Newswise — People who are taking anti tumor necrosis factor therapy for the treatment of rheumatoid arthritis may be at increased risk for developing non-melanoma skin cancer, according to research presented this week at the American College of Rheumatology Annual Scientific Meeting in Philadelphia, Pa.
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
RA is associated with an increased risk of non-melanoma skin cancer, and it is believed that this risk might increase for people taking anti tumor necrosis factor therapy (commonly called anti-TNF therapy), although evidence has been conflicting.
Researchers from the United Kingdom recently set out to explore the influence of anti-TNF therapy relative to other disease modifying therapies on the incidence of non-melanoma skin cancer using data from the BSRBR, a registry that tracks the progress of people with severe rheumatoid arthritis and other rheumatic conditions in the United Kingdom.
During the study, researchers followed 11,757 people on anti-TNF therapy for RA and compared those patients to 3,515 patients with RA who were not on this therapy but were receiving traditional Disease-modifying antirheumatic drugs (often called DMARDS).
Patients, who were followed until December 31, 2008 or death, and their physicians completed questionnaires and these, along with information from a national register for cancer, were used to determine the incidence of non-melanoma skin cancer. Researchers excluded Bowen’s disease (a condition where, on the surface, cells appear to be cancerous, but they have not grown into deeper layers of the skin) in their reporting of non-melanoma cancer, and they considered non-melanoma cancer that occurred after stopping anti-TNF treatment to be attributed to the most-recent anti-TNF drug.
During the study, 221 cases of non-melanoma skin cancer were verified. Of these, 175 cases were found among 149 anti-TNF patients and 46 cases were found in 40 DMARD patients. Researchers received histology data for 135 non-melanoma skin cancers in the anti-TNF patients, which revealed that 122 ( 90 percent) of these skin cancers were basal cell carcinoma and 12 ( nine percent) were squamous cell carcinoma, and a similar ratio of basal cell to squamous cell was found among patients taking DMARDS.
Researchers determined that the strongest predictor of non-melanoma skin cancer in these patients is having previously been diagnosed with it. Other known risk factors were found to be age, being a male, and use of steroid therapy.
Ultimately, researchers found that in patients with RA who had not previously been diagnosed with non-melanoma skin cancer, the risk was increased those who were on anti-TNF therapy compared with those on traditional DMARD therapy, although this increase was not statistically significant. This risk for developing non-melanoma skin cancer was further broken down by specific therapy. The researchers did not examine whether the risk of non-melanoma skin cancer was increased in those on DMARD therapy compared with untreated RA patients or the general population.
“This study has suggested that treatment with anti-TNF may increase the risk of non-melanoma skin cancer in patients with RA,” says Kimme Hyrich, MD, PhD, FRCPC; senior lecturer in rheumatic diseases epidemiology; University of Manchester, Manchester United Kingdom, and lead investigator in the study. “The majority of the cancers were basal cell cancers, which is the most common type of skin cancer and although rarely fatal, can lead to significant scarring. Patients on anti-TNF therapy should be advised on preventative skin care and ongoing skin surveillance, and should be encouraged to report any new, persistent lesions to their doctors.”
The ACR is an organization of and for physicians, health professionals, and scientists that advances rheumatology through programs of education, research, advocacy and practice support that foster excellence in the care of people with or at risk for arthritis and rheumatic and musculoskeletal diseases. For more information on the ACR’s annual meeting, see www.rheumatology.org/annual.
Editor’s Notes: Dr. Hyrich will present this research during the ACR Annual Scientific Meeting at the Pennsylvania Convention Center at 12:15 PM on Wednesday, October 21 in Room 108B. Dr. Hyrich will be available for media questions and briefing at 8:30 AM on Sunday, October 18 in the on-site press conference room, 109 A.
Presentation Number: 2062
The Influence of Anti-TNF Therapy Upon Incidence of Non-Melanoma Skin Cancer (NMSC) in Patients with Rheumatoid Arthritis (RA): Results From the BSR Biologics Register (BSRBR)
L. K. Mercer, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom J. B. Galloway, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom M. Lunt, PhD, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom W. G. Dixon, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom K. D. Watson, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom BSRBR Control Centre Consortium D. P. Symmons, ARC Epidemiology Unit, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom K. L. Hyrich, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom On behalf of the BSRBR, arc Epidemiology Unit, University of Manchester, Manchester, United Kingdom
Purpose: RA is associated with an increased risk of NMSC. Anti-TNF therapy may intensify this risk, although evidence to date is conflicting. Our aim was to explore the influence of anti-TNF therapy on the incidence of NMSC using data from the BSRBR, a prospective cohort study set up in 2001 to monitor the long-term safety of anti-TNF therapy in the UK.
Method: 11757 consecutive anti-TNF treated patients with RA were followed 6 monthly and compared to 3515 biologic-naïve subjects with active RA receiving traditional disease modifying therapy (DMARD). Patients were followed until 12/31/2008 or death, whichever came first. Incident NMSC were identified from consultant and patient questionnaires and record linkage with the UK national register for cancer. Local recurrence was included but carcinoma-in-situ (Bowen's disease) excluded as an incident NMSC. NMSC occurring after stopping anti-TNF was attributed to the most recently received anti-TNF drug. The rates of NMSC in the anti-TNF and DMARD cohorts were compared using multivariate Cox proportional hazards models adjusted for age, gender, disease duration, disease activity, HAQ, baseline steroid use, number of prior DMARDs, smoking and year of registration.
Results: 221 NMSC were verified: 175 in 149 anti-TNF patients (4.2/1000 pyrs) and 46 in 40 DMARD patients (5.1/1000 pyrs). Histology data were received for 135 NMSC in the anti-TNF patients of which 122 (90%) were basal cell carcinoma (BCC) and 12 (9%) squamous cell carcinoma (SCC). A similar ratio of BCC:SCC was seen in the DMARD cohort. The strongest predictor for NMSC was prior NMSC (HR 9.8 (95% CI 5.6, 17.0)), with other known risk factors (age, male gender and steroids) also associated with increased risk. Limiting the analysis to patients with no prior NMSC the fully adjusted hazard ratio (aHR) for anti-TNF vs. DMARD was 1.7 (0.9, 3.4). The aHR was 1.7 (0.8, 3.4) for etanercept (ETA), 2.9 (1.4, 6.1) for infliximab (INF) and 1.1 (0.5, 2.5) for adalimumab (ADA).
Conclusion: In patients with no prior NMSC, the risk of NMSC was increased by 70% in patients with RA treated with anti-TNF therapy, although this was not significant. INF was associated with an almost 3 fold increase in risk of NMSC in this group. Vigilance for NMSC should be maintained in all patients with RA, especially when treated with anti-TNF therapy.
Table: (View the press release with full abstract at www.rheumatology.org.
Disclosure: L. K. Mercer, None; J. B. Galloway, None; M. Lunt, None; W. G. Dixon, None; K. D. Watson, None; D. P. Symmons, The British Society for Rheumatology, 2 ; K. L. Hyrich, The British Society for Rheumatology, 2 ; O. behalf of the BSRBR, The British Society for Rheumatology, 2 .
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