Volume 3 Supplement 2

21st European Workshop for Rheumatology Research

Open Access

Differences between active immunoinflammatory and postinfectious fibromyalgia (FM)

  • I Wittrup1,
  • M Christiansen1,
  • B Jensen1,
  • H Bliddal1,
  • B Danneskiold-Samsøe1 and
  • A Wiik1
Arthritis Research & Therapy20013(Suppl 2):P085

https://doi.org/10.1186/ar254

Received: 15 January 2001

Published: 26 January 2001

Aim

To study immunological and neurochemical markers in cerebrospinal fluid (CSF) and serum of FM patients in two subgroups, one having had a slow onset of symptoms (SO) and the other an acute onset (AO) of FM after a flue-like attack.

Materials

Twenty women with SO and 19 with AO FM, matched as to age and clinical symptoms, were studied for a multitude of antimicrobial and autoantibodies in serum. Markers of inflammation, immune activation and nerve cell damage were looked for in CSF and serum. All patients had longstanding disease.

Results

More patients with AO FM had IgM antibodies to enteroviruses, but PCR amplification showed no signs of enteroviral genome in CSF. All other antimicrobial and autoantibodies were similar in the two groups. However, in the SO FM patients we found strongly increased intrathecal IgA production as shown by extended indices but normal albumin ratio indicating normal blood/CSF barrier function. Intrathecal IgM production was increased in a few SO FM patients but IgG production was normal in all FM patients. Myelin basic protein (MBP) levels were normal in CSF of AO FM patients but very low in the SO patient group.

Conclusions and discussion

In FM characterized by an insidious onset of symptoms an immunoinflammatory mechanism involving IgA production in the brain may be a driving pathogenetic mechanism. Patients having experienced an acute onset of FM after a flue-like episode are likely to suffer from sequelae after earlier encephalitis, showing no signs of immune activation. The abnormally low MBP levels in the CSF of SO FM patients are yet unexplained. Our findings strongly support the concept that FM is a result of brain abnormalities that lead to disordered sensory processing and widespread allodynia.

Authors’ Affiliations

(1)
Parker Research Institute; Frederiksberg Hospital and Departments of Clinical Biochemistry and Autoimmunology, Statens Serum Institut

Copyright

© BioMed Central Ltd 2001

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