ABSTRACT
Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world. It is a complex multifactorial disease, and despite new advances in treatment, many patients still succumb to visual impairment. The complement pathway has been implicated in the pathogenesis of many diseases, and recently variants in several genes encoding complement pathway proteins have been associated with AMD. Complement proteins have been found in histological specimens of eyes with AMD. Altered levels of both intrinsic complement proteins and activated products have been found in the circulation of patients with AMD. Complement activation may be triggered by oxidative stress, resulting from retinal exposure to incoming light; indeed an inter-play between these two pathological processes seems to exist. Finally, complement inhibitors are currently being evaluated in clinical trials. This article reviews the role of the complement system in AMD, and the potential of complement inhibition in preventing the devastating blindness resulting from this disease.
Subject(s)
Complement Activation/immunology , Complement System Proteins/metabolism , Macular Degeneration/pathology , Retina/pathology , Age Factors , Blindness/etiology , Complement Inactivator Proteins/therapeutic use , Complement System Proteins/genetics , Humans , Macular Degeneration/complications , Macular Degeneration/genetics , Macular Degeneration/immunology , Oxidative Stress , Retina/immunologyABSTRACT
PURPOSE: To correlate the response of topical dorzolamide (Trusopt; Merck) in patients with X-linked retinoschisis (XLRS) with genotype. METHODS: We carried out a retrospective evaluation of four patients (seven eyes) with XLRS, treated with topical dorzolamide. The change in best-corrected visual acuity (VA) and central macular thickness (CMT; central 1 mm subfield thickness) from optical coherence tomography (OCT) was analysed over the follow-up period, using Student's t-test. Each patient also had genetic analysis for mutations in the retinoschisisgene (RS1). RESULTS: The mean age at the start of treatment was 14.7±11 years, and mean follow-up duration was 21.7±7.7 months. Mean CMT at the final follow-up was significantly better than at baseline (291±123 vs 352±119 µm, P=0.007); however, mean VA was worse (0.38±0.25 vs 0.31±0.24 logMAR score, P=0.041). All four patients had a mutation in the RS1gene; there was no apparent association between the type of mutation and the response to topical dorzolamide. CONCLUSION: Topical dorzolamide may have some effect in reducing central macular thickness in patients with XLRS, but this does not necessarily correlate with improvement in VA. In our case series, genotypic information did not predict the response to this treatment.
Subject(s)
Eye Proteins/genetics , Genetic Diseases, X-Linked/drug therapy , Genetic Diseases, X-Linked/genetics , Retinoschisis/drug therapy , Retinoschisis/genetics , Sulfonamides/administration & dosage , Thiophenes/administration & dosage , Administration, Topical , Adolescent , Adult , Child , Female , Genotype , Humans , Macula Lutea/pathology , Male , Retinoschisis/physiopathology , Retrospective Studies , Tomography, Optical Coherence , Visual Acuity , Young AdultABSTRACT
AIM: To compare nurse-guided Optomap retinal imaging with examination by an eye casualty officer, in detecting clinically significant peripheral retinal lesions in patients with retinal symptoms. METHODS: 219 patients presenting to eye casualty with retinal symptoms (flashing lights and floaters) were recruited. Retinal images were taken with the Optomap imaging system, and graded by an independent masked ophthalmologist. The findings from the Optomap and casualty officer were compared with a gold-standard examination with scleral indentation performed by a retinal specialist. We calculated the sensitivity and specificity of the Optomap and casualty officer. RESULTS: The final analysis included 205 eyes of 187 patients. The sensitivity of the Optomap for detecting retinal detachment (n = 7) was 100% (95% CI 59-100%), the same as the casualty officer. For retinal holes/tears (n = 18) the Optomap sensitivity was 33% (13-59%), compared with 67% (41-87%) for the casualty officer. Combining all retinal lesions (n = 52), the sensitivity was 62% (47-75%) and 73% (59-84%), with specificity 96% (92-99%) and 98% (94-100%) for the Optomap and casualty officer respectively. CONCLUSION: The Optomap detects retinal detachments successfully but, due to limitations in the optics, is not able to accurately detect retinal holes and tears.
Subject(s)
Emergency Medical Services , Ophthalmoscopy/standards , Retinal Detachment/diagnosis , Emergency Service, Hospital , Female , Humans , Male , Microscopy, Confocal/instrumentation , Middle Aged , Retinal Perforations/diagnosis , Sclera/physiology , Sensitivity and SpecificityABSTRACT
Serum total sialic acid (TSA) has recently been shown to be related to diabetic retinopathy. However, there is some controversy as this may be true in European Type 2 diabetic patients but not South Asians. There are few data looking at serum TSA expression in Arab Type 2 diabetic patients from the United Arab Emirates (UAE) and we wished to test the hypothesis that there may be different serum TSA expression in Arab Type 2 diabetic patients as regard to retinopathy. Sixty-five Type 2 diabetic patients from the UAE were studied (19 male and 46 female, age 57.5+/-9.8 (45-74) years, duration of diabetes 9.4+/-5.7 (0-22) years. The serum TSA in 13 patients with diabetic retinopathy was 757+/-130 mg/l and 782+/-163 mg/l in those without retinopathy (NS). There was no significant correlation between serum TSA and patient age, serum fructosamine, diabetes duration, or blood pressure. As in South Asians serum TSA does not appear to be elevated in Type 2 diabetic patients from the United Arab Emirates with diabetic retinopathy.
