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Case Reports
. 2016 Jul-Sep;60(3):188-194.

Combined etiology for bilateral and simultaneous optic neuropathy in a patient with ciancobalamin deficit and hepatitis C treated with peg-interferon and ribavirin

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Case Reports

Combined etiology for bilateral and simultaneous optic neuropathy in a patient with ciancobalamin deficit and hepatitis C treated with peg-interferon and ribavirin

Anca Delia Pantalon et al. Rom J Ophthalmol. 2016 Jul-Sep.

Abstract

We report the case of a 53-year-old female patient who developed bilateral sudden visual acuity loss after 15 weeks from the initiation of Peg-Interferon and Ribavirin treatment for hepatitis C. Debut was simultaneous and asymmetric, reported in the morning, at awakening. No pain or other symptom was reported by the patient. Results. At presentation, visual acuity was 0.2 in RE and 3/ 50 in LE. Pupillary reflexes were sluggish and severe dyschromatopsia was documented in both eyes (Ishihara plates). Fundus examination revealed bilateral pale optic disc edema, more prominent in LE, with splinter hemorrhages in the RNFL around the optic disk. Visual field exam demonstrated severe defects in 3 quadrants of the RE, whereas in the LE, it was impossible to perform the investigation due to VA<0.1. Neurologic evaluation was normal; other possible causes of systemic vasculitis were excluded by negative lab tests. Acute inflammatory markers (fibrinogen and ESR) and mild pancytopenia were the only documented laboratory changes in this patient. Anamnesis cleared the traditional risk factors for conventional AION (hypertension, diabetes, ischemic heart disease, and hypercholesterolemia). Cranial and orbital CT scan and MRI findings were normal. Patient was withdrawn from the Interferon and Ribavirin treatment and was administered methyl prednisolone pulse therapy (1g/ day) for 3 days, continued with oral Prednisone (60 mg/ day) tapered slowly for over 12 weeks. VA increased to 0.8 during treatment in the RE, but visual recovery in the LE was not as spectacular (0.16) as in the fellow eye. Modified latencies and amplitudes in evoked visual potentials examination during 4 months time emphasized bilateral optic atrophy. Optic nerve sufferance was amplified by a low level of vitamin B12, detected by chance at the last eye visit. Due to the general condition, dietary supplementation was not possible. Conclusion. A case of a patient with bilateral and simultaneous NAION caused by IFN and Ribavirin treatment for hepatitis C, who was also vitamin B12 deficient, was analyzed. Therefore, a combined etiology for optic atrophy was explained.

Keywords: Peg-Interferon; bilateral simultaneous AION; hepatitis C; vitamin B12 deficit.

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Figures

Fig. 1
Fig. 1
Bilateral NAION – Optic disc edema. Visible splinter peridiscal hemorrhages and mild macular edema (LE)
Fig. 2
Fig. 2
Visual field examination RE (at presentation) – Full Field 120*, 3 zones – severe vision loss, absolute defects in 3 quadrants; LE could not be performed due to VA<0.1
Fig. 3a
Fig. 3a
OCT aspect in RE at presentation (visible optic disc edema, no macular lesions)
Fig. 3b
Fig. 3b
OCT aspect in LE at presentation (optic disc edema, macular edema)
Fig. 4
Fig. 4
Visual field changes at 3 months after presentation – Full field 120*, 3 zones (RE – slight improvement of visual field defects compared to baseline; LE – altitudinal defect). 30-2 Threshold test. General reduction of retinal sensitivity (RE MD = -22.48 dB; LE MD = -25.04 dB) and significant visual loss in both hemifields (RE PSD = 12.04 dB; LE PSD = 11.4 dB)
Fig. 5
Fig. 5
RE – increased latencies and decreased amplitudes in visual evoked potentials (VEP) examination at presentation and 4 months follow up
Fig. 6
Fig. 6
LE - non-recordable parameters in VEP exam at presentation. Recordable data only in channel A2 (fibers from the temporal side) showing severe optic atrophy at 4 months follow up
Fig. 7
Fig. 7
Fundus appearance – optic atrophy (pale discs) in both eyes at the last follow up visit

References

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