Laurent Azoulay

Lady Davis Institute for Medical Research, Montréal, Quebec, Canada

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Publications (81)558.61 Total impact

  • Adi Klil-Drori · Laurent Azoulay
    JAMA Internal Medicine 07/2015; 175(7):1243-1244. DOI:10.1001/jamainternmed.2015.1277 · 13.25 Impact Factor
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    ABSTRACT: Few observational studies have investigated the association between androgen deprivation therapy (ADT) and venous thromboembolism (VTE) in patients with prostate cancer (PCa). To determine whether the use of different types of ADT in patients with PCa is associated with an increased incidence of VTE. A population-based cohort study was conducted using the UK Clinical Practice Research Datalink linked to the Hospital Episode Statistics repository. The cohort consisted of men newly diagnosed with PCa between April 1, 1998, and March 31, 2014. Cox proportional hazards models with a time-varying exposure definition were used to estimate adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of patients hospitalized for VTE associated with current and past ADT use compared with nonuse. A secondary analysis was conducted to assess the risk with current use of specific types of ADT. The cohort included 21 729 patients, of whom 609 were hospitalized for VTE during follow-up. Current ADT use was associated with an 84% increased risk of VTE (incidence rates: 10.1 vs 4.8 per 1000 person-years; HR: 1.84; 95% CI, 1.50-2.26), whereas there was no association with past use (HR: 1.07; 95% CI, 0.81-1.42). In the secondary analysis, most types of ADT were associated with a high risk of VTE. Residual confounding is possible given the observational nature of the study. The use of ADT was associated with an overall 84% increased risk of VTE, with the risk elevated for most ADT types. In this study, we investigated whether androgen deprivation therapy was associated with the risk of blood clots in a cohort of patients with prostate cancer. We observed that the risk was nearly doubled in patients who used ADT compared with those who never used it. This treatment should be reserved for patients for whom the benefits outweigh the risks. Copyright © 2015 European Association of Urology. Published by Elsevier B.V. All rights reserved.
    European Urology 06/2015; DOI:10.1016/j.eururo.2015.06.022 · 12.48 Impact Factor
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    Laurent Azoulay · Maria Eberg · Serge Benayoun · Michael Pollak
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    ABSTRACT: 5α-Reductase inhibitors (5-ARIs) are widely used in the treatment of benign prostatic hyperplasia. However, randomized clinical trials have raised concerns that their use may be associated with an increased risk of high-grade prostate cancer tumors that would ultimately lead to worse prostate cancer outcomes. To date, few observational studies have addressed this important safety concern. To determine whether the use of 5-ARIs before prostate cancer diagnosis is associated with an increased risk of cancer-specific and all-cause mortality in men with a new diagnosis of prostate cancer in the real-world setting. A retrospective cohort study was conducted in a cohort of 13 892 men with a new diagnosis of prostate cancer between January 1, 1999, and December 31, 2009, who were followed up until October 1, 2012. Patients were individually linked across 4 databases from the United Kingdom: National Cancer Data Repository, Clinical Practice Research Datalink, Hospital Episodes Statistics database, and Office for National Statistics database. Cox proportional hazards models were used to estimate hazard ratios (HRs) with 95% CIs of prostate cancer-specific and all-cause mortality associated with prediagnostic use of 5-ARIs. For each outcome, 2 models were constructed, one adjusted for predefined covariates (conventional model) and another adjusted for high-dimensional propensity score (HD-PS) deciles. During a mean (SD) of 4.5 (3.1) years, 5001 deaths occurred, including 2429 from prostate cancer (crude incidence rate of 3.86 per 100 person-years [95% CI, 3.71-4.02]). In the conventional model, use of 5-ARIs before prostate cancer diagnosis was not associated with an increased risk of prostate cancer-specific mortality (crude incidence rates, 3.76 [95% CI, 3.04-4.59] [use] vs 3.87 [95% CI, 3.71-4.03] [nonuse] per 100 person-years; adjusted hazard ratio [aHR], 0.86 [95% CI, 0.69-1.06]) and all-cause mortality (crude incidence rates, 8.42 [95% CI, 7.32-9.64] [use] vs 7.93 [95% CI, 7.71-8.16] [nonuse] per 100 person-years; aHR, 0.87; 95% CI, 0.75-1.00). Similar results were observed with the HD-PS adjusted model (prostate cancer-specific mortality: aHR, 0.90 [95% CI, 0.73-1.13]; and all-cause mortality: aHR, 0.92 [95% CI, 0.80-1.07]). The use of 5-ARIs was not associated with an increased risk of prostate cancer-specific and all-cause mortality in men with a new diagnosis of prostate cancer. While these results provide reassurance, additional studies are needed to replicate these findings.
    06/2015; 1(3). DOI:10.1001/jamaoncol.2015.0387
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    Laurent Azoulay
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    ABSTRACT: Over the past few years, substantial clinical data have been presented showing that incretin-based therapies are effective glucose-lowering agents. Specifically, glucagon-like peptide 1 receptor agonists demonstrate an efficacy comparable to insulin treatment with minimal hypoglycemia and have favorable effects on body weight. Thus, many of the unmet clinical needs noted from prior therapies are addressed by these agents. However, even after many years of use, many continue to raise concerns about the long-term safety of these agents and, in particular, the concern with pancreatitis. This clearly remains a complicated topic. Thus, in this issue of Diabetes Care, we continue to update our readers on this very important issue by presenting two studies evaluating incretin-based medications and risk of pancreatitis. Both have undergone significant revisions based on peer review that provided significant clarification of the data. We applaud both author groups for being extremely responsive in providing the additional data and revisions requested by the editorial team. As such, because of the critical peer review, we feel both articles achieve the high level we require for Diabetes Care and are pleased to now present them to our readers. In keeping with our aim to comprehensively evaluate this topic, we asked for additional commentaries to be prepared. In the narrative outlined below, Dr. Laurent Azoulay provides a commentary about the remaining uncertainty in this area and also discusses the results from a nationwide population-based case-control study. In the narrative preceding Dr. Azoulay's contribution, Prof. Edwin A.M. Gale provides a commentary on the report that focuses on clinical trials of liraglutide in the treatment of diabetes. From the journal's perspective, both of the articles on pancreatitis and incretin-based therapies reported in this issue have been well vetted, and we feel both of the commentaries are insightful.-William T. CefaluEditor in Chief, Diabetes Care. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes care 06/2015; 38(6):951-3. DOI:10.2337/dc15-0347 · 8.57 Impact Factor
  • Revue d Épidémiologie et de Santé Publique 05/2015; 63:S79. DOI:10.1016/j.respe.2015.03.096 · 0.66 Impact Factor
  • Oriana Hoi Yun Yu · Hui Yin · Laurent Azoulay
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    ABSTRACT: To determine whether the combination of dipeptidyl-peptidase 4 (DPP-4) inhibitors vs. sulfonylureas with metformin after failure of first-line treatment is associated with a decreased risk for major adverse cardiovascular events (myocardial infarction and stroke) and for all-cause mortality. Using the UK Clinical Practice Research Datalink, a cohort of patients newly treated with metformin or sulfonylurea monotherapy between January 1, 1988, and December 31, 2011, was identified and was followed until December 31, 2012. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models to compare the DPP-4 inhibitor-metformin combination to the sulfonylurea-metformin combination so as to study the risk for a composite endpoint consisting of myocardial infarction, stroke and all-cause mortality. The models were adjusted for high-dimensional propensity score deciles. The cohort consisted of 11,807 patients that included 2286 on a DPP-4 inhibitor-metformin combination and 9521 on a sulfonylurea-metformin combination. The crude incidence rates (95% CIs) of the composite endpoint were 1.2% (0.8% to 1.7%) and 2.2% (1.9% to 2.5%) per year for the DPP-4 inhibitor-metformin and sulfonylurea-metformin combinations, respectively. In the high-dimensional propensity score-adjusted model, the use of the DPP-4 inhibitor-metformin combination was associated with a 38% decreased risk for the composite endpoint (adjusted HR: 0.62; 95% CI 0.40 to 0.98), compared with the sulfonylurea-metformin combination. The use of a DPP-4 inhibitor combination with metformin, compared with a sulfonylurea-metformin combination, was associated with decreased risks for major cardiovascular events and all-cause mortality. Copyright © 2015 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.
    04/2015; DOI:10.1016/j.jcjd.2015.02.002
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    ABSTRACT: AimDipeptidyl peptidase-4 (DPP-4) inhibitors may alter the immune response and increase the risk of infections, but evidence for this association is limited. Thus, the objective of this study was to determine whether the use of DPP-4 inhibitors is associated with an increased risk of community-acquired pneumonia.Materials and methodsThe United Kingdom Clinical Practice Research Datalink (CPRD) and the Hospital Episodes Statistics (HES) database were used to conduct a nested case-control analysis within a cohort of new users of anti-diabetic drugs between 2007 and 2012. Incident cases of hospitalized community-acquired pneumonia were matched with up to 20 controls on age, duration of treated diabetes, calendar year, and duration of follow-up. Conditional logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) of hospitalized community-acquired pneumonia associated with current use of DPP-4 inhibitors compared with current use of two or more oral anti-diabetic drugs.ResultsThe cohort included 49,653 patients, of whom 562 were hospitalized for community-acquired pneumonia during follow-up (incidence rate: 5.2/1000 person-years). Compared with current use of two or more oral anti-diabetic drugs, current use of DPP-4 inhibitors was not associated with an increased risk of hospitalized community-acquired pneumonia overall (adjusted OR: 0.80, 95% CI: 0.50–1.29) or according to duration of use (p-trend = 0.57).Conclusions The use of DPP-4 inhibitors was not associated with an increased risk of hospitalization for community-acquired pneumonia. Additional research is needed to assess the association between these drugs and other serious infections.
