BACKGROUND: Electroretinographic (ERG) abnormalities have been reported in multiple sclerosis (MS), as well as the presence of circulating antiretinal antibodies. We and others have reported cases of impaired vision and diminished ERGs in MS patients with alpha-enolase autoantibodies. Anti-enolase antibodies have been implicated in autoimmune retinopathy. We performed this study to further explore the relationship between antiretinal antibodies and ERG changes in patients with MS. METHODS: Patients with clinically definite MS and normal visual acuity were recruited for this study, along with healthy controls. All patients and controls had ERG testing done according to ISCEV standards. Patient and control sera were analyzed for the presence of antiretinal antibodies using Western blot and ELISA techniques, and HLA class II typing was performed using polymerase chain reaction. RESULTS: We found a statistically significant difference between MS patients and controls in the rod-cone b-wave implicit time (p < 0.005). We found autoantibodies against alpha-enolase in 38% of MS patients and 11% of controls (p < 0.02). There was no statistically significant difference between ERG parameters of MS patients with alpha-enolase autoantibodies compared to those without alpha-enolase antibodies. Furthermore, the presence of alpha-enolase did not associate with a particular HLA haplotype. CONCLUSIONS: Factors affecting the retina other than alpha-enolase antibodies may account for the delayed rod-cone b-wave implicit times observed in MS patients in this study. Anti-enolase antibodies are likely an epiphenomenon of autoimmune disease, and are not causing retinopathy in MS patients with normal visual acuity. However, the possibility of rare cases of patients with pathogenic alpha-enolase autoantibodies can not be excluded. The pathogenic contribution of these antibodies in MS patients with visual impairment deserves further investigation.
BACKGROUND: Electroretinographic (ERG) abnormalities have been reported in multiple sclerosis (MS), as well as the presence of circulating antiretinal antibodies. We and others have reported cases of impaired vision and diminished ERGs in MS patients with alpha-enolase autoantibodies. Anti-enolase antibodies have been implicated in autoimmune retinopathy. We performed this study to further explore the relationship between antiretinal antibodies and ERG changes in patients with MS. METHODS: Patients with clinically definite MS and normal visual acuity were recruited for this study, along with healthy controls. All patients and controls had ERG testing done according to ISCEV standards. Patient and control sera were analyzed for the presence of antiretinal antibodies using Western blot and ELISA techniques, and HLA class II typing was performed using polymerase chain reaction. RESULTS: We found a statistically significant difference between MS patients and controls in the rod-cone b-wave implicit time (p < 0.005). We found autoantibodies against alpha-enolase in 38% of MS patients and 11% of controls (p < 0.02). There was no statistically significant difference between ERG parameters of MS patients with alpha-enolase autoantibodies compared to those without alpha-enolase antibodies. Furthermore, the presence of alpha-enolase did not associate with a particular HLA haplotype. CONCLUSIONS: Factors affecting the retina other than alpha-enolase antibodies may account for the delayed rod-cone b-wave implicit times observed in MS patients in this study. Anti-enolase antibodies are likely an epiphenomenon of autoimmune disease, and are not causing retinopathy in MS patients with normal visual acuity. However, the possibility of rare cases of patients with pathogenic alpha-enolase autoantibodies can not be excluded. The pathogenic contribution of these antibodies in MS patients with visual impairment deserves further investigation.
Authors: Krishnakumar N Menon; David L Steer; Martin Short; Steven Petratos; Ian Smith; Claude C A Bernard Journal: Mol Cell Proteomics Date: 2011-03-18 Impact factor: 5.911
Authors: Yuyi You; Elizabeth C Graham; Ting Shen; Con Yiannikas; John Parratt; Vivek Gupta; Joshua Barton; Michael Dwyer; Michael H Barnett; Clare L Fraser; Stuart L Graham; Alexander Klistorner Journal: Neurol Neuroimmunol Neuroinflamm Date: 2017-12-15