Glaucoma is the most commonly acquired optic neuropathy. It represents a public health challenge because it causes an irreversible blindness. Emerging evidence indicates that the pathogenesis of glaucoma depends on several interacting pathogenetic mechanisms, which include mechanical effects by an increased intraocular pressure, decreased neutrophine-supply, hypoxia, excitotoxicity, oxidative stress, and the involvement of autoimmune processes. In particular, alterations in serum antibody profiles have been described. However, it is still unclear whether the autoantibodies seen in glaucoma are an epiphenomenon or causative. Oxidative stress appears to be a critical factor in the neurodestructive consequences of mitochondrial dysfunction, glial activation response, and uncontrolled activity of the immune system during glaucomatous neurodegeneration. In addition, hearing loss has been identified in association with glaucoma. A higher prevalence of antiphosphatidylserine antibodies of the immunoglobulin G class was seen in normal-tension glaucoma patients with hearing loss in comparison with normal-tension glaucoma patients with normacusis. This finding suggests a similar pathological pathway as a sign for generalized disease. Glaucoma is the second leading cause of blindness globally, after cataracts. It presents an even greater public health challenge than cataracts because the blindness it causes is irreversible.1 Numerous interesting studies investigate the involvement of immunological mechanisms. Wax et al,2 in 1998, detected antibodies against endogenous antigens such as heat shock protein 60 in the serum of normal-tension glaucoma patients. Recently, glaucoma patients were found to develop antibody alterations against specific retina and optic nerve proteins. In the experimental autoimmune glaucoma model, Grus and Gramlich3 demonstrated that an immunization with these proteins causes retinal ganglion cell loss in an autoimmune context. Despite these results, it is still unclear whether the changes in antibody patterns have a causal connection with glaucoma development or are epiphenomena of the disease.
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-Antonio Greco, MD, Maria Ida Rizzo, MD, Armando De Virgilio, MD, Andrea Gallo, MD, Massimo Fusconi, MD, Marco de Vincentiis, MD
This article originally appeared in the September 2016 issue of The American Journal of Medicine.