Abstract
Pseudoexfoliation (PXF) glaucoma is classically diagnosed by slit lamp visualization of white powdery deposits (PXF material) in a bull’s eye configuration on the lens capsule. PXF glaucoma is the most common form of open-angle worldwide with an identifiable etiology.1 The presence of PXF material is associated with an increased risk of developing glaucoma, but can be present in the eye without associated glaucoma. This disorder also has an association with narrow angles secondary to zonular weakness, increased rate and risk of cataract formation, and increased risk of complications during cataract extraction associated with zonular dehiscence. PXF glaucoma’s primary manifestations and morbidity are ocular. However, PXF is a systemic condition with PXF material present throughout the body. The presence of PXF material has been weakly associated with cardiovascular and cerebrovascular morbidity and sensorineural hearing loss.2–10 Unlike PXF and glaucoma, a direct cause-effect relationship remains to be clearly established between the presence of PXF material and the aforementioned systemic associations. PXF syndrome was first described by Lindbergh in the year 1917, followed by Vogt, and initially termed “glaucoma capsulare.” The classic white flaky dandrufflike material was initially thought to originate from the lens capsule.11 Immunohistologic and electron microscopy studies suggest the PXF material deposited on the lens capsule and throughout the anterior segment of the eye (ie, the angle, corneal endothelium, etc.) is a product of abnormal extracellular matrix material metabolism.1 PXF is distinct from true exfoliation syndrome observed in glass blowers, where a schisis of the anterior lens capsule occurs. Recent molecular and genetic studies have revealed clues as to the molecular pathogenesis of PXF material formation and the association of PXF with the extracellular matrix and cellular metabolism.12,13 This paper reviews current concepts in the medical and surgical management of PXF glaucoma.
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