 2, 3. Experiments in rodents have demonstrated the potential of this approach, and preliminary studies in humans have been reported 1. The theory of endogenous microflora in IBD can be supported by the long clinical observations that the two most important medications used for treatment of IBD, sulfasalazine and its derivative 5-aminosalicylate mesalasine, 5-ASA , have some antibacterial activity.
Therefore it was postulated that the flare of UC and CD might have some linkage with intestinal bacteria 4. Sulfasalazine is used for more than 50 years and is highly effective for UC. On the contrary, the randomized trials showed that sulfasalazine was only marginally superior to a placebo for the induction of remission in active CD 1, 4.
An ideal treatment for active CD should rapidly and reliably induce remission of symptoms, and chronic maintaining therapy is recommended to prevent relapses of the disease.
