Sir,

It is recognized that standard interferon therapy can rarely cause ocular toxicity, including retinopathy and optic neuropathy,1 but the frequency and severity of adverse effects of the pegylated form is not known.

This 46-year-old man with a 4-month history of hepatitis C, whose risk factor for this infection was past blood transfusion, had been treated with PEG interferon alpha 2B at 0.5 ml subcutaneously per week. He was not taking any other medications. After 3 weeks of treatment, he presented with acute bilateral visual loss. He described sudden blackout of his vision upon awakening without any headache or ocular pain. He had no diabetes, hypertension, heart disease, or past history of alcohol, smoking or drug abuse.

His visual acuity was 20/400 OD and 20/100 OS without relative afferent pupillary defect. Extraocular motility was full. Automated perimetry revealed bilateral inferior altitudinal defects. Slit-lamp examination and intraocular pressures were normal. He had bilateral swollen optic discs without hemorrhages or cotton wool spots. Macular and peripheral retinal exam was normal. Magnetic resonance imaging and magnetic resonance angiography of the brain and orbits with and without gadolinium were normal. Alanine transaminase and aspartate transaminase were elevated. Complete blood count, platelets, ferritin, % saturation, ceruloplasmin, antinuclear antibody, sedimentation rate, rheumatoid factor, RPR, angiotensin-1-converting enzyme, Lyme titers, serum and urine methylmalonate, folate, 24-h urine for heavy metals, and Leber's hereditary optic neuropathy genetic testing were normal. Cerebrospinal fluid protein, glucose, cell count, gram stain, immunoglobulin index, oligoclonal bands, neuromyelitis optica antibody and cytology were all unremarkable. The patient chose to stop treatment after his visual loss, and his visual acuity improved slightly to 20/80 OU with residual inferior field defects.

Comment

This report describes bilateral non-arteritic ischemic optic neuropathy (NAION) associated with only PEG interferon alpha 2B and poor functional visual recovery. The prompt onset of visual loss after initiation of therapy, the rare occurrence of simultaneous NAION2 and the lack of vascular risk factors in this young patient suggests that his NAION was related to PEG interferon alpha 2B. Central nervous system disorders and other autoimmune, vasculitic, nutritional and genetic optic neuropathies that could cause acute bilateral visual loss were ruled out. Another report described a similar presentation in a patient treated with both PEG interferon alpha 2B and ribavarin.3 At least eight cases of NAION4 associated with standard interferon have been reported in the literature. Although new pegylated interferons have improved pharmacokinetics and better antiviral efficacy,5 idiosyncratic ocular toxicity has been associated with variable doses and duration of interferon therapy. Lohmann et al6 postulated that interferon-alpha can produce autoantibodies that lead to deposition of immune complexes in the posterior ciliary arteries to cause NAION. Interferon-alpha can also stimulate other cytokines to cause an inflammatory reaction in blood vessels leading to ischemia.6

Therefore, physicians treating chronic hepatitis C patients with pegylated interferon should be aware of the potential complication of severe NAION that can occur at any time after the initiation of this drug.