UNLABELLED: Currently, the importance of autoimmune phenomenon in the genesis of inner ear disease is difficult to evaluate because the clinical and biological criteria of autoimmune deafness has not yet been well defined. Among patients with sensorineural hearing loss, is it possible to define a group presenting clinical and biological findings suggesting autoimmune disease? What are the most sensitive and selective biological tests for autoimmune disease of the inner ear? Do patients with autoimmune deafness present a particular clinical, genetic and for biological profile? In order to answer these questions, we retrospectively studied 35 patients followed in our service from June 1990 to August, 1992 for sensorineural hearing loss of an unknown origin. All patients had had a complete biological work-up including examinations which would detect inflammation (erythrocyte sedimentation rate immunoglobulin IgG, IgA, IgM assays, protein electrophonesis) or dysimmunity (circulating immune complexes, marked depression of serum complement levels the presence of antinuclear antiorgan antibodies, or anticardiolipid and type II anticollagen antibodies). HLA typing had also been done. RESULTS. Only 4 patients had a biological profile suggesting dysimmunity. These patients presented no common clinical or genetic characteristic which would distinguish them as a separate subgroup. Biologically, anticardiolipid antibodies were found in all 4 of these patients and only in these patients. These 4 patients also had circulating immune complexes and 3 of the 4 patients also had elevated levels of IgA and IgM. IN CONCLUSION: including assays for antiphospholipid antibodies in the work-up of sensorineural hearing loss could reveal an antiphospholipid syndrome affecting the inner ear. Theoretically, the use of anticoagulants and agents decreasing platelet aggregation could provide effective treatment.
UNLABELLED: Currently, the importance of autoimmune phenomenon in the genesis of inner ear disease is difficult to evaluate because the clinical and biological criteria of autoimmune deafness has not yet been well defined. Among patients with sensorineural hearing loss, is it possible to define a group presenting clinical and biological findings suggesting autoimmune disease? What are the most sensitive and selective biological tests for autoimmune disease of the inner ear? Do patients with autoimmune deafness present a particular clinical, genetic and for biological profile? In order to answer these questions, we retrospectively studied 35 patients followed in our service from June 1990 to August, 1992 for sensorineural hearing loss of an unknown origin. All patients had had a complete biological work-up including examinations which would detect inflammation (erythrocyte sedimentation rate immunoglobulin IgG, IgA, IgM assays, protein electrophonesis) or dysimmunity (circulating immune complexes, marked depression of serum complement levels the presence of antinuclear antiorgan antibodies, or anticardiolipid and type II anticollagen antibodies). HLA typing had also been done. RESULTS. Only 4 patients had a biological profile suggesting dysimmunity. These patients presented no common clinical or genetic characteristic which would distinguish them as a separate subgroup. Biologically, anticardiolipid antibodies were found in all 4 of these patients and only in these patients. These 4 patients also had circulating immune complexes and 3 of the 4 patients also had elevated levels of IgA and IgM. IN CONCLUSION: including assays for antiphospholipid antibodies in the work-up of sensorineural hearing loss could reveal an antiphospholipid syndrome affecting the inner ear. Theoretically, the use of anticoagulants and agents decreasing platelet aggregation could provide effective treatment.