Ocular hypertension (increased pressure within the eye) is the largest risk factor in most glaucomas, but in some populations only 50% of patients with primary open angle glaucoma actually have elevated ocular pressure.
Those of African descent are three times more likely to develop primary open angle glaucoma. People who are older, have thinner corneal thickness, and myopia also are at higher risk for primary open angle glaucoma. People with a family history of glaucoma have about a six percent chance of developing glaucoma.
Many East Asian groups are prone to developing angle closure glaucoma due to their shallower anterior chamber depth, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Inuit also have a twenty to forty times higher risk than Caucasians of developing primary angle closure glaucoma. Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallower anterior chambers.
Other factors can cause glaucoma, known as "secondary glaucomas," including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle recession glaucoma); and uveitis (uveitic glaucoma).
Primary open angle glaucoma (POAG) has been found to be associated with mutations in genes at several loci. Normal tension glaucoma, which comprises one third of POAG, is associated with genetic mutations.
There is increasing evidence that ocular blood flow is involved in the pathogenesis of glaucoma. Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.
A number of studies also suggest a possible correlation between hypertension and the development of glaucoma. In normal tension glaucoma, nocturnal hypotension may play a significant role.
There is no clear evidence that vitamin deficiencies cause glaucoma in humans. It follows then that oral vitamin supplementation is probably not useful in glaucoma treatment.
Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally, failure of the normal third trimester gestational atrophy of the hyaloid canal and the tunica vasculosa lentis is associated with other anomalies. Angle closure induced ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies. and modelled in mice .
Those at risk for glaucoma are advised to have a dilated eye examination at least once a year.
Further Reading
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