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Chloroquine retinopathy is a form of toxic retinopathy (damage of the retina) caused by the drugs chloroquine or hydroxychloroquine, which are sometimes used in the treatment of autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus. This eye toxicity limits long-term use of the drugs. [3]
Macular toxicity is related to the total cumulative dose rather than the daily dose. Regular eye screening, even in the absence of visual symptoms, is recommended to begin when either of these risk factors occurs. [22] Toxicity from hydroxychloroquine may be seen in two distinct areas of the eye: the cornea and the macula.
In weeks to a month times the lesions begin to clear and disappear (with prednisone) leaving behind areas of retinal pigment epithelial atrophy and diffuse fine pigmentation (scarring). Rarely choroidal neovascularization occur as a late onset complication.
A Hollenhorst plaque (also known as a retinal cholesterol embolus) is a cholesterol embolus that is seen in a blood vessel of the retina.It is usually found when a physician performs ophthalmoscopy, during which a plaque will appear as a small, bright crystal that is refractile (reflects the light from the ophthalmoscope) and yellow. [1]
Cocaine is associated with retinal toxicity mainly through its negative impacts on the retinal vasculature. [18] Cocaine use causes increased norepinephrine levels and the resulting sympathetic activation leads to vasospasm and hypertension, [19] both of which are risk factors to retinal blood vessel damage.
Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder. Toxic optic neuropathy is treated by identification and removal of the offending agent. Depending upon the individual affected, the nature of the agent, total exposure prior to removal, and degree of vision loss at the time of diagnosis, the prognosis ...
Symptoms include blurred vision in both eyes, but the onset may occur at a different time in each eye. There are yellow-white placoid lesions in the posterior pole at the level of the retinal pigment epithelium. Some suggest a genetic predisposition to the disease, while others postulate an abnormal immune response to a virus. [2]
The blood–ocular barrier is a barrier created by endothelium of capillaries of the retina and iris, ciliary epithelium and retinal pigment epithelium. [1] It is a physical barrier between the local blood vessels and most parts of the eye itself, and stops many substances including drugs from traveling across it. [2]