Potential use of TNF-α inhibitors in systemic sclerosis.
Systemic sclerosis (SSc) is a rare connective tissue disease characterized by chronic inflammation and fibrosis of the skin, vascular abnormalities and variable involvement of organs. TNF-α has a central role in initial host response to infections and in the pathogenesis of various systemic immune-mediated diseases. Serum levels of TNF-α are elevated in patients with SSc and favor the development of pulmonary fibrosis and pulmonary arterial hypertension. Inflammatory arthritis can occur in patients with SSc. Infliximab and etanercept may improve the inflammatory arthritis and disability in SSc. TNF-α inhibitors reduce the systemic inflammation, improve the endothelial function decreasing the risk of pulmonary arterial hypertension progression and of acute cardiovascular and/or cerebrovascular events. Physicians need to be aware of the potential risks of tuberculosis reactivation and opportunistic infections. Randomized controlled trials with TNF-α inhibitors in patients with SSc are needed to confirm the potential role of these agents in the treatment of SSc.
Department of Internal Medicine, Clinical Immunology Unit, University of Genova, Viale Benedetto XV, n. 6, 16132 Genova, Italy.
Giuseppe
G
Murdaca
Francesca
F
Spanò
Miriam
M
Contatore
Andrea
A
Guastalla
Francesco
F
Puppo
D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D057134:Antibodies, Neutralizing / Q000096:biosynthesis; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D001168:Arthritis / Q000209:etiology / Q000517:prevention & control; D000068582:Certolizumab Pegol; D004341:Drug Evaluation; D004359:Drug Therapy, Combination; D004730:Endothelium, Vascular / Q000503:physiopathology; D000068800:Etanercept; D005544:Forecasting; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000517:prevention & control; D007140:Immunoglobulin Fab Fragments / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D007074:Immunoglobulin G / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D000069285:Infliximab; D055985:Latent Tuberculosis / Q000150:complications / Q000503:physiopathology; D009894:Opportunistic Infections / Q000209:etiology / Q000517:prevention & control; D011092:Polyethylene Glycols / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D011658:Pulmonary Fibrosis / Q000209:etiology / Q000517:prevention & control; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012595:Scleroderma, Systemic / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000502:physiology
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D057134:Antibodies, Neutralizing; D018501:Antirheumatic Agents; D007140:Immunoglobulin Fab Fragments; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D011092:Polyethylene Glycols; C529000:golimumab; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept; D000068582:Certolizumab Pegol