Steroid induced ocular hypertension

Posterior capsular opacification, also known as after-cataract, is a condition in which months or years after successful cataract surgery, vision deteriorates or problems with glare and light scattering recur, usually due to thickening of the back or posterior capsule surrounding the implanted lens, so-called 'posterior lens capsule opacification'. Growth of natural lens cells remaining after the natural lens was removed may be the cause, and the younger the patient, the greater the chance of this occurring. Management involves cutting a small, circular area in the posterior capsule with targeted beams of energy from a laser, called Nd:YAG laser capsulotomy, after the type of laser used. The laser can be aimed very accurately, and the small part of the capsule which is cut falls harmlessly to the bottom of the inside of the eye. This procedure leaves sufficient capsule to hold the lens in place, but removes enough to allow light to pass directly through to the retina. Serious side effects are rare. [56] Posterior capsular opacification is common and occurs following up to one in four operations, but these rates are decreasing following the introduction of modern intraocular lenses together with a better understanding of the causes.

Long term use of topical & systemic steroids produce secondary open angle glaucoma similar to chronic simple glaucoma. The increased IOP caused by prolonged steroid therapy is reversible but the damage produced by it is irreversible. In this study, we analysed 25 patients (44 eyes) with steroid induced glaucoma, who reported to us with dimness of vision, haloes and elevated . and were using steroids for long duration due to various causes. The behaviour of the . due to different steroid preparations, the type of lenticular change, and the management of those cases are discussed in this paper. From our study we conclude that dexamethasone and betamethasone both topical as well as systemic are more potent in producing glaucoma and cataract than medrysone and prednisolone. The condition is reversible without permanent damage when the duration of steroid therapy is short and vice versa.

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Steroid-induced posterior subcapsular cataracts (PSCs) exhibit three main distinctive characteristics: (i) association only with steroids possessing glucocorticoid activity, (ii) involvement of aberrant migrating lens epithelial cells, and (iii) a central posterior location. The first characteristic suggests a key role for glucocorticoid receptor activation and subsequent changes to the transcription of specific genes. Glucocorticoid receptor activation is associated in many cell types with proliferation, suppressed differentiation, a reduced susceptibility to apoptosis, altered transmembrane transport, and enhancement of reactive oxygen species activity. Glucocorticoids may be capable of inducing changes to the transcription of genes in lens epithelial cells that are related to many of these cellular processes. This review examines the various mechanisms that have been proposed to account for the development of PSC in the context of recent DNA array studies. Additionally, given that the glucocorticoid receptor can also engender wide-ranging indirect activities, glucocorticoids could also indirectly affect the lens through the responses of other cells within the ocular compartment and/or through effects on cells at more remote locations. These indirect mechanisms, which, for example, could be mediated through alterations to the intraocular levels of growth factors that normally orchestrate lens development and maintain lens homeostasis, are also discussed. Although the mechanism of steroid cataract induction remains unknown, glucocorticoid-induced gene transcription events in lens epithelial cells, and also other intraocular or systemic cells, likely interact to generate steroid cataracts. Finally, although evidence for glucocorticoid-protein adduct formation in the lens is inconclusive, the generation of such adducts cannot yet be discounted as a contributing factor and must necessarily be retained in discussions of the etiology of steroid cataract.

Steroid induced ocular hypertension

steroid induced ocular hypertension

Steroid-induced posterior subcapsular cataracts (PSCs) exhibit three main distinctive characteristics: (i) association only with steroids possessing glucocorticoid activity, (ii) involvement of aberrant migrating lens epithelial cells, and (iii) a central posterior location. The first characteristic suggests a key role for glucocorticoid receptor activation and subsequent changes to the transcription of specific genes. Glucocorticoid receptor activation is associated in many cell types with proliferation, suppressed differentiation, a reduced susceptibility to apoptosis, altered transmembrane transport, and enhancement of reactive oxygen species activity. Glucocorticoids may be capable of inducing changes to the transcription of genes in lens epithelial cells that are related to many of these cellular processes. This review examines the various mechanisms that have been proposed to account for the development of PSC in the context of recent DNA array studies. Additionally, given that the glucocorticoid receptor can also engender wide-ranging indirect activities, glucocorticoids could also indirectly affect the lens through the responses of other cells within the ocular compartment and/or through effects on cells at more remote locations. These indirect mechanisms, which, for example, could be mediated through alterations to the intraocular levels of growth factors that normally orchestrate lens development and maintain lens homeostasis, are also discussed. Although the mechanism of steroid cataract induction remains unknown, glucocorticoid-induced gene transcription events in lens epithelial cells, and also other intraocular or systemic cells, likely interact to generate steroid cataracts. Finally, although evidence for glucocorticoid-protein adduct formation in the lens is inconclusive, the generation of such adducts cannot yet be discounted as a contributing factor and must necessarily be retained in discussions of the etiology of steroid cataract.

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