الفهرس 
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Abstract
HCV infection most often leads to an asymptomatic chronic state, which can later progress to active liver disease, liver failure, or primary hepatocellular carcinoma. Treatment of HCV is costly, beyond the reach of most patients in less-developed countries, requires 48 or more weeks to complete, and has serious adverse effects and low efficiency. HCV in a family member can be socially and economically detrimental. There is no vaccine for HCV. Hepatitis C is primarily acquired following contact with infected blood. Needle sharing among intravenous drug users (IDUs) currently represents the most common route of acquisition of HCV in the developed world. HCV infected persons should be counseled on preventing spread of the virus to others. Eighty to ninety percent of acute hepatitis C infections are asymptomatic. In symptomatic infections, abdominal pain, nausea, loss of appetite, jaundice and dark urine begin about seven weeks after infection. Chronic infection with HCV develops in 75% to 85% of infected individuals. Most chronic infections eventually lead to hepatic inflammation and varying degrees of fibrosis. The current treatment is combination therapy with interferon-alfa and ribavarin for 24 to 48 weeks. HCV infection may result in various HCV related extrahepatic abnormalities. The ocular surface considered as one of the most important sites of these manifestations. Cornea, conjunctiva, and accessory lacrimal glands together with the meibomian glands, main lacrimal gland, and interconnecting neural reflex loops constitute a functional unit. Dry eye seems to be a common ocular manifestation in patients with chronic hepatitis C infection, especially in those with advanced stages of hepatic fibrosis. A possible pathogenetic association between Mooren ulcer, recurrent keratitis, and CHC has been proposed. Other forms of ocular involvement in patients with chronic hepatitis C include episcleritis, retinopathy, and retinal vasculitis Interferons (IFNs) were discovered by Isaacs and Lindemann in 1957. IFNs are proteins made and released by host cells in response to the presence of pathogens such as viruses, bacteria, parasites or tumor cells. IFNs were simply classifi ed in 3 groups: IFN alpha, IFN beta and IFN gamma. Pegylation is a process in which a polyethylene glycol (PEG) moiety is attached to the molecules used for the treatment. This results in alteration of the pharmacokinetic and immunologic properties of the drug which in turn results in longer duration of action of the pegylated molecule allowing for using lower doses of the drug and better efficacy. Two pegylated molecules of interferon are pegylated interferon (PEG-IFN)-α2a (Pegasys) and -α2b (PegIntron). Both IFN-alpha and PEG-IFN-alpha share the same side effect profile, even though PEG-IFN-alpha has been reported to provoke less frequent systemic effects. The rate of interferon complications is reported to be higher in patients with diabetes or hypertension, but is not related with HCV genotypes, platelet counts or types or dose of interferon. Most of ophthalmological side effects occurring during IFN-α treatment are benign, transient, and are mainly represented by the classical IFN-related retinopathy. Atypical ocular side effects associated with the use of IFN-α are branch retinal artery occlusion, central retinal vein occlusion, anterior ischemic optic neuropathy ,retinal detachment, subconjunctival haemorrhage, optic disc edema, neovascular glaucoma, vitreous hemorrhage, panophthalmitis and central retinal artery occlusion. There are two severe forms of intraocular complications of IFN which result in severe visual impairment. The first form is represented by VKH, one of the inflammatory intraocular disorders and the second form is retinal vascular disorders including central retinal arterial/venous occlusion. Retinopathy developed by week 14 in most of the patients after the start of therapy and disappeared in the majority of the patients during the 4–8 week period in which the patients were receiving the treatment. This suggests that treatment can be continued despite the development of retinopathy in many patients. The exact pathogenesis of retinopathy is not known but is presumably related to the disturbance in retinal microcirculation, thus, preexisting arteriosclerosis that affects microcirculation may promote interferon induced retinopathy. There is no classification for IFN-induced retinopathy, like diabetic retinopathy. Therefore there is no rule for suspending the use of interferon in patients who develop retinopathy or any other ocular side effects. The prevalence of retinopathy in children with HCV treated with PEG α2a was low (1%) compared to adult data (19–29%). Health care providers who treat children with interferon for chronic HCV should be vigilant for the complication and other potential ophthalmologic complications in children. Because of the potential severity, prospective assessment for ocular complications should remain part of the monitoring strategy for children who are treated with interferon for HCV.