Neuroinflammatory (demyelinating) disease is a rare but feared complication of treatment with anti-tumour necrosis factor (TNF)α in patients with polyarthritis. In this study, blood and cerebrospinal fluid markers of inflammation were analysed in 10 people with polyarthritis before and during treatment with infliximab. An increased systemic expression of interferon (IFN)γ was detected. Systemic administration of IFNγ is known to exacerbate multiple sclerosis. However, the present study failed to detect signs of inflammation in the cerebrospinal fluid samples—that is, pleocytosis, oligoclonal immunoglobulin G bands, increased expression of IFNγ, TNFα or interleukin 10, or increased levels of nitric oxide oxidation products. Our initial hypothesis, that the few cases of clinical neuroinflammatory disorders observed during treatment of polyarthritis with anti-TNFα represent the extreme end of a commonly occurring minor intrathecal immune activation, which in most cases does not give any overt neurological dysfunction, was not supported. Induction of systemic IFNγ production may still be relevant in neuroinflammation associated with treatment with anti-TNFα.
- CNS, central nervous system
- CRP, C reactive protein
- CSF, cerebrospinal fluid
- IFN, interferon
- NOx, nitric oxide oxidation product
- PCR, polymerase chain reaction
- TNF, tumour necrosis factor
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Published Online First 10 April 2006
Funding: This work was supported by grants from the Swedish Research Council, the Swedish Rheumatism Association, the Centre of Gender-related Medicine at Karolinska Institutet, the King Gustaf V 80th Birthday Fund and the R&D committee at the Karolinska University Hospital.
Competing interests: None declared.
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