[Chronic inflammatory bowel disease--current status]

Chronic inflammatory bowel disease (IBD) encompasses the disease entities, ulcerative colitis (UC) and Crohn's disease (CD). An aetiologic agent has not yet been defined and the diagnosis is based, therefore, on the sum of clinical, paraclinical, radiologic, endoscopic and histopathologic features. In recent years pathogenetic studies have focused on immune mechanisms, transmissible infectious agents, the potential role of the normal intestinal flora, dietary factors, enzymatic alterations and genetic features, in addition to vascular, neuromotor, allergic and psychologic factors. The prevalence of IBD is increased in first-degree relatives of patients and there is a high rate of disease concordance among monozygotic twins. Thus abnormal genes may encode for one or several immunoregulatory factors, while bacterial wall products seem to activate colonic inflammatory cells in a non-specific way, leading to increased production of cytokines, complement-derived peptides, eicosanoids, platelet activating factor, biogenic amines, kinins, chemotactic oligopeptides, and neuropeptides. The named soluble inflammatory mediators, in addition to free oxygen radicals, are considered responsible for the secondary amplification of the inflammatory process. The corner stones in medical therapy of IBD are still corticosteroids and sulphasalazine (SAZ). The new oral salicylates, which are analogues of SAZ or "slow release" preparations of 5-aminosalicylic acid (mesalazine), have provided a therapeutic progress, because they are tolerated better than SAZ. Immunosuppressive agents, such as azathioprine and 6-mercaptopurine, reduce the requirement for corticosteroids and are effective in refractory CD, but the effect is delayed up to several months. The therapeutic action of cyclosporine A is not sustained, but often associated with side effects. Metronidazole has a beneficial effect on perineal disease.(ABSTRACT TRUNCATED AT 250 WORDS)