PURPOSE: To investigate the possible link between normal tension glaucoma (NTG) and autoimmunity. METHODS: We studied the serum of 95 patients: 31 with NTG, 32 with primary open-angle glaucoma (POAG), and 32 age- and sex-matched controls. Blood was drawn from each patient and serum was examined for the presence of antinuclear antigens (ANA), autoantibodies to extractable nuclear antigens (ENA), anti-double-strand DNA, serum protein electrophoresis, and immunoglobulin (IgG, IgA, and IgM) levels. RESULTS: In the NTG group, the relative risks for ANA and ENA positivity were 2.5 and 4.4 times, respectively, that of the control group. There was a statistically significant difference between IgA levels in the NTG and control group (P=0.024), but there was no statistically significant difference between both groups regarding IgM or IgG levels. In the POAG group, the relative risks for ANA and ENA positivity were 0.77 and 2.9 times, respectively, that of the control group. The relative risk for detection of paraprotein in the POAG group was 0.97 times that of the control group. Also, there was a statistically significant difference between IgA levels in the POAG and control group (P=0.011), but there was no statistically significant difference between both groups regarding IgM or IgG. CONCLUSION: These results support the hypothesis that humoral immune mechanisms may have a role in the pathogenesis of NTG.
PURPOSE: To investigate the possible link between normal tension glaucoma (NTG) and autoimmunity. METHODS: We studied the serum of 95 patients: 31 with NTG, 32 with primary open-angle glaucoma (POAG), and 32 age- and sex-matched controls. Blood was drawn from each patient and serum was examined for the presence of antinuclear antigens (ANA), autoantibodies to extractable nuclear antigens (ENA), anti-double-strand DNA, serum protein electrophoresis, and immunoglobulin (IgG, IgA, and IgM) levels. RESULTS: In the NTG group, the relative risks for ANA and ENA positivity were 2.5 and 4.4 times, respectively, that of the control group. There was a statistically significant difference between IgA levels in the NTG and control group (P=0.024), but there was no statistically significant difference between both groups regarding IgM or IgG levels. In the POAG group, the relative risks for ANA and ENA positivity were 0.77 and 2.9 times, respectively, that of the control group. The relative risk for detection of paraprotein in the POAG group was 0.97 times that of the control group. Also, there was a statistically significant difference between IgA levels in the POAG and control group (P=0.011), but there was no statistically significant difference between both groups regarding IgM or IgG. CONCLUSION: These results support the hypothesis that humoral immune mechanisms may have a role in the pathogenesis of NTG.
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