Eosinophilia myalgia syndrome: absence of immunoglobulin reactivity suggests a cellular rather than humoral mechanism
Villanova, M.; De Clerck, L.S.; Cras, P.; Guazzi, G.C.; Martin, J.J.
Acta Neurologica Belgica 94(3): 200-204
1994
ISSN/ISBN: 0300-9009 PMID: 7976226 Document Number: 433315
The idiopathic disorder Eosinophilia Myalgia Syndrome (EMS), characterized by peripheral eosinophilia, myalgia and frequently fasciitis, can be triggered by ingestion of some commercial preparations of L-Tryptophan. Activated T-lymphocytes and macrophages are involved in the pathogenesis of EMS. We investigated immunohistochemically the potential role of immunoglobulins and of the terminal C5b-9 complement factor (membrane attack complex) in EMS. We found no evidence for direct involvement of immunoglobulins. However, membrane attack complex immunoreactivity was present in vessel walls in EMS, but completely absent in controls. These observations suggest that the fasciitis in EMS involves a cellular rather than a humoral reaction and that complement activation could be of importance.