title: [Risk of infection through use of selective  immunomodulating drugs for rheumatoid arthritis].
abstract: BACKGROUND
  New drugs for rheumatoid arthritis (RA) have resulted in an improvement in patients' functioning and morbidity, but are linked with increased risk of infections. Traditional immunosuppressant drugs are often used in combination with anti-tumour necrosis factor-alpha (TNF-α) inhibitors or anti-CD20 (rituximab).
  
  
  METHODS
  The review is based on a search in PubMed and on the authors' own experience of treating infections in patients who receive immunosuppressant treatment.
  
  
  RESULTS
  Traditional immunomodulating treatment results in an increased risk of infection. The disease RA in itself increases the risk of infections. There is evidence of an increased incidence of infections with both extracellular bacteria and intracellular microorganisms such as mycobacteria, including Mycobacterium tuberculosis, and viruses in patients who are treated with TNF-α inhibitors. Patients who are about to start taking TNF-α inhibitors must therefore undergo a tuberculosis-risk assessment. Rituximab may increase the incidence of infection, but long-term observations are limited. Combination therapy involving different drugs that selectively modulate immune response is normally contraindicated because of the increased risk of infection.
  
  
  CONCLUSIONS
  The benefit of TNF-α inhibitors and rituximab treatment for RA must be weighed up against the increased risk of infections. Symptoms, findings and laboratory test results pertaining to serious infections may be influenced by immunomodulation therapy and thereby make clinical assessment difficult.
authors.affiliation: Infeksjonsseksjonen, Medisinsk divisjon, Stavanger universitetssjukehus, Norway. hare@sus.no
authors.forename: Erna
authors.initials: E
authors.lastname: Harboe
authors.forename: Jan Kristian
authors.initials: JK
authors.lastname: Damås
authors.forename: Roald
authors.initials: R
authors.lastname: Omdal
authors.forename: Stig S
authors.initials: SS
authors.lastname: Frøland
authors.forename: Haakon
authors.initials: H
authors.lastname: Sjursen
mesh_terms: D058846:Antibodies, Monoclonal, Murine-Derived / Q000008:administration & dosage / Q000009:adverse effects*; D018501:Antirheumatic Agents / Q000009:adverse effects; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000188:drug therapy*; D004359:Drug Therapy, Combination / Q000009:adverse effects; D016174:Hepacivirus / Q000502:physiology; D006509:Hepatitis B / Q000209:etiology; D006515:Hepatitis B virus / Q000502:physiology; D006526:Hepatitis C / Q000209:etiology; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000009:adverse effects*; D007239:Infections / Q000139:chemically induced*; D018570:Risk Assessment; D012307:Risk Factors; D000069283:Rituximab; D014376:Tuberculosis / Q000139:chemically induced; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014775:Virus Activation / Q000187:drug effects
chemical_list: D058846:Antibodies, Monoclonal, Murine-Derived; D018501:Antirheumatic Agents; D007166:Immunosuppressive Agents; D014409:Tumor Necrosis Factor-alpha; D000069283:Rituximab