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العنوان
Retinal Toxicity Induced by Systemic Drugs/
المؤلف
Zayed,Samar Osama Ahmed EL Gharib
هيئة الاعداد
باحث / سمر أسامة أحمد الغريب زايد
مشرف / شريف زكي منصور
مشرف / ريهام فوزي الشناوي
الموضوع
Retinal Toxicity Induced
تاريخ النشر
2014
عدد الصفحات
97.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
طب العيون
تاريخ الإجازة
10/3/2014
مكان الإجازة
جامعة عين شمس - كلية الطب - Ophthalmology
الفهرس
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Abstract

The retina is the light-sensitive tissue that lines the inside of the eye. The optical elements within the eye focus an image onto the retina of the eye, initiating a series of chemical and electrical events within the retina. Nerve fibers within the retina send electrical signals to the brain, which then interprets these signals as visual images.
The retina is relatively protected from systemic drug administration because of the blood-retinal barrier, a highly selective mechanism adapted to providing a regulated homeostatic environment for this highly specialized tissue. However, a number of drugs have been associated with retinal toxicity.
The toxicity of systemic drugs has different mechanisms. This toxicity can be grouped into:
1. Pigmentary retinopathies:.
• Chloroquine, hydroxychloroquine: Retinal effects include retinal parafoveal granularity of the retinal pigment epithelium (RPE) with loss of the foveal light reflex and bilateral paracentral visual field change, best seen with red test (early in disease); bull’s-eye appearance of the macula (late in the disease); vascular attenuation and peripheral fine granular pigmentary changes.
• Thioridazine: Thioridazine toxicity has been described as a progressive chorioretinopathy’, but this designation can be misleading. During the first year after thioridazine exposure retinal pigmentation evolves from a granular to a patchy or nummular appearance. However, visual function and the electroretinogram typically improve during this period. Some cases may show chorioretinal atrophy and functional loss many years later, but there is little evidence for ongoing drug-related progression. Late atrophy may represent degeneration of cells that were injured subclinically at the time of initial drug exposure. Although thioridazine toxicity produces an evolving pigmentary disturbance, functional changes must be monitored independently of fundus appearance.
• Desferrioxamines: Macular and/or peripheral pigmentary degeneration are the most common changes described. The earliest fundus changes described are subtle opacification or loss in transparency of the outer retina and retinal pigment epithelium (RPE). These changes precede the development of RPE mottling.
2. Crystalline retinopathies :
• Tamoxifen: Birdshot retinochoroidopathy associated with ocular toxicity due to tamoxifen is due to the presence of yellow-white dots in the paramacular region and the fovea and by modifications of the retinal epithelial pigments. Ocular toxicity should be suspected as it may be reversible if recognized and stopped early.
• Canthaxanthin: A high intake of canthaxanthin lead to the deposition of crystal-like birefringent inclusions in the inner layers of the peripheral retina and, to some extent, the central retina that are glistening and arranged in a donut shaped ring .
• Talc: It may lodge in the macular arterial vasculature, causing a granulomatous reaction with focal occlusion, leading to eventual macular ischemia.
3. Vascular Retinopathies:
• Quinine: Dilated fundus examination reveals optic nerve pallor with retinal atrophy and severely attenuated retinal arterioles and venules spectral time-domain OCT reveals severe atrophy of the neuroretina in both eyes.
• Interferon: Typical ocular lesions include cotton wool spots and retinal haemorrhages at the posterior fundus, particularly around the optic disc. Retinal haemorrhages appear as superficial linear and patchy forms or as white centred bleeding. The retinopathy may develop unilaterally or bilaterally.
4. Other Retinnal affection:
• Topiramate: Topiramate toxicity may present with macular folds TPM even if discontinued, vision fail to improve significantly over 6 months of follow-up.
• Meclofenamic acid: visual side effects, such as temporary blindness, visual field defect, blurred vision, scotomata, and color vision changes subsequent to short- or long-term use.
• Digoxin Retinal toxicity: Ocular side effects are common with high doses, with symptoms ranging from decreased vision to photopsias, xanthopsia and scotomas.
Ophthalmological screening and monitoring is recommended during prescription of certain drugs. The retina is the site for multiple adverse drug reactions and the dose of therapy may be important in determining the likelihood of retinal toxicity.