title: Tumor necrosis factor-α antagonists: Side effects and their management.
abstract: As elevated levels of tumor necrosis factor-alpha (TNF-α) are associated with disease severity in psoriasis and psoriatic arthritis, TNF-α antagonists are being used to treat moderate to severe disease in patients who have contraindications, fail to respond or develop side effects to conventional systemic therapies. It is of utmost importance to be well versed with the possible adverse effects and contraindications of TNF-α antagonists so that they can be used effectively and safely. Many of their adverse effects have been well studied in patients of rheumatoid arthritis (RA) and inflammatory bowel disease (IBD) and may not be completely applicable in psoriasis. This is because patients with RA and IBD are on multiple immunosuppressants while those with psoriasis are mostly receiving single systemic therapy and often have comorbidities that distinguish them from those with RA or IBD. Also, some of the side effects are still controversial and debated. Long-term prospective randomized controlled studies are needed to better understand the associated risk in patients of psoriasis. Baseline screening and periodic monitoring during treatment can reduce and help in early identification and appropriate management of the adverse outcomes. This article reviews the side effects known to be associated with TNF-α antagonists, their pathomechanisms and management guidelines. Some of the common side effects include infusion and injection site reactions, infections particularly reactivation of tuberculosis, autoantibody formation and drug induced lupus erythematosus, liver function abnormalities, hematological, and solid organ malignancies.
authors: Department of Dermatology, Venereology and Leprology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
authors: Sunil
authors: S
authors: Dogra
authors: Geeti
authors: G
authors: Khullar
mesh_terms: D000014:Abnormalities, Drug-Induced / Q000209:etiology; D000068879:Adalimumab; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects; D004342:Drug Hypersensitivity / Q000209:etiology / Q000628:therapy*; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects; D000069285:Infliximab; D007267:Injections / Q000009:adverse effects; D055985:Latent Tuberculosis / Q000139:chemically induced* / Q000188:drug therapy; D008099:Liver / Q000187:drug effects / Q000503:physiopathology; D009369:Neoplasms / Q000139:chemically induced; D009422:Nervous System Diseases / Q000139:chemically induced; D011565:Psoriasis / Q000139:chemically induced; D018124:Receptors, Tumor Necrosis Factor; D013921:Thrombocytopenia / Q000139:chemically induced; D013923:Thromboembolism / Q000139:chemically induced; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept