anti-TNF agents as therapeutic choice in immune-mediated inflammatory diseases: focus on adalimumab.
The complex pathogenesis of immune-mediated inflammatory diseases (IMIDs) has been extensively investigated and dysregulation of cytokines, such as tumour necrosis factor (TNF) has been shown to play a dominant role in the pathogenesis of various IMIDs, such as rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, ulcerative colitis, psoriasis and psoriatic arthritis. The subsequent development of biological agents capable of blocking TNF has led to important advances in the pharmacotherapy of such diseases and confirmed the concept of a common pathophysiology among IMIDs with TNF having a predominant role. Five TNF inhibitors have currently been approved for treatment of one or more IMIDs; these include infliximab, etanercept, adalimumab, golimumab and certolizumab pegol. Given the similarities in the pathogenic background of IMIDs, one could expect that anti-TNF agents be similarly effective and with comparable tolerability profiles; however, this may not be the case. Structural and pharmacological differences among the anti-TNF drugs are likely to result in differences in efficacy and tolerability among the agents in the different IMIDs, together with differences in potency, therapeutic dose ranges, dosing regimens, administration routes, and propensity for immunogenicity. Among the five TNF inhibitors approved for treatment of IMIDs, adalimumab has the widest range of indications. Data from controlled clinical trials of adalimumab, showing its excellent efficacy and tolerability in a wide range of indications, are supported by real-world long-term data from observational studies, which confirm the value of adalimumab as a suitable choice in the management of IMIDs.
IBD Unit, Complesso Integrato Columbus, Catholic University, Rome, Italy.
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Armuzzi
Gastroenterology Unit, Anna Meyer Childrens Hospital, Department of Paediatrics, University of Firenze, Firenze, Italy.
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Lionetti
Division of Pharmacology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
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Blandizzi
Chair and Division of Rheumatology, IRCCS Policlinico San Matteo Foundation, Pavia, Italy.
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Caporali
Department of Dermatology, University of Rome Tor Vergata, Rome, Italy.
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Chimenti
Ocular Immunology Unit, Ophthalmology, Unit, Arcispedale S Maria Nuova Reggio, Reggio, Emilia, Italy.
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Cimino
IBD Unit, Department of Medical and Surgical Sciences, S. Orsola-Malpighi Hospital, University of Bologna, Italy.
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Gionchetti
Department of Medicine, Section of Dermatology and Venereology, University of Verona, Verona, Italy.
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Girolomoni
Rheumatology Unit, Interdisciplinary Department of Medicine, Medical School, University of Bari, Bari, Italy.
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Lapadula
G. Pini Orthopedic Institute, Milano, Italy.
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Marchesoni
CEIS  Economic Evaluation and HTA (EEHTA), IGF Department, University of Tor Vergata, Rome, Italy.
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Marcellusi
CEIS  Economic Evaluation and HTA (EEHTA), IGF Department, University of Tor Vergata, Rome, Italy.
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Mennini
Rheumatology Unit, Department of Internal Medicine, Azienda Ospedaliera ASMN, Istituto di Ricovero e Cura a Carattere Scientifico, Reggio Emilia, Italy.
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Salvarani
Department of Paediatrics, Rheumatology Unit, Anna Meyer Childrens Hospital, University of Florence, Firenze, Italy.
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Cimaz
D000068879:Adalimumab; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects / Q000737:chemistry / Q000493:pharmacokinetics / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000737:chemistry / Q000493:pharmacokinetics / Q000627:therapeutic use*; D001327:Autoimmune Diseases / Q000188:drug therapy* / Q000276:immunology*; D002986:Clinical Trials as Topic; D006801:Humans; D007249:Inflammation; D013329:Structure-Activity Relationship; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000893:Anti-Inflammatory Agents; D061067:Antibodies, Monoclonal, Humanized; D014409:Tumor Necrosis Factor-alpha; D000068879:Adalimumab