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Arch Ophthalmol. 2002;120:985-987.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Tumor necrosis factor (TNF) is a cytokine derived chiefly from macrophages.¹ The liberation of TNF- is thought to stimulate the inflammatory process by binding to cell surface receptors. Infliximab is a chimeric antibody of the IgG class, which binds TNF-, inhibiting its activity.² The Food and Drug Administration has approved infliximab, as an intravenous infusion, for the treatment of rheumatoid arthritis and Crohn disease.³

Cytokine-targeted therapy in patients with rheumatoid arthritis has been increasing and has generally been reported to be safe, although headache and respiratory congestion may occur. Review of the package insert for infliximab lists "neurologic events" as possible adverse affects and adds that "Infliximab and other agents that inhibit TNF have been associated in rare cases with exacerbation of clinical symptoms and/or radiographic evidence of de-myelinating disease."⁴

Inhibition of TNF- has also been studied in multiple sclerosis (MS), in which high TNF- levels have been noted . . . [Full Text of this Article]

Report of a Case


Comment
Corresponding author and reprints: Robert C. Sergott, MD, Neuro-Ophthalmology Service, Wills Eye Hospital, 900 Walnut St, Philadelphia, PA 19107.

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