Selected autoantibodies and normal-tension glaucoma

Abstract

BackgroundAlthough intraocular pressure is an important risk factor in glaucoma, there is growing body evidence indicating an immunological component in the pathogenesis of normal-tension glaucoma (NTG). The aim of this study was to determine if NTG coexists with elevated levels of autoantibodies detected in rheumatic diseases.Material/MethodsWe enrolled 105 patients into the study: 35 with NTG, 34 with primary open-angle glaucoma (POAG), and 36 controls. All patients underwent ophthalmic examination and blood tests. Blood was examined for the level of: antibodies against antinuclear antibodies (ANA), antibodies to extractable nuclear antigens (ENA), immunoglobulins (IgG, IgA, IgM), rheumatoid factor, anti-citrullinated protein antibodies (ACPA), and antiphospholipid antibodies (anticardiolipin antibodies, beta2-glycoprotein I antibodies, antiprothrombin antibodies).ResultsThe level of ANA was increased among 6 patients in the NTG group (17.1%), 8 in the POAG group (23.5%), and 6 in the control group (16.5%). The difference was not statistically significant (p=0.97). None of the patients in the NTG, POAG, or control group had positive antibodies to ENA. The level of immunoglobulins IgG, IgM, and IgA in the 3 groups was similar and within normal values. The median level of rheumatoid factor and ACPA was the highest in the NTG group, but it was within normal laboratory values. There was a statistically significant difference between antiprothrombin antibodies IgG between the NTG and POAG group (p=0.01), but not between the NTG and control group (p=0.24).ConclusionsThe results of our study do not confirm the hypothesis that NTG coexists with elevated blood levels of antibodies, which are a characteristic feature of rheumatic diseases.

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“…Elevated intraocular pressure (IOP) is one of the most common risk factors for the development of glaucoma and can be detected in approximately 70% of all patients; it has been termed the primary open-angle glaucoma (POAG) [1]. Next to other factors, the participation of an autoimmune component, including autoantibodies (AAB), has become a focus of attention in glaucoma research, providing new attractive targets for future diagnostic or therapeutic purposes [2,3,4,5,6,7]. A multitude of AABs against different kinds of retinal or optic nerve antigens have been identified, such as several heat shock proteins (HSP27, HSP60 and HSP70) [8,9], various crystallins (α- and β-crystallin) [8,10], vimentin [10], glycosaminoglycans [11] and α-fodrin [12].…”

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“…Consequently, the RGC axons bend and slow down the axonal transport of mitochondria and trophic factors from the brain to the RGC somas and vice versa [ 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 ] thereby reducing the communication between the eye and the brain. Soon the retinal blood vessels also exhibit increased tortuosity, and periods of ischemia occur that cause hypoxia and oxidative stress, resulting in mitochondrial dysfunction in the vulnerable RGCs, LC cells, and RGC axons [ 67 , 90 , 91 , 92 , 93 , 94 , 95 , 96 ]. Malfunctions and reduced activity of the transport systems in the compromised RGCs result in the extrusion of excess glutamate, endothelin, ATP, and other cytosolic constituents such as tumor necrosis factor-α [ 68 , 86 , 92 , 95 , 97 , 98 ].…”

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“…Antibodies to myelin basic protein and IgG-antibodies were found in the retinas of POAG, NTG and pseudoexfoliation glaucoma patients suggesting that a generalized autoimmune response against visual cell/tissue components can occur (Joachim et al, 2007a,b;Grus et al, 2008;Hammam et al, 2008). Clearly, much more research is needed to find and confirm such etiological aspects of the immune response in OHT and various forms of glaucoma (Gramlich et al, 2013;Joachim et al, 2014;Gramlich et al, 2016;Joachim et al, 2013;Skonieczna and Grabska-Liberek, 2014;Beutgen et al, 2019). Nevertheless, it is clear that age-related and/or pathological events occurring at the ANC-level (i.e., OHT) and at the LC/ONH-level cause progressive loss of RGCs and their axons, resulting in thinning of the RNFL and reduced connectivity to the brain, which leads to visual impairment and can cause blindness unless treatment(s) are started for the patient (Figure 8).…”