Biologic Disease-Modifying Antirheumatic Drugs and Risk of High-Grade Cervical Dysplasia and Cervical Cancer in Rheumatoid Arthritis: A Cohort Study

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Abstract

<div class="section"> <a class="named-anchor" id="S1">  </a> <h5 class="section-title" id="d6436124e178">Objective</h5> <p id="P1">Recent research showed an increased risk of high-grade cervical dysplasia and cervical cancer associated with rheumatoid arthritis (RA). We examined whether this risk was associated with biologic disease-modifying antirheumatic drug (DMARD) versus non-biologics. </p> </div><div class="section"> <a class="named-anchor" id="S2">  </a> <h5 class="section-title" id="d6436124e183">Methods</h5> <p id="P2">We identified RA patients starting either a biologic or a non-biologic DMARD in the US Medicaid and commercial insurance databases (2000–2012). We identified high-grade cervical dysplasia or cervical cancer with a validated claims-based algorithm and assessed utilization of gynecologic procedures. To control for potential confounders, biologic DMARD initiators were 1:1 matched to non-biologic DMARD initiators on the propensity score (PS). Hazard ratios (HR) and rate ratios (RR) from the PS-matched Medicaid and commercial cohorts were pooled by an inverse variance-weighted, fixed-effects model. </p> </div><div class="section"> <a class="named-anchor" id="S3">  </a> <h5 class="section-title" id="d6436124e188">Results</h5> <p id="P3">We included 14,729 pairs of biologic and non-biologic DMARD initiators from Medicaid and 7,538 pairs from the commercial cohort. During 73,388 person-years of active treatment with either biologic or non-biologic DMARDs, 95 cases of high-grade cervical dysplasia or cervical cancer occurred in the 2 cohorts. The HR of high-grade cervical dysplasia or cervical cancer associated with biologic DMARD was 1.25 (95%CI 0.78–2.01) in Medicaid and 1.63 (95%CI 0.62–1.89) in the commercial cohort with the pooled HR of 1.32 (95%CI 0.86–2.01). The rate of gynecologic procedures involving the uterine cervix was not different between the two groups (pooled RR 0.96, 95%CI 0.90–1.02). </p> </div><div class="section"> <a class="named-anchor" id="S4">  </a> <h5 class="section-title" id="d6436124e193">Conclusion</h5> <p id="P4">Among women with RA, initiation of biologic DMARDs was associated with a numerically, but not statistically significant, increase in the risk of high-grade cervical dysplasia or cervical cancer versus non-biologics. </p> </div>

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Sexually transmitted infections among US women and men: prevalence and incidence estimates, 2008.

Catherine Lindsey Satterwhite, Elizabeth Torrone, Elissa Meites … (2013)

Most sexually active people will be infected with a sexually transmitted infection (STI) at some point in their lives. The number of STIs in the United States was previously estimated in 2000. We updated previous estimates to reflect the number of STIs for calendar year 2008. We reviewed available data and literature and conservatively estimated incident and prevalent infections nationally for 8 common STIs: chlamydia, gonorrhea, syphilis, herpes, human papillomavirus, hepatitis B, HIV, and trichomoniasis. Where available, data from nationally representative surveys such as the National Health and Nutrition Examination Survey were used to provide national estimates of STI prevalence or incidence. The strength of each estimate was rated good, fair, or poor, according to the quality of the evidence. In 2008, there were an estimated 110 million prevalent STIs among women and men in the United States. Of these, more than 20% of infections (22.1 million) were among women and men aged 15 to 24 years. Approximately 19.7 million incident infections occurred in the United States in 2008; nearly 50% (9.8 million) were acquired by young women and men aged 15 to 24 years. Human papillomavirus infections, many of which are asymptomatic and do not cause disease, accounted for most of both prevalent and incident infections. Sexually transmitted infections are common in the United States, with a disproportionate burden among young adolescents and adults. Public health efforts to address STIs should focus on prevention among at-risk populations to reduce the number and impact of STIs.

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Some methods of propensity-score matching had superior performance to others: results of an empirical investigation and Monte Carlo simulations.

Peter C Austin (2009)

Propensity-score matching is increasingly being used to reduce the impact of treatment-selection bias when estimating causal treatment effects using observational data. Several propensity-score matching methods are currently employed in the medical literature: matching on the logit of the propensity score using calipers of width either 0.2 or 0.6 of the standard deviation of the logit of the propensity score; matching on the propensity score using calipers of 0.005, 0.01, 0.02, 0.03, and 0.1; and 5 --> 1 digit matching on the propensity score. We conducted empirical investigations and Monte Carlo simulations to investigate the relative performance of these competing methods. Using a large sample of patients hospitalized with a heart attack and with exposure being receipt of a statin prescription at hospital discharge, we found that the 8 different methods produced propensity-score matched samples in which qualitatively equivalent balance in measured baseline variables was achieved between treated and untreated subjects. Seven of the 8 propensity-score matched samples resulted in qualitatively similar estimates of the reduction in mortality due to statin exposure. 5 --> 1 digit matching resulted in a qualitatively different estimate of relative risk reduction compared to the other 7 methods. Using Monte Carlo simulations, we found that matching using calipers of width of 0.2 of the standard deviation of the logit of the propensity score and the use of calipers of width 0.02 and 0.03 tended to have superior performance for estimating treatment effects. 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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Natural history and possible reactivation of human papillomavirus in human immunodeficiency virus-positive women.

R D Burk, A. Levine, Lee Silverberg … (2005)

Little is known in human immunodeficiency virus (HIV)-positive women about how the combination of plasma HIV RNA level and CD4+ T-cell count is associated with the natural history of human papillomavirus (HPV) infection or about HPV reactivation--whether it occurs and with what frequency in HIV-positive women. HIV-positive (n = 1848) and -negative (n = 514) women were assessed at semiannual visits (total person-years = 5661) for cervicovaginal HPV with polymerase chain reaction assays and for squamous intraepithelial lesions (SILs) by Pap smear. We studied the prevalent detection of HPV and SILs with generalized estimating equations and the incident detection and persistence of HPV and SILs with multivariable Cox models. All statistical tests were two-sided. We observed a strong interaction between the associations of CD4+ and plasma HIV RNA strata with both prevalent (P(interaction) = .002) and incident (P(interaction) = .001) detection of HPV. Indeed, the hazard ratio for incident HPV detection peaked between 4.0 and 5.0, with either a CD4+ count of less than 200 cells per mm3 or an HIV RNA level of more than 100,000 copies per mL. Although incident HPV detection in all women was associated with the number of recent sex partners (P(trend)<.001), 22% of sexually inactive HIV-positive women with a CD4+ count of less than 200 cells/mm3 also had at least one incidentally detected HPV type. The association between CD4+/HIV RNA strata and HPV persistence was statistically significantly smaller (P<.001) than for incident HPV detection. SIL prevalence, incident detection, and persistence had similar associations with CD4+/HIV RNA strata as HPV (above). In HIV-positive women, plasma HIV RNA level and CD4+ count in combination appear to have a strong and statistically interactive association with incident detection of HPV, some of which may reflect HPV reactivation (e.g., in sexually inactive women). The more moderate association between HIV coinfection and HPV persistence could partly explain why cervical cancer rates have not reached more epidemic proportions in HIV-positive women.