A case report of adalimumab-associated optic neuritis

被引:13
作者
Alice Kim
Norman Saffra
机构
[1] Division of Ophthalmology, Maimonides Medical Center, Brooklyn, NY, 11219
关键词
Adalimumab; Multiple sclerosis; Optic neuritis; Tumor necrosis factor;
D O I
10.1007/s12348-011-0058-2
中图分类号
学科分类号
摘要
Purpose: To describe a case of retrobulbar optic neuritis that presented within 3 weeks of adalimumab treatment initiation. Methods: This index case was evaluated with visual field testing, brain magnetic resonance imaging, lumbar puncture, and laboratory evaluation, and treated with intravenous methylprednisolone followed by a steroid taper. Results: Our patient made a full visual recovery, but was found to have extensive T2/FLAIR foci of hyperintensities that enhanced and had restricted diffusion on magnetic resonance imaging (MRI). Six months later, these demyelinating lesions still persisted and our patient was initiated on immunomodulatory treatment. Conclusion: With the extensive burden of disease at presentation and persistence of lesions on follow-up MRI, this unusual case seems to suggest an unmasking of an underlying demyelinating process by adalimumab. The clinician should be mindful of this association and monitor for any manifestations and treat appropriately. © 2012 The Author(s).
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页码:145 / 147
页数:2
相关论文
共 13 条
[1]  
Chung J.H., van Stavern G.P., Frohman L.P., Turbin R.E., Adalimumab-associated optic neuritis, J Neurol Sci, 244, pp. 133-136, (2006)
[2]  
Mohan N., Edwards E.T., Cupps T.R., Et al., Demyelination occurring during anti-tumor necrosis factor alpha therapy for inflammatory arthritides, Arthritis Rheum, 44, pp. 2862-2869, (2001)
[3]  
Thomas Jr. C.W., Weinshenker B.G., Sandborn W.J., Demyelination during anti-tumor necrosis factor alpha therapy with infliximab for Crohn's disease, Inflamm Bowel Dis, 10, pp. 28-31, (2004)
[4]  
Shin I.S., Baer A.N., Kwon H.J., Et al., Guillain-Barre and Miller Fisher syndromes occurring with tumor necrosis factor alpha antagonist therapy, Arthritis Rheum, 54, pp. 1429-1434, (2006)
[5]  
Sharief M.K., Hentges R., Association between tumor necrosis factor alpha and disease progression in patients with multiple sclerosis, N Engl J Med, 325, pp. 467-472, (1991)
[6]  
Selmaj K., Raine C.S., Cross A.H., Anti-tumor necrosis factor therapy abrogates auto-immune demyelination, Ann Neurol, 30, pp. 694-700, (1991)
[7]  
Ruddlen H., Bergman C.M., McGrath M.L., An antibody to lymphotoxin and tumor necrosis factor prevents transfer of experimental allergic encephalomyelitis, J Exp Med, 172, pp. 1193-1200, (1990)
[8]  
Selmaj K., Papierz W., Glabinski A., Kohn O.T., Prevention of chronic relapsing experimental autoimmune encephalomyelitis by soluble TNF receptor 1, J Neuroimmunol, 56, pp. 135-141, (1995)
[9]  
Probert L., Akassoglou K., Pasparakis M., Et al., Spontaneous inflammatory demyelinating disease in transgenic mice showing central nervous system-specific expression of tumor necrosis factor-α, Neurobiology, 92, pp. 11294-11298, (1995)
[10]  
van Oosten B.W., Barkhof F., Truyen L., Et al., Increased MRI activity and immune activation in two multiple sclerosis patients treated with the monoclonal anti-tumor necrosis factor antibody cA2, Neurology, 47, pp. 1531-1534, (1996)