آنتی بادی های ضد استرپتوکوکی افزایش یافته در بیماران مبتلا به سندرم تورت

Infection or postinfectious phenomena have been postulated to play a role in the pathogenesis of children afflicted with the typical symptoms of Tourette’s syndrome (TS). We investigated whether an increase of titers of antistreptococcal antibodies can be reproduced in our children with TS, and whether this increase is restricted to children. We examined the titers of two different antistreptococcal antibodies, antistreptolysin (ASL) and antiDNase B, both in children and adults. Titers of ASO and antiDNase B were measured (1) in 13 children/adolescents suffering from TS and in an age-matched comparison group; (2) in 23 adult patients, a comparison group of 23 age-matched controls, and in another group of 17 age-matched, non-medicated acute schizophrenics. ASO and antiDNase B titers were determined by laser nephelometry using a commercially available kit. Two antistreptococcal cut-off levels were compared (>250 U/ml and >400 U/ml). As expected, increased ASO titers (>400 IU/ml) were found in a higher proportion of children/adolescents with TS compared to healthy controls. In parallel, high antiDNase titers (>250 U/ml or >400 U/ml) were also observed in significantly more children/adolescents with TS compared to controls. Regarding adults, titers >250 U/ml for both antistreptococcal antigens were found in significantly more TS patients than in schizophrenic patients or healthy control subjects. The mean values of ASO and antiDNase titers were significantly higher in both groups of TS patients compared to control children/adolescents, to the comparison groups of healthy adults and to schizophrenics. No difference in antistreptococcal titers was found between schizophrenics and the group of healthy adults. TS patients exhibited higher antistreptococcal titers than age-matched comparison groups of both children/adolescents and adults using different types of calculation. Our findings support the theory that a postinfectious immune mechanism may play a role in the pathogenesis of TS. The mechanism still needs to be elucidated.