ABSTRACT
Glaucoma is one of the leading causes of blindness worldwide. The current view of glaucoma is that it is a multifactorial disease. Elevated IOP is a recognized etiologic factor which can trigger initial damage through biomechanical and ischemic injury to the retinal ganglion cells. However, elevated intraocular pressure cannot be entirely responsible for the development of glaucoma. Accumulating evidence suggests that abnormal immunity may be contributing to the glaucomatous optic neuropathy. Autoimmunity may be responsible for initiating or exacerbating glaucoma. This review provides an evaluation of the potential role of autoimmunity in some patients with glaucoma.
Subject(s)
Autoimmunity/physiology , Glaucoma/physiopathology , Optic Nerve Diseases/physiopathology , Glaucoma/immunology , Humans , Immune System/physiology , Optic Nerve Diseases/immunology , Oxidative Stress , Retinal Ganglion Cells/pathologyABSTRACT
In 1948, Posner and Schlossman first reported glaucomatocyclitic crisis, an uncommon form of glaucoma characterized by recurrent unilateral episodes of markedly elevated intraocular pressure (IOP) with mild idiopathic anterior chamber inflammation. The exact etiology of glaucomatocyclitic crisis is not clear. Although it is typically a self-limited condition, some cases with advanced optic nerve cupping and associated visual field loss have been reported. Diagnosis of Posner-Schlossman syndrome is difficult, and it may mimic a variety of ocular disorders. Treatment of this syndrome is directed towards controlling the inflammation and associated IOP elevation.
