The case for autoimmunity in glaucoma

Although the majority of patients with glaucoma have elevated intraocular pressure as the presumed etiology for their resultant neuropathy, it is well known that approximately 25% of patients with glaucoma have intraocular pressure within the normal range for their race. These patients may have conditions that facilitate non-pressure related stress to the retina and optic nerve that might directly contribute to their glaucomatous neuropathy and include chronic or intermittent ischemia (i.e atherosclerosis, heart disease, vasospasm, migraine, sleep apnea), altered scleral/optic nerve head morphology that predisposes to glaucomatous stress (i.e myopia); genetic mutations that predispose to glaucoma damage at normal IOP (OPA-1,optineurin, myocilin) and evidence of aberrant immunity that suggests that their glaucoma might be a form of an autoimmune neuropathy (i.e. presumed autoimmune glaucoma). This review provides a critical assessment of the potential role for autoimmunity as an initiating or exacerbating etiology in some patients with glaucoma.

► Autoimmunity may underlie the etiology or the progression of glaucoma in some patients.
► The presence of anti-retinal or optic nerve antibodies in patients with glaucoma may represent a normal physiological process; may be representative of epiphenomenon that accompanying the disease process; may be representative of biomarkers of a specific pathological process; or may be of genuine pathogenic importance.
► The diagnosis of “presumed autoimmune glaucoma” is a diagnosis of exclusion. Unfortunately therapeutic options are limited if autoimmunity is indeed autoimmunity the cause of the glaucomatous neuropathy