Antimeasles immunoglobulin G in sera of patients with otosclerosis is lower than that in healthy people

There is some evidence for an inflammatory process as a driving force in otosclerosis. Two popular hypotheses for the induction of this chronic inflammation have been proposed: an autoimmune phenomenon induced by an otic capsule specific antigen and measles virus infection. Antibodies against measle...

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Veröffentlicht in:Otology & neurotology 2001-11, Vol.22 (6), p.766-770
Hauptverfasser: LOLOV, Stephan R, ENCHEVA, Vessela I, KYURKCHIEV, Stanimir D, EDREV, George E, KEHAYOV, Ivan R
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Sprache:eng
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Zusammenfassung:There is some evidence for an inflammatory process as a driving force in otosclerosis. Two popular hypotheses for the induction of this chronic inflammation have been proposed: an autoimmune phenomenon induced by an otic capsule specific antigen and measles virus infection. Antibodies against measles virus hemagglutinin, polymerase, nucleocapsid, and matrix proteins were evaluated in sera from otosclerotic patients and in sera from healthy age-and sex-matched controls by use of the Western blot analyses. Significant differences were not detected between healthy men and women or between otosclerotic men and women. There were significantly stronger reactions against all viral proteins in the group of healthy women as compared with otosclerotic women despite a high standard deviation. The group of healthy male blood donors demonstrated significantly stronger reactions against polymerase and nucleocapsid proteins. Healthy blood donors again demonstrated stronger reaction compared with respective otosclerotic patients in a separate reaction for viral matrix protein. Our observation is consistent with viral participation in otosclerotic pathogenesis, but it is difficult to say if the diminished antimeasles humoral response is a consequence or the cause for a local measles infection. In light of the present data, we can discuss autoantibodies in otosclerosis as a sign of autoimmunity triggered by measles virus.
ISSN:1531-7129
1537-4505
DOI:10.1097/00129492-200111000-00009