[Therapeutic use of "biologics" in inflammatory joint and spinal diseases].
At present, two principles of biologic treatment for rheumatoid arthritis and other chronic inflammatory joint and spine diseases (juvenile polyarticular idiopathic arthritis, spondarthritides) are available for use in clinical practice. These are the TNF-alpha antagonists etanercept and infliximab as well as the human recombinant IL-1 receptor antagonist anakinra. All three biologics have significant short and long-term therapeutic effects on clinical and humoral inflammatory activity compared to placebo treatment in controlled clinical trials and even radiological progression of rheumatoid arthritis can be with halted. Principally, safety and tolerability of TNF- and IL-1 antagonist are good. However, local skin reactions at injection sites and infections of the upper respiratory tract and urinary tract have to be considered. Severe infections are rare except for an increased frequency of tuberculous infection observed with infliximab worldwide. The induction of autoantibodies including antibodies to double-stranded DNA and neuralizing antibodies to etanercept and infliximab themselves can occur though their clinical significance is still upon debate. It is important to notice that the advantages of the use of biologics in individual patients has carefully to be balanced against their high costs and the increased risk of infectious side effects. Therefore, guidelines of international experts recommend the clinical use of biologics mostly for patients resistant or intolerable to conventional treatment.
Seitz
M
M
Klinik für Rheumatologie und Klinische Immunologie/Allergologie, Universität Bern, Inselspital, Bern. michael.seitz@insel.ch
D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000627:therapeutic use*; D000069285:Infliximab; D053590:Interleukin 1 Receptor Antagonist Protein; D016032:Randomized Controlled Trials as Topic; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors* / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012795:Sialoglycoproteins / Q000009:adverse effects / Q000627:therapeutic use*; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000276:immunology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000502:physiology
D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; C507763:IL1RN protein, human; D007074:Immunoglobulin G; D053590:Interleukin 1 Receptor Antagonist Protein; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept