[Chronic inflammatory bowel disease--pathogenic concepts and therapeutic perspectives].
Chronic inflammatory bowel disease (IBD) is considered to be a consequence of inappropriate upregulation of immune reactions evoked by the colonic microflora. Abnormalities observed in IBD may be explained, at least in part, by an unfavourable balance between pro- and anti-inflammatory cytokines. Conventional drug treatment of IBD may soon be replaced by more selective inhibitors that act centrally in the inflammatory process. Immunoneutralisation with chimeric anti-tumour necrosis factor-alpha (TNF alpha) antibodies reduces treatment refractory IBD, including fistular Chrons' disease, but recombinant human TNF alpha-receptor fusion proteins may be equally effective with potentially fewer side effects. This view also applies to chimeric antibodies directed against cytokines or adhesion molecules. Potentially more promising are antisense oligonucleotides and matrix-metalloproteinase inhibitors. Whether sustained remission can be achieved probably depends on successful unravelling of the aetiology of IBD.
Madsen
J R
JR
Medicinsk Gastroenterologisk Afdeling C, Amtssygehuset i Herlev.
D000906:Antibodies / Q000627:therapeutic use; D003093:Colitis, Ulcerative / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D003106:Colon / Q000276:immunology / Q000382:microbiology; D003424:Crohn Disease / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000502:physiology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy / Q000209:etiology / Q000276:immunology*; D061965:Matrix Metalloproteinase Inhibitors; D016376:Oligonucleotides, Antisense / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000502:physiology
D000906:Antibodies; D016207:Cytokines; D061965:Matrix Metalloproteinase Inhibitors; D016376:Oligonucleotides, Antisense; D014409:Tumor Necrosis Factor-alpha