RESUMO
The discovery in 1985 in Martinique of an association between human T lymphotrophic virus type (HTLV -1) and tropical spastic paraparesis (TSP) (Gessain et al, 1985) opened a new chapter in the search for viruses in chronic human neurological disease. A few HTLV-1 seropositive patients have been reported to present with a clinical picture of a slowly progressive disorder resembling amyotrophic lateral sclerosis (ALS), but with a slower evolution (Vernant et al, 1989). In addition, pathological findings in some TSP cases have included anterior horn neuron depletion (Robertson and Cruickshank, 1972; Arimura et al, 1989). We have monitored selected humoral immune factors as well as levels of inflammatory proteins in asymptomatics and normal controls, using a computer-aided electrophoresis technique. The results showed a significant presence of hypergamma-globulinaemia, predominantly IgC in TSP patients. Interestingly enough, as well, immune complexes, complement cascade activation in those HTLV-1 seropositive patients with anterior horn-like neurological disorders. These data are consistent with the hypothesis of the occurrence of an immune complex-mediated vasculitis phenomenon in the latter subjects. Monitoring of these biological factors may represent a useful tool in the diagnosis and understanding of the physiopathological mechanisms of these disorders (AU)
Assuntos
Humanos , Paraparesia Espástica Tropical/imunologia , Manifestações Neurológicas , Esclerose Lateral Amiotrófica , MartinicaRESUMO
Tropical spastic paraparesis (TSP), a neuromyelopathy predominantly involving the pyramidal tract and commonly observed in tropical and equatorial areas, was recently found to be associated with human T lymphotropic virus type I (HTLV-I). We investigated sera and cerebrospinal fluid (CSF) from 19 patients with TSP who were from the Caribbean area, French Guiana, and Africa. Our results showed an elevated intra-blood-brain barrier IgG synthesis rate and an elevated IgG index, with an increased HTLV-I antibody-to-albumin ratio and the presence of CSF oligoclonal bands in the majority of the patients. These data, in association with similar HTLV-I antibody patterns between patients with TSP who were from these three regions, strenghten the probable etiologic role of HTLV-I in the pathogenesis of such chronic neuromyelopathies. (AU)