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Arthritis Res. 2001; 3(Suppl A): P085.
Published online Jan 26, 2001. doi:  10.1186/ar254
PMCID: PMC3273269
Differences between active immunoinflammatory and postinfectious fibromyalgia (FM)
I Wittrup,1 M Christiansen,1 B Jensen,1 H Bliddal,1 B Danneskiold-Samsøe,1 and A Wiik1
1Parker Research Institute; Frederiksberg Hospital and Departments of Clinical Biochemistry and Autoimmunology, Statens Serum Institut, Copenhagen, Denmark
Supplement
21st European Workshop for Rheumatology Research
Conference
21st European Workshop for Rheumatology Research
1-4 March 2001
Vienna, Austria
Received January 15, 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.
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