    Diabetes Obesity and Metabolism 01/2015; 17(4). DOI:10.1111/dom.12431 · 5.46 Impact Factor
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    ABSTRACT: Tramadol is a weak opioid analgesic whose use has increased rapidly, and it has been associated with adverse events of hypoglycemia. To assess whether tramadol use, when compared with codeine use, is associated with an increased risk of hospitalization for hypoglycemia. A nested case-control analysis was conducted within the United Kingdom Clinical Practice Research Datalink linked to the Hospital Episodes Statistics database of all patients newly treated with tramadol or codeine for noncancer pain between 1998 and 2012. Cohort and case-crossover analyses were also conducted to assess consistency of the results. Cases of hospitalization for hypoglycemia were matched with up to 10 controls on age, sex, and duration of follow-up. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated comparing use of tramadol with codeine. A cohort analysis, with high-dimensional propensity score-adjusted hazard ratios (HRs) and 95% CIs, was performed comparing tramadol with codeine in the first 30 days after treatment initiation. Finally, a case-crossover analysis was also performed, in which exposure to tramadol in a 30-day risk period immediately before the hospitalization for hypoglycemia was compared with 11 consecutive 30-day control periods. Odds ratios and 95% CIs were estimated using conditional logistic regression analysis. The cohort included 334 034 patients, of whom 1105 were hospitalized for hypoglycemia during follow-up (incidence, 0.7 per 1000 per year) and matched to 11 019 controls. Compared with codeine, tramadol use was associated with an increased risk of hospitalization for hypoglycemia (OR, 1.52 [95% CI, 1.09-2.10]), particularly elevated in the first 30 days of use (OR, 2.61 [95% CI, 1.61-4.23]). This 30-day increased risk was confirmed in the cohort (HR, 3.60 [95% CI, 1.56-8.34]) and case-crossover analyses (OR, 3.80 [95% CI, 2.64-5.47]). The initiation of tramadol therapy is associated with an increased risk of hypoglycemia requiring hospitalization. Additional studies are needed to confirm this rare but potentially fatal adverse event.
    JAMA Internal Medicine 12/2014; 175(2). DOI:10.1001/jamainternmed.2014.6512 · 13.25 Impact Factor
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    ABSTRACT: Serotonin has been implicated in the development of idiopathic pulmonary arterial hypertension (IPAH). Drugs modulating serotonin pathways, including antidepressants, have been associated with the incidence of IPAH, with conflicting reports as to the direction of the effect. We aimed to determine whether antidepressant exposure is associated with the incidence of IPAH. A nested case-control study was conducted using the United Kingdom Clinical Practice Research Datalink and the Hospital Episodes Statistics repository between January 1, 1988 and September 30, 2011. Incident cases of IPAH were identified and matched to all controls in the case's risk set on age, sex, general practice, and date of registration with the practice. Rate ratios (RRs) and 95% confidence intervals (CIs) were estimated for the use of antidepressants on the risk of IPAH, with an 18-month lag period before the diagnosis. One hundred ninety-five IPAH cases were identified (incidence 3.84/million per year). Use of any antidepressant was associated with a 67% increased risk of IPAH (RR, 1.67; 95% CI, 1.17-2.37). The rate of IPAH was similar across antidepressant classes, whether with selective serotonin reuptake inhibitors (SSRIs) (RR, 1.67; 95% CI, 1.09-2.57) or non-SSRI antidepressants (RR, 1.66; 95% CI, 1.07-2.59). In sensitivity and exploratory analyses, no change in risk was observed with different lag times, serotonin transporter affinities, or durations of exposure. The use of antidepressants was associated with a significantly increased risk of IPAH. However, the consistency of this risk across all antidepressants and absence of a dose-response relationship suggests a noncausal association. Copyright © 2014 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
    The Canadian journal of cardiology 12/2014; 30(12):1633-9. DOI:10.1016/j.cjca.2014.09.031 · 3.94 Impact Factor
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    ABSTRACT: Case reports have signaled a possible association between tramadol, a weak opioid analgesic, and hyponatremia. The objective of this study was to determine whether the use of tramadol is associated with an increased risk of hyponatremia, when compared with codeine.Methods Using the UK Clinical Practice Research Datalink and Hospital Episodes Statistics database, a population-based cohort of 332,880 patients initiating tramadol or codeine was assembled between 1998 through 2012. Cox proportional hazards models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) of hospitalization for hyponatremia associated with the use of tramadol, compared with codeine, in the first 30 days after initiation. A similar analysis was conducted within a highly-restricted sub-cohort, which additionally excluded patients with any serum sodium level abnormality in the year before cohort entry. All models were adjusted for propensity score quintiles.ResultsThe incidence rates of hospitalization for hyponatremia were 4.6 (95% CI: 2.4-8.0) and 1.9 (95% CI: 1.4-2.5) per 10,000 person-months for tramadol and codeine users, respectively. In the adjusted model, the use of tramadol was associated with a 2-fold increased risk of hospitalization for hyponatremia, compared with codeine (adjusted HR: 2.05; 95% CI: 1.08-3.86). In the highly-restricted sub-cohort, the use of tramadol was associated with an over 3-fold increased risk of hospitalization for hyponatremia, compared with codeine (adjusted HR: 3.54; 95% CI: 1.32-9.54).Conclusions In this first population-based study, the use of tramadol was associated with an increased risk of hyponatremia requiring hospitalization.
