Prostate cancer in systemic lupus erythematosus

Authors

  • S. Bernatsky,

    Corresponding author
    1. Division of Rheumatology, McGill University Health Centre, Montreal, QC, Canada
    2. Division of Clinical Epidemiology, McGill University Health Centre, Montreal, QC, Canada
    • Division of Clinical Epidemiology, Research Institute of the McGill University Health Centre, 687 Pine Avenue West, V-Building, V2.09, Montreal QC H3A 1A1, Canada
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    • Fax: +1-514-934-8293

  • R. Ramsey-Goldman,

    1. Division of Rheumatology, Northwestern University, Chicago, IL
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  • C. Gordon,

    1. Department of Rheumatology, Sandwell and West Birmingham Hospitals NHS Trust, City Hospital, Birmingham, United Kingdom
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  • A.E. Clarke

    1. Division of Clinical Epidemiology, McGill University Health Centre, Montreal, QC, Canada
    2. Division of Clinical Immunology/Allergy, McGill University Health Centre, Montreal, QC, Canada
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Abstract

Our research objective was to estimate prostate cancer risk in systemic lupus erythematosus (SLE), relative to the age-matched general population. A progressive literature review was performed to identify SLE cohort studies with cancer registry linkage for cancer ascertainment. Data were pooled from four studies of large SLE cohorts who met these criteria. The total number of prostate cancers observed was derived by pooling the incident cases across all studies. The total expected number of prostate, derived from applying appropriate general population cancer incidence data to the observed number of patient-years of follow-up for each study, was similarly determined. The parameter of interest was the standardized incidence ratio (SIR), the ratio of observed to expected malignancies. The four studies together provided a pool of 6,068 male SLE patients observed for a total of 38,186 patient-years (mean 6.3 years). Within these subjects, 80 prostate cancers were observed. In each contributing study, the number of cancers expected far exceeded that observed. The pooled SIR estimate for prostate cancer risk in males with SLE, compared to the general population, was 0.72 (95% CI 0.57, 0.89). These data suggest a decreased risk of prostate cancer in SLE; more definite conclusions require additional data. As alterations in androgen pathways can potentially alter prostate risk, a lower risk of prostate cancer in SLE could possibly be due to low hypoadrenergic states which some believe may occur in men with SLE; underlying genetic factors could also be at play. Further study of these issues in large cohorts is needed.

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