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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steroid treatment has gained notoriety due to its tendency to induce multiple side effects, including a variety of ocular side effects. Administration of local, regional, inhalation or systemic steroids may induce the development of ocular hypertension, which might even result in subsequent open angle glaucoma. About one in every three people is considered a potential "steroid responder". A significant elevation of intraocular pressure might result in these patients in response to steroid treatment. Included in this group are patients with first degree relatives suffering from open angle glaucoma. Morphologic changes in the trabecular meshwork (which serves as the site of aqueous humor drainage from the eye) are suggested as the proposed mechanism through which steroid treatment results in glaucoma. Steroids are said to induce the expression of a gene that is located on chromosome 1 and is known as TIGR or GLCIA. its product is a protein called myocilin. Ocular hypertension secondary to steroid treatment is usually reversible, when treatment is limited to a period of less than 12 months. The fear of ocular hypertension, which is usually unnoticed by the patient, obligates regular ophthalmologic follow-up examinations, including tonometry, visual fields and optic disc examinations.
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PMID:[Steroid induced glaucoma]. 1265 48

Glaucoma patients present a unique set of challenges to physicians performing corneal refractive surgery. Corneal thickness, which is modified during corneal refractive surgery, plays an important role in monitoring glaucoma patients because of its effect on the measured intraocular pressure. Patients undergo a transient but significant rise in intraocular pressure during the laser-assisted in situ keratomileusis (LASIK) procedure with risk of further optic nerve damage or retinal vein occlusion. Glaucoma patients with filtering blebs are also at risk of damage to the bleb by the suction ring. Steroids, typically used after refractive surgery, can increase intraocular pressure in steroid responders, which is more prevalent among glaucoma patients. Flap interface fluid after LASIK, causing an artificially low pressure reading and masking an elevated pressure has been reported. The refractive surgeon's awareness of these potential complications and challenges will better prepare them for proper management of glaucoma patients who request corneal refractive surgery.
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PMID:Considerations of glaucoma in patients undergoing corneal refractive surgery. 1626 74

Steroids in susceptible individuals can cause a clinical condition similar to primary open-angle glaucoma. Five percent of the population are high steroid responders and develop an intraocular pressure (IOP) elevation of more than 15 mm Hg above baseline. IOP elevation may occur as early as 1 day to as late as 12 weeks after intravitreal triamcinolone in 20-65% of patients. On average, 75% of eyes with steroid implants require IOP-lowering therapy at some point within 3 years of follow-up. The exact mechanism of steroid-induced glaucoma is not totally understood, but decreased trabecular meshwork outflow is regarded as the main cause of IOP elevation. High-risk patients who receive steroids should be monitored closely and if they develop elevated IOP, steroids with lower potency or steroid-sparing agents should be used. The IOP usually returns to normal within 2-4 weeks after stopping the steroid. About 1-5% of patients do not respond to medical therapy and need surgery. Trabeculectomy, trabeculotomy, shunt surgery, and cyclodestructive procedures are among the methods employed. Removal of residual sub-Tenon or intravitreal steroids may help hasten the resolution of the steroid response. Early results with anecortave acetate, an analog of cortisol acetate with antiangiogenic activity, in controlling IOP have been promising.
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PMID:Steroid-induced iatrogenic glaucoma. 2175 64

With the current widespread use of anti-VEGFs in the treatment of central retinal vein occlusion (CRVO), the role for steroids has become greatly diminished. Recent large scale randomized control trials (RCTs) have established the efficacy and safety of anti-VEGFs in the treatment of CRVO. Steroids are known to cause elevations in intraocular pressure as well as increase the risk of cataract formation. With that in mind many ophthalmologists are injecting steroids less frequently. This paper aims to review some of the data pertaining to the use of steroids either as a first line monotherapy, adjunct therapy, or an alternative therapy to help answer the question: Is there currently any role for steroids in the management of CRVO?
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PMID:Steroids in Central Retinal Vein Occlusion: Is There a Role in Current Treatment Practice? 2663 73

Steroids are a group of anti-inflammatory drugs, commonly used to treat ocular and systemic conditions. Unmonitored use of steroids especially in eye drop formulations is common in situations when it is easily available over-the-counter, resulting in undesirable side effects. Among the ocular side effects, cataract and glaucoma are common. Steroid-induced ocular hypertension was reported in 1950, when long-term use of systemic steroid was shown to increase the intraocular pressure (IOP). Chronic administration of steroids in any form with raised IOP can cause optic neuropathy resulting in steroid-induced glaucoma. This review describes the pathophysiology and epidemiology of steroid-induced glaucoma, recognition of side effects, and principles of management. The purpose is to familiarize all clinicians with the potential dangers of administering steroids without monitoring the eye and the dangers of irreversible blind -ness in some instances of habitual self-prescription by patients.
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PMID:Steroid-induced Glaucoma: An Avoidable Irreversible Blindness. 2892 42

Inflammation is substantially contributing to the development and worsening of diabetic retinopathy in general and diabetic macular edema (DME) in particular, which provides the rationale to treat DME with corticosteroids. While anti-vascular endothelial growth factor (VEGF) agents are mostly chosen as a first-line treatment, there is an important role for steroids in the treatment algorithm for DME. A slow-release bioerodible dexamethasone implant and an extended-release nonbioerodible fluocinolone acetonide insert are both approved for the treatment of DME and provide the advantage of sustained drug delivery and reduced treatment burden. Steroids bare the complications of cataract progression and increase of intraocular pressure (IOP). However, with dexamethasone implant, IOP rise is well manageable with topical treatment in almost all cases. Dexamethasone implant has been shown to be effective in the treatment of naive DME as well as in eyes nonresponding to anti-VEGF agents. In these cases, early switching to steroids may be considered and has been shown to be beneficial. Fluocinolone acetonide is reserved for severe cases of chronic DME insufficiently responsive to other available therapies. Future randomized controlled trials are needed to realize the role of steroids in the current treatment algorithm of DME.
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PMID:The Role of Steroids in the Management of Diabetic Macular Edema. 3104 80

The aim of this article is to provide an overview of characteristics and principles of use of dexamethasone implant in patients with diabetic macular edema (DME). The condensed information about patient selection, dosing, and postinjection management is provided to make the clinician's decisions easier in real-life practice. DME is a common complication of diabetes and the leading cause of visual loss in the working-age population. Inflammation plays an important role in the pathogenesis of DME. The breakdown of the blood-retinal barrier involves the expression of inflammatory cytokines and growth factors, including vascular endothelial growth factor (VEGF). Steroids have proved to be effective in the treatment of DME by blocking the production of VEGF and other inflammatory cytokines, by inhibiting leukostasis, and by enhancing the barrier function of vascular endothelial cell tight junctions. Dexamethasone intravitreal implant has demonstrated efficacy in the treatment of DME resistant to anti-VEGF therapy and in vitrectomized eyes. Data from clinical trials suggest that dexamethasone implant can be considered as first-line treatment in pseudophakic eyes. Dexamethasone implant is also the first-line therapy in patients not suited for anti-VEGF therapy, pregnant women, and patients unable to return for frequent monitoring. It has been shown that the maximum effect of dexamethasone implant on visual gain and retinal thickness occurs approximately 2 months after injection. Various treatment regimens are used in real-life situations, and reported reinjection intervals were usually <6 months. The number of retreatments needed decreased over time. Treatment algorithms should be personalized. Postinjection management and follow-up should consider potential adverse events such as intraocular pressure elevation and cataract.
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PMID:Dexamethasone implant in the management of diabetic macular edema from clinician's perspective. 3119 Jul 26