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Logo of arthresbiomed central web sitesearch.manuscript submission.see also journal with issn 1478-6354registration.reference to the article.journal front page.
 
Arthritis Res. 2001; 3(Suppl A): P085.
Published online 2001 January 26. doi:  10.1186/ar254
PMCID: PMC3273269

Differences between active immunoinflammatory and postinfectious fibromyalgia (FM)

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.


Articles from Arthritis Research are provided here courtesy of BioMed Central