Autoimmunity · 2007
Antibodies to myelin protein zero (P0) protein as markers of auto-immune inner ear diseases.
СтатьяМногоцентровое исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Pham Bach-Nga, Rudic Milan, Bouccara Didier, Sterkers Olivier, Belmatoug Nadia, Bébéar Jean-Pierre, Couloigner Vincent, Fraysse Bernard, Gentine André, Ionescu Eugène, Robier Alain, Sauvage Jean-Pierre, Truy Eric, Van Den Abbeele Thierry, Ferrary Evelyne
Аннотация
BACKGROUND/AIMS: The inner ear can be the target of autoimmune disorders. Recognition of autoimmune inner ear disease is important, as it is one of the very few forms of sensorineural hearing loss (HL) that can be successfully treated by medical therapy. The aim of this study was to evaluate whether the detection of antibodies to myelin protein P0 (MPZ) could be a diagnostic test for inner ear disease of autoimmune cause.
METHODS: This multicentric prospective study included 129 patients: patients with progressive sensorineural HL or with Menière's disease, together with their control group corresponding to patients with similar symptoms, but of presumably known origin. Detection of antibodies to myelin P0 protein was performed by using western blots. NORMAL: The prevalence of antibodies to myelin P0 protein in patients with rapidly progressive HL was not statistically different from that of the control group corresponding to genetic HL patients (30 versus 28%). In patients with Menière's disease, the prevalence was lower than that of the control group corresponding to patients with benign paroxysmal positional vertigo (5.4 versus 18.7%). No patient with auto-immune disease had antibodies to myelin P0 protein.
CONCLUSIONS: The sole presence of antibodies to myelin P0 may not be used as a marker of inner ear disease of autoimmune origin.
METHODS: This multicentric prospective study included 129 patients: patients with progressive sensorineural HL or with Menière's disease, together with their control group corresponding to patients with similar symptoms, but of presumably known origin. Detection of antibodies to myelin P0 protein was performed by using western blots. NORMAL: The prevalence of antibodies to myelin P0 protein in patients with rapidly progressive HL was not statistically different from that of the control group corresponding to genetic HL patients (30 versus 28%). In patients with Menière's disease, the prevalence was lower than that of the control group corresponding to patients with benign paroxysmal positional vertigo (5.4 versus 18.7%). No patient with auto-immune disease had antibodies to myelin P0 protein.
CONCLUSIONS: The sole presence of antibodies to myelin P0 may not be used as a marker of inner ear disease of autoimmune origin.