At present, there is no treatment capable of modifying the evolution of Sjögren's syndrome (SS) and the therapeutic approach is based mainly on symptomatic replacement or stimulation of glandular secretions, while extraglandular involvement requires an organ-specific therapy. New therapeutic approaches for sicca manifestations include oral muscarinic agonists (e.g., pilocarpine and cevimeline) for dry mouth, as well as topical agents (e.g., cyclosporine A and diquafosol) for dry eye. Turning to biological agents, recent studies have demonstrated the lack of efficacy of anti-tumor necrosis factor (TNF) agents in primary SS. By contrast, a promising treatment is rituximab (anti-CD20). Advances in our knowledge of etiopathogenic mechanisms will allow the development of future treatments for SS, including localized gene transfer and agents antagonizing B cell-activating factor from the TNF family and CD22-positive cells.
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Ramos‐Casals et al. (2007) studied this question.
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