[Biologicals in treatment of rheumatoid arthritis and other inflammatory arthropathies].
The ongoing evaluation of the cytokine-cascade and the steadily growing knowledge about cytokine mediated processes seem to open striking therapeutical options in the fields of sepsis, autoimmune and chronic inflammatory joint or bowel diseases via modulation or inhibition of the cytokine-cascade. There is no doubt about the efficacy of the various anticytokine-treatments in the therapy of chronic inflammatory rheumatic diseases. A large number of preclinical and clinical studies forms the scientific basis for these almost widely established therapies. These so-called "biologicals" are fully accepted as disease modifying antirheumatic drugs, equal to or even more potent than the classical substances. On the one hand, these agents are acting as tumor necrosis factor-alpha-blockers, like a chimeric (human/mouse) monoclonal anti-tumor-necrosis-factor-alpha-antibody (Infliximab), a recombinant soluble tumor necrosis factor-receptor p75 fusion protein (Etanercept), and a fully humanized anti-tumor-necrosis-factor-alpha-antibody (Adalimumab); on the other hand a recombinant human interleukin-1 receptor antagonist (Anakinra) is used in clinical practice. Generally these drugs are very well tolerated; the most common adverse events are higher infection rates (including tuberculosis) and injection-site reactions for the subcutaneously administered agents. Of course one should be aware of the possibly elevated risk for malignancies although there is no evidence for that so far, but the observation time since launching of these drugs is considerably short. To conclude, involved physicians should use these new "tools" very carefully and critically, because long-term tolerance and safety is a matter of ongoing investigation and last but not least because of the growing importance of cost effectiveness when using such expensive medications. Above all initiation and monitoring of those therapies should be restricted to rheumatologists
Sautner
Judith
J
II. Medizinischen Abteilung, NO Zentrum für Rheumatologie, Humanisklinikum Niederösterreich, Landstrasse 18, A-2000 Stockerau.
Leeb
Burkhard F
BF
D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D016207:Cytokines / Q000037:antagonists & inhibitors*; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000627:therapeutic use; D000069285:Infliximab; D053590:Interleukin 1 Receptor Antagonist Protein; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012795:Sialoglycoproteins / Q000009:adverse effects / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D016207:Cytokines; C507763:IL1RN protein, human; C507764:Il1rn protein, mouse; D007074:Immunoglobulin G; D053590:Interleukin 1 Receptor Antagonist Protein; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept