Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cystoid macular edema (CME), a common complication following cataract surgery, is routinely medically treated with topical nonsteroidal anti-inflammatory drugs (NSAIDs), alone or in combination with steroids. In this paper, we describe 6 patients with CME and 1 patient with diabetic macular edema (DME), all of whom were treated with nepafenac 0.1%, a novel prodrug NSAID. Three (3) patients with acute CME following cataract surgery were treated for 3-4 weeks with nepafenac 0.1%, with or without concomitant steroids. Both retinal thickness and visual acuity improved in all 3 cases. The 3 patients with chronic CME, each of whom had been previously treated with steroids with or without concomitant NSAID therapy, were started on nepafenac 0.1% three times daily. Retinal thickness and visual acuity improved in each case, except for 1 patient with 20/25 pretreatment visual acuity. The mean improvement in visual acuity of all 6 CME patients was 2.5 lines and the mean decrease in retinal thickness was 282.8 microm. The patient with DME also showed improvement in retinal thickness and visual acuity after 6 months of treatment with nepafenac. These clinical data strongly suggest that nepafenac 0.1% is a promising drug for the treatment of posterior segment inflammation, including CME, and warrants further investigation.
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PMID:Cystoid and diabetic macular edema treated with nepafenac 0.1%. 1800 Dec 48

Intravitreal pharmacotherapies have been used with increasing frequency in the treatment of retinal disease. Indications for their use include choroidal neovascular membranes, diabetic macular edema, ischemic neovascularization, inflammatory and infectious processes, and neoplasia. Complications of intravitreal therapies include cataract formation, glaucoma, and endophthalmitis. Recent developments of pharmacologic agents administered intravitreally and the new applications of systemic medications in retinal disease present the practitioner with expanded treatment options. Current and emerging data will help guide therapy in order to maximize the benefits and limit the systemic and ocular complications of these new treatment options.
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PMID:Intravitreal pharmacotherapy: applications in retinal disease. 1820 13

Macular edema, a condition usually associated with an underlying disease process, is a common cause of severe visual loss. There have been a variety of approaches to the treatment of macular edema; within the past few years, however, intravitreal corticosteroid treatments have emerged as an increasingly used treatment option for patients with macular edema. Intravitreal delivery allows the steroid to bypass the blood-retinal barrier, leading to a more concentrated dose of steroid for a prolonged period of time. Corticosteroids have likely been successful in the treatment of various forms of macular edema, due to their known anti-angiogenic, anti-edematous, anti-inflammatory, anti-apoptotic, and anti-proliferative effects. Intravitreal triamcinolone acetonide has been repeatedly successful in reducing macular edema and improving visual acuity, although the duration of action is typically short-term. Due to the recurrent and chronic nature of macular edema, biodegradable implants may be the future of intravitreal steroids. Intravitreal corticosteroids are not without risks. Steroid-related side effects include cataract formation and elevated intraocular pressure. Injection-related side effects include retinal detachment, vitreous hemorrhage, bacterial endophthalmitis, and sterile endophthalmitis. This article reviews the evolving role of intravitreal corticosteroids in the treatment of macular edema secondary to uveitis, diabetes, and retinal vascular disorders.
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PMID:Intravitreal steroids for macular edema: the past, the present, and the future. 1942 73

My prime years as an ophthalmologist began as intraocular lenses (IOLs) were just entering into the developmental stage, and I took on as my mission to contribute to perfecting safe and reproducible cataract/IOL implantation surgery. Identifying surgical and/or IOL-related complications consumed time; however, these complications soon became predictable and even preventable with the use of sensitive biological parameters and preclinical evaluation. This was a simple goal for me to pursue my studies on cataract/IOL implantation surgery. I discuss in this review article, based on my previous research, clinico-pathophysiological problems of these intra- and postoperative eyes. The early phase of cataract/IOL implantation surgery development began with a debate as to which is physiologically superior: intracapsular cataract extraction (ICCE) or extracapsular cataract extraction (ECCE). From the perspective of transporting substances from intraocular fluids to extraocular space, which we studied using a nonphysiological substance, fluorescein, ECCE was confirmed to be physiologically superior to ICCE. The transport mechanism of both physiological and nonphysiological substances from intraocular fluids (such as vitreous and aqueous humor) is believed to be related to the pathogenesis of various ocular disorders. Following the fluorescein study, I next focused my attention on biosynthesis and active transport of prostaglandin (PG), which are inflammatory mediators. My studies revealed that PG were more likely to accumulate in ICCE eyes than in ECCE eyes; higher intraocular concentration of PG was also confirmed in eyes with persistent aphakic or pseudophakic cystoid macular edema (CME). While conducting the above studies and having made some observations, I postulated another hypothesis on the pathogenesis of aphakic or pseudophakic CME as follows: topical application of nonsteroidal antiinflammatory drugs (NSAIDs) to eyes with PG, which are biosynthesized intra- and postoperatively during the healing process of uveal tissues and lens epithelial cells, prevents CME. Based on this hypothesis experimental studies were then started, and in 1977 I became the first in the world to prove that topical application of indomethacin, one of the NSAIDs, controls the incidence of CME in ICCE eyes. Thereafter, some 40 follow-up studies have been conducted worldwide, and recent meta-analysis has established the efficacy of indomethacin. Macular edema and CME are recently of significant interest as complications in various ocular disorders. Compared to other forms of CME, the pathophysiology of CME associated with aphakic/ pseudophakic eyes is relatively simple, its natural history is well understood and its reproducibility is high. It is possible that the other forms of macular edema or CME having more complicated pathogenesis may be interpreted by understanding the formation mechanism of aphakia/pseudophakic CME. Our studies have shown how chemical mediators (PG) are systematically involved in the development of aphakic/pseudophakic CME, and that they concurrently cause blood-aqueous barrier disruption and CME, decrease oscillatory potential of the full field ERG, and decrease choroidal blood flow at an early postoperative period, and this has recently been proven. All these phenomena, however, can be effectively prevented by topical application of NSAIDs. I believe these findings provide significant information when considering the pathogenesis and treatment of CME associated with other ocular disorders. Using the primitive method of an early phase, I discovered that anti-PG eye drops can treat disrupted blood-aqueous barrier, and confirmed that the blood-aqueous barrier function is indeed a very sensitive function. I next applied fluorophotometry and laser flaremetry. Using blood-aqueous barrier function as a parameter, the following were evaluated: consensual reaction of blood-aqueous barrier disruption, method of IOL fixation, racial differences in disruption of the aqueous barrier function, drugs used perioperatively, biocompatibility of IOL materials, and effects of preservative agents. Research on preservative agents disclosed that the preservative agent in anti-glaucoma drops more strong by induced pseudophakic CME than the anti-glaucoma agent itself. Thus, this introduced a new concept called Our desire to closely observe the endosurface of the iris, ciliary processes and anterior vitreous face, all of which are closely related to phacoemulsification techniques, posterior chamber lens fixation, and active transport of PG, led me to the development of "Posterior video technique" (Miyake-Apple View). The technique since then has been used to evaluate cataract surgical techniques, to analyze complications, to review IOL designs and fixation techniques, to pre-clinically evaluate surgical devices, and to study variations of local anatomy related to cataract/IOL surgery. The method is also useful as an educational as well as a presentational tool, and it has now been accepted world-wide. The pathogenesis of aphakic/pseudophakic CME, physiological evaluation centering on blood-aqueous barrier function, and preclinical evaluation using the Posterior video technique have all played a significant role in establishing today's safe cataract/IOL implantation surgery.
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PMID:[Studies on clinical pathophysiology of pseudophakic/aphakic eyes--a journey of 4 decades]. 1841 12

Blindness or low vision affects more than 3 million Americans 40 years and older, and this number is projected to reach 5.5 million by 2020. In addition to treating a patient's vision loss and comorbid medical issues, physicians must be aware of the physical limitations and social issues associated with vision loss to optimize health and independent living for the visually impaired patient. In the United States, the four most prevalent etiologies of vision loss in persons 40 years and older are age-related macular degeneration, cataracts, glaucoma, and diabetic retinopathy. Exudative macular degeneration is treated with laser therapy, and progression of nonexudative macular degeneration in its advanced stages may be slowed with high-dose antioxidant and zinc regimens. The value of screening for glaucoma is uncertain; management of this condition relies on topical ocular medications. Cataract symptoms include decreased visual acuity, decreased color perception, decreased contrast sensitivity, and glare disability. Lifestyle and environmental interventions can improve function in patients with cataracts, but surgery is commonly performed if the condition worsens. Diabetic retinopathy responds to tight glucose control, and severe cases marked by macular edema are treated with laser photocoagulation. Vision-enhancing devices can help magnify objects, and nonoptical interventions include special filters and enhanced lighting.
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PMID:The visually impaired patient. 1981 33

Diabetes Mellitus (DM) is a serious medical problem that causes long-term systemic complications and considerable associated morbidity. DM can cause retinopathy (DRP), maculopathy, cataract, optic neuropathy, defects of eye muscles. DM is a risk factor for acute infectious conjunctivitis, bacterial keratitis, herpes virus infections and endophtalmitis. Elevated blood glucose induces structural, physiological and hormonal changes which affect retinal capillaries. DRP is recognized by loss of pericyte function and capillary occlusions together leading to breakdown of blood-retinal barrier, edematous changes and proliferation of vessels and fibrous tissue. Depending on stage of DRP, there are different preferable therapeutic approaches applied. In the case of ETDRS, in the area of leakage focal treatment should be performed, while panretinal photocoagulation is applied towards ischemic areas or beginning proliferations. Vitreal haemorrhage followed by fibroproliferative changes or tractional retinal detachment is treated by vitrectomy alone or in combination with ILM peeling. In pathogenesis of DRP, Insulin Growth Factor (IGF-1) can play an important role in production of VEGF (Vascular Endothelial Growth Factor). Hypoxia can up-regulate VEGF expression levels leading to pathologic ocular neovascularisation. An application of intravitreal corticosteroid treatment modulates vascular permeability by suppressing the production of VEGF, reducing both extracellular matrix metalloproteinase activity and basic fibroblast growth factor, decreasing major histocompatibility complex 2 Ag expression levels, and inhibiting activity of inflammatory cells. Clinical effects of treatment using intravitreal corticosteroids are evaluated by reduction of macular thickness and visual improvement. Intravitreal use of Anti-VEGF drugs, Pegaptanib, Ranibizumab and Bevacizumab can modify vasoproliferation, trigger macular edema, and, therefore, influence a prognosis for visual loss.
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PMID:Eye disorders in diabetes: potential drug targets. 1853 2

Optical coherent tomography (OCT) shows that in patients with diabetes mellitus (DM), a macular morphological response to cataract phacoemulsification (CPE) with intaocular lens (IOL) implantation proceeds as 3 types: 1) areactive without macular morphological changes; 2) hyperreactive with the development of reversible subclinical macular edema; and 3) aggressive with the transition of stress-induced retinal morphological lesions to clinically significant diabetic macular edema. Morphological differences in OCT parameters were established to have impact on the effect of visual rehabilitation. Following 3-4 months of CPE with IOL implantation in DM patients with the areactive type of a macular morphological response to surgical stress, the increase in visual acuity exceeded that observed in the hyperactive and aggressive types of a macular response by 12.8 and 57.7%, respectively. The findings suggest that medical preventive measures reducing the negative consequences of surgical stress should be implemented in DM patients at catarrhal surgery.
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PMID:[Clinical and morphometric macular changes in patients with diabetes mellitus after cataract phacoemulsification]. 1875 95

This review describes the possible interactions between several retinal diseases, their treatment, and intraocular pressure (IOP). The use of the intravitreal route in the delivery of drugs to the retina has recently gained widespread acceptance with the development of the VEGF inhibitors and glucocorticoids such as triamcinolone. Although the intravitreal route offers high local concentrations in the vitreous, in the retina these advantages are offset by side effects, particularly short-term and chronic elevation of IOP. This review describes the clinical features of steroid glaucoma induced by triamcinolone or sustained-release systems of glucocorticoid drugs. Another aspect of the relationships between glaucoma and retina is also described: published reports of the occurrence of cystoid macular edema (CME) in eyes being treated with the prostaglandin analogs (PGAs) have led to concern regarding a possible causal relationship between the two. A review of the literature suggests that most PGA-treated eyes with CME had independent risk for development of CME, with a disruption of the blood-aqueous barrier: open or absent posterior capsule, history of dipivefrin-associated CME, epiretinal membrane, complicated cataract surgery, history of macular edema associated with branch retinal vein occlusion, ocular inflammation, and diabetes mellitus. In eyes at risk for CME, the use of PGAs is acceptable but must be prudent.
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PMID:[Retina and glaucoma: therapeutic considerations]. 1895 16

Vitreous surgery has various physiological and clinical consequences, both beneficial and harmful. Vitrectomy reduces the risk of retinal neovascularization, while increasing the risk of iris neovascularization, reduces macular edema and stimulates cataract formation. These clinical consequences may be understood with the help of classical laws of physics and physiology. The laws of Fick, Stokes-Einstein and Hagen-Poiseuille state that molecular transport by diffusion or convection is inversely related to the viscosity of the medium. When the vitreous gel is replaced with less viscous saline, the transport of all molecules, including oxygen and cytokines, is facilitated. Oxygen transport to ischemic retinal areas is improved, as is clearance of VEGF and other cytokines from these areas, thus reducing edema and neovascularization. At the same time, oxygen is transported faster down a concentration gradient from the anterior to the posterior segment, while VEGF moves in the opposite direction, making the anterior segment less oxygenated and with more VEGF, stimulating iris neovascularization. Silicone oil is the exception that proves the rule: it is more viscous than vitreous humour, re-establishes the transport barrier to oxygen and VEGF, and reduces the risk for iris neovascularization in the vitrectomized-lentectomized eye. Modern vitreous surgery involves a variety of treatment options in addition to vitrectomy itself, such as photocoagulation, anti-VEGF drugs, intravitreal steroids and release of vitreoretinal traction. A full understanding of these treatment modalities allows sensible combination of treatment options. Retinal photocoagulation has repeatedly been shown to improve retinal oxygenation, as does vitrectomy. Oxygen naturally reduces VEGF production and improves retinal hemodynamics. The VEGF-lowering effect of photocoagulation and vitrectomy can be augmented with anti-VEGF drugs and the permeability effect of VEGF reduced with corticosteroids. Starling's law explains vasogenic edema, which is controlled by osmotic and hydrostatic gradients between vessel and tissue. It explains the effect of VEGF-induced vascular permeability changes on plasma protein leakage and the osmotic gradient between vessel and tissue. At the same time, it takes into account hemodynamic changes that affect the hydrostatic gradient. This includes the influence of arterial blood pressure, and the effect oxygen (laser treatment) has in constricting retinal arterioles, increasing their resistance, and thus reducing the hydrostatic pressure in the microcirculation. Reduced capillary hydrostatic pressure and increased osmotic gradient reduce water fluxes from vessel to tissue and reduce edema. Finally, Newton's third law explains that vitreoretinal traction decreases hydrostatic tissue pressure in the retina, increases the pressure gradient between vessel and tissue, and stimulates water fluxes from vessel into tissue, leading to edema.
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PMID:Physiology of vitreous surgery. 1903 81

We review the epidemiology, pathophysiology, and etiology of cystoid macular edema (CME). Inflammatory, diabetic, post-cataract, and macular edema due to age-related macular degeneration is described. The role of chronic inflammation and hypoxia and direct macular traction is evaluated in each case according to different views from the literature. The different diagnostic methods for evaluating the edema are described. Special attention is given to fluoroangiography and the most modern methods of macula examination, such as ocular coherence tomography and multifocal electroretinography. Finally, we discuss the treatment of cystoid macular edema in relation to its etiology. In this chapter we briefly refer to the therapeutic value of laser treatment especially in diabetic maculopathy or vitrectomy in some selected cases. Our paper is focused mainly on recent therapeutic treatment with intravitreal injection of triamcinolone acetonide and anti-VEGF factors like bevacizumab (Avastin), ranibizumab (Lucentis), pegaptamid (Macugen), and others. The goal of this paper is to review the current status of this treatment for macular edema due to diabetic maculopathy, central retinal vein occlusion and post-cataract surgery. For this reason the results of recent multicenter clinical trials are quoted, as also our experience on the use of intravitreal injections of anti-VEGF factors and we discuss its value in clinical practice.
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PMID:Cystoid macular edema. 1966 45


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