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Empyema in a patient treated with infliximab: it is not what it seems
  1. A Bossink1,
  2. S Thijsen2,
  3. A J van Houte3
  1. 1Heart Lung Centre, and Diakonessenhuis, Utrecht, The Netherlands
  2. 2Diakonessenhuis, Utrecht, The Netherlands
  3. 3Diakonessenhuis, Utrecht and Antonius Ziekenhuis, Nieuwegein, The Netherlands
  1. Correspondence to:
    Dr A Bossink
    Bosboomstraat 1, Utrecht, The Netherlands; aikbossinkmac.com

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A 68 year old woman, treated with prednisone and infliximab for rheumatoid arthritis, presented with two periods of thoracic empyema in two subsequent winters. H influenzae was cultured in the first infectious period and S pneumoniae during the second. Direct stains, polymerase chain reaction, and cultures for mycobacteria remained negative in both periods. She was treated with intravenous antibiotics and a closed drainage system. Infliximab was discontinued after the first infectious period. Recovery was complete. Last winter no infections occurred.

Six month after the last infectious period a chest computed tomographic scan was made and immunoglobulins and mannose binding lectin (MBL, a key mediator of innate host immunity) were determined. Radiology showed no abnormalities. IgG2 was significantly decreased. IgG1, IgG3, and IgG4, IgA, and IgM levels were normal. Functional serum MBL was markedly low, correlating with the genotype heterozygote XA/YD MBL codon 1 variant in combination with a heterozygous promoter genotype, resulting in deficient production of functional MBL. One year after the second infection, after tapering prednisone to 10 mg daily, she was vaccinated with a 23-valent pneumococcal polysaccharide vaccine and H influenzae B polysaccharide conjugated with tetanus toxoid. The immune response against pneumococcal polysaccharide types 3, 4, and 9 was absent and against H influenzae type B polysaccharide the response was normal.

Reduced IgG levels can be the result of long term prednisone treatment or chronic infection.1 Isolated IgG2 subclass deficiency may result in enhanced susceptibility to encapsulated bacteria.2 Another report suggests an increased susceptibility to invasive pneumococcal disease in homozygotes for MBL codon variants.3 It is tempting to speculate that the immunomodulating effect of infliximab contributed to the two episodes of thoracic empyema. However, to date, no reports have mentioned this kind of infection as a result of anti-tumour necrosis factor treatment.

We suggest that the combination of an IgG2 subclass deficiency with a heterozygote MBL codon variant and the use of steroids made this host more vulnerable to infection with encapsulated bacteria. In our opinion, in patients with infections with encapsulated bacteria after treatment with immunomodulating drugs, an assessment of the immune state should be considered.

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