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R. Foroozan, L. Buono, R. Sergott, P. Savino (2002)
Retrobulbar optic neuritis associated with infliximab.Archives of ophthalmology, 120 7
J. Keltner, Chris Johnson, John Spurr, Roy Beck (1993)
Baseline visual field profile of optic neuritis. The experience of the optic neuritis treatment trial. Optic Neuritis Study Group.Archives of ophthalmology, 111 2
William Robinson, M. Genovese, L. Moreland (2001)
Demyelinating and neurologic events reported in association with tumor necrosis factor alpha antagonism: by what mechanisms could tumor necrosis factor alpha antagonists improve rheumatoid arthritis but exacerbate multiple sclerosis?Arthritis and rheumatism, 44 9
M. Fernández‐Arquero, R. Arroyo, A. Rubio, C. Martin, P. Vigil, L. Conejero, M. Figueredo, E. Concha (1999)
Primary association of a TNF gene polymorphism with susceptibility to multiple sclerosisNeurology, 53
Rubio A, Neurology. (1999)
Primary association of a TNF gene polymorphism with susceptibilityto MS., 53
Iread with great interest the article by Foroozan et al1 onretrobulbar optic neuritis associated with infliximab in a patient with rheumatoidarthritis. I have also encountered a similar manifestation in a 50-year-oldwoman treated with infliximab for advanced Crohn disease. She developed visualloss in the left eye associated with ocular pain 3 weeks after the last infliximabinfusion. There was no preceding illness or travel. She had no previous visualsymptom or neurologic dysfunction. Her examination results were consistentwith retrobulbar optic neuropathy in the left eye. Furthermore, she had asuperior altitudinal visual field defect in the left eye and a superior visualfield depression in the right eye at automated perimetry (Figure 1). Gadolinium-enhanced magnetic resonance imaging revealedenhancement of the retrobulbar portion of the left optic nerve (Figure 2). There were no other abnormalities to suggest demyelinationwithin the brain. Her visual function spontaneously improved in the subsequent6 weeks. At follow-up examination, she had normal visual acuity, color vision,pupillary function, and funduscopic appearance, along with striking improvementof visual fields (Figure 3). Thepatient had not received further infliximab treatment. Figure 1. View LargeDownload Automated perimetry Humphrey central30-2 threshold test (Zeiss Humphrey Systems, Dublin, Calif) gray scale (right)and pattern deviation (left) show a superior visual field depression in theright eye (A) and a superior altitudinal visual field defect in the left eye(B). Figure 2. View LargeDownload Gadolinium-enhanced T1-weightedaxial (A) and coronal (B) magnetic resonance images show enhancement of theretrobulbar portion of the left optic nerve. Figure 3. View LargeDownload Automated perimetry Humphrey central30-2 threshold test (Zeiss Humphrey Systems, Dublin, Calif) gray scale (right)and pattern deviation (left) show a superior visual field depression in theright eye (A) and a mild nasal depression in the left eye (B). Although the association of optic neuritis with infliximab therapy mighthave been coincidental in these 2 cases, mounting evidence suggests that treatmentwith tumor necrosis factor (TNF) α blockers may predispose patientsto developing demyelinating disease.2 Itis unknown why TNF-α antagonists are not beneficial in multiple sclerosisor by what mechanisms they could predispose patients to or worsen demyelinatingdisease. On the one hand, it is believed that these molecules are unable tocross the blood-brain barrier, even in active multiple sclerosis. In addition,TNF has been implicated in the pathogenesis of multiple sclerosis.2 On the other hand, TNF-α antagonists aresuspected of enhancing disease activity in multiple sclerosis by increasingperipheral autoreactive T cells, some of which may be myelin specific.2 Alternatively, the reduction of TNF-α levelsin joint or bowel may cause a gradient across the blood-brain barrier andpromote up-regulation of central nervous system TNF or TNF-receptor expressionand lead to TNF-mediated central nervous system injury.2 Thepossibility that genetic susceptibility might be influenced by TNF gene polymorphismhas been proposed as an alternative explanation.3 It is interesting that our patient had a visual field defect similarto the one described by Foroozan et al.1 However,it is clear that a variety of visual field defects may occur in optic neuritis.In the optic neuritis treatment trial, altitudinal visual field defects werepresent in 15% of affected eyes.4 Therefore,more cases of infliximab-associated optic neuritis are needed to ascertainthe possibility that altitudinal visual field defects are common in this condition. Corresponding author: Luis J. Mejico, MD, Neuro-Ophthalmology Unit,State University of New York Upstate Medical University, 90 Presidential Plaza,Syracuse, NY 13202 (e-mail: mejicol@upstate.edu). References 1. Foroozan RBuono LMSergott RCSavino PJ Retrobulbar optic neuritis associated with infliximab. Arch Ophthalmol. 2002;120985- 987PubMedGoogle Scholar 2. Robinson WHGenovese MCMoreland LW Demyelinating and neurologic events reported in association with tumornecrosis factor alpha antagonism: by what mechanisms could tumor necrosisfactor alpha antagonists improve rheumatoid arthritis but exacerbate multiplesclerosis? Arthritis Rheum. 2001;441977- 1983PubMedGoogle ScholarCrossref 3. Fernandez-Arquero MArroyo RRubio A et al. Primary association of a TNF gene polymorphism with susceptibilityto MS. Neurology. 1999;531361- 1363PubMedGoogle ScholarCrossref 4. Keltner JLJohnson CASpurr JOBeck RW Baseline visual field profile of optic neuritis: the experience ofthe optic neuritis treatment trial: Optic Neuritis Study Group. Arch Ophthalmol. 1993;111231- 234PubMedGoogle ScholarCrossref
Archives of Ophthalmology – American Medical Association
Published: May 1, 2004
Keywords: optic neuritis,infliximab
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