Drugs that inhibit tumor necrosis factor α (TNF-α) are now widely used for management of a variety of inflammatory processes (eg, rheumatologic disorders, inflammatory bowel diseases) proven refractory to conventional therapy. As with many medical advances, benefit comes with a price, and an important consequence of anti–TNF-α therapy is increased risk of infection, especially tuberculosis.1 Other studies have linked anti–TNF-α therapy with increased risk of serious bacterial2 and fungal3 infections. Associations between TNF-α antagonists and viral infections have not been as clearly defined, though case reports of severe episodes of herpes zoster in patients receiving these drugs have appeared in the literature.4 Prior analyses of large databases have yielded conflicting results regarding a causal association between treatment with biologic agents and herpes zoster.5,6
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