title: Pneumocystis jirovecii colonization in patients treated with infliximab.
abstract: BACKGROUND
  Infliximab, a chimeric antitumour necrosis factor (TNF) monoclonal antibody, has become an established effective therapy for inflammatory rheumatic disease. However, TNF is a critical factor in host defence, and the suppression of its biological activity may be associated with the increased risk of opportunistic infections. The frequent use of infliximab in clinical practice has identified Pneumocystis jirovecii pneumonia (PcP) as a serious complication. Individuals colonized with Pneumocystis may be at high risk of development of PcP when they have undergone immunosuppression. Hence, we addressed the question of the frequency of Pneumocystis colonization among patients treated with infliximab.
  
  
  METHODS
  We examined 125 oropharyngeal washes collected from 78 individuals with rheumatoid arthritis, 30 with ankylosing spondylitis and 17 with psoriatic arthritis, half of them underwent infliximab therapy, using a real-time polymerase chain reaction assay that employs specific primers from a portion of the mitochondrial large-subunit rRNA gene of P. jirovecii.
  
  
  RESULTS
  Pneumocystis jirovecii colonization was detected in 32 (25·6%) patients. In a multivariate regression model, only duration of infliximab treatment for more than 3 years and use of corticosteroid were significantly and independently associated with risk of Pneumocystis colonization. However, the effect of corticosteroid on P. jirovecii colonization rate was not linearly dose dependent as showed other logistic regression analysis.
  
  
  CONCLUSIONS
  There is a high rate of P. jirovecii colonization among patients with rheumatologic diseases treated with infliximab. The identification of patients colonized by P. jirovecii before starting the treatment with infliximab could be a strategy for PcP prevention.
authors.affiliation: Pneumocystis Study Group, Infectology Unit, Clinical Hospital of Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Wissmann
authors.forename: Rubén
authors.initials: R
authors.lastname: Morilla
authors.forename: Isabel
authors.initials: I
authors.lastname: Martín-Garrido
authors.forename: Vicente
authors.initials: V
authors.lastname: Friaza
authors.forename: Nieves
authors.initials: N
authors.lastname: Respaldiza
authors.forename: Juan
authors.initials: J
authors.lastname: Povedano
authors.forename: Juan M
authors.initials: JM
authors.lastname: Praena-Fernández
authors.forename: Marco A
authors.initials: MA
authors.lastname: Montes-Cano
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Medrano
authors.forename: Luciano Z
authors.initials: LZ
authors.lastname: Goldani
authors.forename: Carmen
authors.initials: C
authors.lastname: de la Horra
authors.forename: José M
authors.initials: JM
authors.lastname: Varela
authors.forename: Enrique J
authors.initials: EJ
authors.lastname: Calderón
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D005260:Female; D006801:Humans; D016867:Immunocompromised Host; D000069285:Infliximab; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009894:Opportunistic Infections / Q000139:chemically induced* / Q000382:microbiology; D045363:Pneumocystis carinii / Q000302:isolation & purification; D011020:Pneumonia, Pneumocystis / Q000139:chemically induced* / Q000382:microbiology; D025242:Spondylarthropathies / Q000188:drug therapy*; D055815:Young Adult
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D000069285:Infliximab