| Popis: |
Devon Hori Harvey,1,2 Chenna Kesavulu Sugali,1,2 Weiming Mao1– 5 1Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN, USA; 2Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, IN, USA; 3Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA; 4Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA; 5Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USACorrespondence: Weiming Mao, Department of Ophthalmology, Indiana University School of Medicine, RM305v, 1160 W. Michigan St, Indianapolis, IN, 46202, USA, Tel +1 317 278 0801, Email weimmao@iu.eduAbstract: Glucocorticoid (GC) therapy is indicated in many diseases, including ocular diseases. An important side-effect of GC therapy is GC-induced ocular hypertension (GIOHT), which may cause irreversible blindness known as GC-induced glaucoma (GIG). Here, we reviewed the pathological changes that contribute to GIOHT including in the trabecular meshwork and Schlemm’s canal at cellular and molecular levels. We also discussed the clinical aspects of GIOHT/GIG including disease prevalence, risk factors, the type of GCs, the route of GC administration, and management strategies.Keywords: glucocorticoid, intraocular pressure, trabecular meshwork, aqueous humor outflow, mechanism, treatment |
