Risk of skin cancer in the drug treatment of rheumatoid arthritis

Stanford University School of Medicine, Division of Immunology and Rheumatology, 1000 Welch Road, Suite 203, Palo Alto, Stanford, CA 94304, USA.
Expert Opinion on Drug Safety (Impact Factor: 2.91). 10/2008; 7(5):539-46. DOI: 10.1517/14740338.7.5.539
Source: PubMed


It is well established that rheumatoid arthritis (RA) is associated with an increased risk of lymphoproliferative disorders when compared to the general population. It remains unclear whether this risk is owing to underlying inflammation and immune dysregulation, effects of disease modifying medications or a combination of the two. With increasing use of targeted biologic therapies, including those that may theoretically interfere with innate tumor surveillance, there is increasing concern about the development of other malignancies.
The English language literature was searched to identify observational studies and clinical trials reporting incidence and relative risk of melanoma and non-melanoma skin cancer (NMSC) among RA patients.
The numbers of melanomas reported were too small to draw conclusions regarding increased or decreased risk with underlying RA or commonly used medications. Relative incidence of NMSCs is difficult to assess given the lack of standardized reporting in the general population. No safety signal concerning skin cancer with RA or its therapies is at present identified.

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    ABSTRACT: The risk of malignancies in patients with rheumatoid arthritis (RA) has raised some concern, particularly with immunosuppressive approaches to disease management. We conducted a systematic review of the literature and meta-analysis characterizing the associated risk of overall malignancy and four site-specific malignancies (lymphoma, lung, colorectal, and breast cancer) in patients with RA. A Medline search from 1990 to 2007 was conducted using specified search terms and predefined inclusion criteria for identification of relevant observational studies that provide estimates of relative risk of malignancy associated with RA. Study-specific estimates of the relative risk, as measured by standardized incidence ratios (SIRs) and estimated in comparison with the general population, were combined using a random effects model. A total of 21 publications were identified, of which 13 reported the SIR for overall malignancy, 14 for lymphoma, 10 for colorectal, 12 for lung, and 9 for breast cancer. Compared with the general population, the overall SIR estimates suggest that RA patients have approximately a two-fold increase in lymphoma risk (SIR 2.08, 95% confidence interval [CI] 1.80 to 2.39) and greater risk of Hodgkin than non-Hodgkin lymphoma. The risk of lung cancer was also increased with an SIR of 1.63 (95% CI 1.43 to 1.87). In contrast, a decrease in risk was observed for colorectal (SIR 0.77, 95% CI 0.65 to 0.90) and breast (SIR 0.84, 95% CI 0.79 to 0.90) cancer. The SIR for overall malignancy was 1.05 (95% CI 1.01 to 1.09). Patients with RA appear to be at higher risk of lymphoma and lung cancer and potentially decreased risk for colorectal and breast cancer compared with the general population.
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    ABSTRACT: Several cases of skin cancer have been reported after treatment with etanercept although the causal relationship remains uncertain. We report the case of a patient who rapidly developed multiple basal cell carcinomas (BCC) after discontinuation of this treatment. A 42-year-old man presented severe plaque psoriasis after receiving topical therapy, less than 100 sessions of PUVA-therapy, retinoids and repeated solar exposure. Severe worsening of the psoriasis led us to use etanercept for seven months with excellent results. However, 11 BCCs gradually appeared within a year starting one month after the end of treatment. There is some controversy about the risk of non melanoma skin cancer associated with etanercept treatment. However, even the most recent studies are contradictory and they mostly concern rheumatological indications. In the past four years, a dozen cases of BCC have been reported following treatment for cutaneous psoriasis. As regards our patient, a genetic predisposition is possible but a potentiating effect of solar exposure is strongly suspected. This observation should lead to reinforced screening for BCC and restriction of anti-TNFalpha therapy to patients who have received less than 1000 J of PUVA-therapy, as recommended by the British Society of Rheumatology for psoriatic rheumatism. Levels of natural solar exposure must be also be taken into account.
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