Malignancy and biologic therapy in rheumatoid arthritis : Current Opinion in Rheumatology (original) (raw)
Rheumatoid arthritis: Edited by Eric Matteson
aDepartment of Medicine, Clinical Epidemiology Unit, Karolinska University Hospital and Karolinska Institute, Sweden
bDivision of Rheumatology and Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
Correspondence to Johan Askling, MD, PhD, Department of Medicine Solna, Clinical Epidemiology Unit M9:01, Karolinska University Hospital Solna, SE-171 76 Stockholm, Sweden Tel: +46 8 517 79321; fax: +46 8 517 79304; e-mail: [email protected]
Abstract
Purpose of review
Owing to the complex functions of the inflammatory response systems – potentially or clearly of importance in human carcinogenesis – that biological therapies interfere with uncertainty regarding their safety profile for malignancy is more or less expected. This uncertainty has been further sparked by the apparent discordance between trial data and observational studies of anti-TNF agents, and the methodological challenges inherent in addressing the safety profile of new drugs for delayed and multifactorial events like cancer.
Recent findings
This review provides a summary of the pattern of cancer seen in patients with rheumatoid arthritis not treated with biologics, and the currently published data on cancer risk following treatment with biologics in patients with rheumatoid arthritis, primarily anti-TNF therapy.
Summary
Published data currently do not exclude clinically important increased risks, nor do they refute beneficial effects. As per definition, much of the currently available safety data from trials or clinical practice do not capture the impact of either any effect that biological therapy might have on early events in carcinogenesis, or of sustained exposure to biologics. Beyond the risk of de-novo cancer development, several other clinically important aspects of cancer safety remain to be addressed, including issues of prognosis, progression, and relapse.
© 2008 Lippincott Williams & Wilkins, Inc.