title: The use of biologic agents in the treatment of ocular manifestations of Behcet's disease.
abstract: Behçet's Disease (BD) is a multisystem inflammatory disorder of uncertain etiology with a variety of potential manifestations throughout the body, and its ocular complications are some of its most devastating. Treatment with immunosuppressive agents has improved outcomes, but many patients suffer from disease that responds poorly to conventional therapies. Because of this, therapy with a variety of biological response modifiers has been employed. The earliest was interferon-α, and a multitude of reports have described its benefits for the uveitis associated with Behçet's Disease. Many patients enjoy durable remissions of their ocular inflammatory disease even after discontinuation of therapy, but side-effects are almost universal and some can be dangerous. Of the newer biological response modifiers, infliximab, a monoclonal antibody to TNF-α, has been most extensively studied. It is reported to be rapidly effective in many cases of Behçet's Disease uveitis, though with conflicting data as to the ability to induce durable remission after cessation of treatment. Side-effects are relatively rare, but may be serious. Several reports have been published on the use of other biologic agents, including adalimumab (a humanized antibody to TNF-α), etanercept (a molecule that resembles the TNF-α receptor), and rituximab (an antibody to CD20 that depletes the body of CD20-positive B cells). Of the three of these, adalimumab has the most promising initial evidence, etanercept has very few positive reports in patients with BD uveitis (and is likely ineffective in uveitis in general), and rituximab is lacking data. Although randomized controlled trials are almost completely lacking, currently available evidence is promising that biologic agents can prove an invaluable addition to the armamentarium of the practitioner treating patients with BD uveitis.
authors.affiliation: Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA.
authors.forename: Nicole R
authors.initials: NR
authors.lastname: Benitah
authors.forename: Lucia
authors.initials: L
authors.lastname: Sobrin
authors.forename: George N
authors.initials: GN
authors.lastname: Papaliodis
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use; D001528:Behcet Syndrome / Q000188:drug therapy*; D001688:Biological Products / Q000627:therapeutic use*; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069285:Infliximab; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D000069283:Rituximab; D014605:Uveitis / Q000188:drug therapy*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D001688:Biological Products; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D000069283:Rituximab; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept