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Reversible toxic optic neuropathy: case report A 30-year-old man developed reversible toxic optic neuropathy following an overdose of tacrolimus. Additionally, the treatment with voriconazole also contributed in the development of reversible toxic optic neuropathy [not all routes, indications and durations of treatments to reaction onset stated]. The man with cystic fibrosis, had undergone bilateral lung transplantation on 15 July 2014. Subsequently, he started receiving immunosuppressive treatment with oral tacrolimus [FK506] 2.5mg two times a day along with prednisone and mycophenolate mofetil. On 11 December 2015, he had undergone a second bilateral transplant due to accelerated bronchiolitis obliterans syndrome and type 1A rejection. In January 2016, he had mild A2 rejection, for which he was initiated on immune globulin and photophoresis. He was found to be rejection free by June 2016. Since starting tacrolimus in 2014, he was continued on the same dose. On 26 September 2016, bronchoscopy was performed with balloon dilation of his proximal airways and Argon beam assisted removal of granulation tissue. During the hospitalisation, his tacrolimus levels were found to be below target, and the dose of tacrolimus was increased. On 05 October 2016, an ophthalmological evaluation was performed due to progressive, bilateral blurring of vision, which started 4–6 months previously. Records showed a visual acuity of 20/40 right eye (OD), 20/60 left eye (OS). Two weeks afterwards, optometric exam showed best corrected visual acuity of 20/400 OS and 20/200 OD with a manifest refraction of –4.00 + 0.75 x 004 OS and –3.50 + 0.75 x 008 OD, similar to his original spectacle correction. A neuro-ophthalmology service was consulted. He showed significant dyschromatopsia. Exam of the posterior pole indicated bilateral temporal pallor of the optic disc associated with mild elevation of the disc margins OU. The arcuate fibers appeared mildly oedematous OU. Macular reflex was blunted OU. Optical coherence tomography (OCT) showed papillomacular atrophy. An MRI of the orbits and brain was recommended, but he declined. Considering his presentation of painless, progressive bilateral symmetric loss vision associated with atrophy of the papillomacular bundle, nutritional and toxic optic neuropathies were considered most likely. At that time, he was receiving treatment with voriconazole 200mg two times a day and tacrolimus along with multiple concomitant medications. Tacrolimus level during that time was 8.9 ng/mL; however, it was increased for several days, reaching as high as 25.0 ng/mL, in the preceding weeks. The increased tacrolimus levels was a consequence of his dosing adjustments (overdose) as his levels had dropped below target. The man’s tacrolimus therapy was changed to ciclosporin on 08 November 2016, and idebenone was initiated. Owing to a concern of voriconazole contributing to his visual decline, it was replaced with isavuconazonium [isavuconazonium sulfate]. Within 2 months following these intervention a subjective impr