    The American Journal of Medicine 11/2014; 128(4). DOI:10.1016/j.amjmed.2014.10.046 · 5.30 Impact Factor
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    Jonathan Assayag · Michael N Pollak · Laurent Azoulay
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    ABSTRACT: The association between the use of aspirin and mortality in patients with prostate cancer remains uncertain. The objective of this study was to determine whether the use of aspirin in patients with prostate cancer is associated with a decreased risk of prostate cancer mortality and all-cause mortality. Using the United Kingdom National Cancer Data Repository, Clinical Practice Research Datalink, and associated databases, we identified a cohort of men with non-metastatic prostate cancer between 1998 and 2009, followed until 2012. Cox proportional hazards models were used to estimate adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of mortality outcomes associated with post-diagnostic use of aspirin defined as a time-varying exposure. Effect modification by pre-diagnostic aspirin use was also assessed. The cohort included 11,779 men followed for 5.4 years (SD: 2.9). Post-diagnostic aspirin use was associated with an increased risk of prostate cancer mortality (HR: 1.46, 95% CI: 1.29-1.65) and all-cause mortality (HR: 1.37, 95% CI: 1.26-1.50). These increased risks were restricted to patients initiating aspirin after the prostate cancer diagnosis (HR: 1.84, 95% CI: 1.59-2.12, and HR: 1.70, 95% CI: 1.53-1.88, respectively), and not in patients who were already exposed to aspirin before the diagnosis (HR: 0.97, 95% CI: 0.81-1.16 and HR: 0.98, 95% CI: 0.87-1.18, respectively). The post-diagnostic use of aspirin is not associated with a decreased risk of prostate cancer outcomes; increased risks were restricted to patients initiating these drugs after their diagnosis, suggesting a non-causal association. Copyright © 2014 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
    The Journal of Urology 11/2014; 193(4). DOI:10.1016/j.juro.2014.11.018 · 3.75 Impact Factor
  • Niklas Schmedt · Laurent Azoulay · Sabrina Hense
    American Journal of Epidemiology 11/2014; 180(12). DOI:10.1093/aje/kwu311 · 4.98 Impact Factor
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    ABSTRACT: Serotonin stimulation of the 5HT4 receptor might be responsible for an increased risk of atrial fibrillation (AF). Thus, we assessed whether the use of antidepressants (ADs) is associated with an increased risk of chronic AF (cAF). Using the UK Clinical Practice Research Datalink, a nested case-control analysis was conducted within a cohort of new AD users having a diagnosis of depression and/or anxiety. Cases of cAF occurring during follow-up were individually matched with up to 10 controls on age, sex, year of cohort entry, and duration of follow-up. Conditional logistic regression was used to estimate rate ratios (RRs) and 95% confidence intervals (CIs) of cAF associated with current and recent use of ADs, when compared to past use. The cohort included 116,125 new AD users, of whom 1271 were diagnosed with cAF during follow-up (incidence rate: 1.6 per 1000 person-years). The adjusted RR of cAF associated with current and recent use of ADs was 0.98 (95% CI: 0.86–1.12) and 1.02 (95% CI: 0.86–1.30), respectively. No association was observed when ADs were classified according to their potency in reducing serotonin reuptake. These findings suggest that exposure to ADs is not associated with an increased risk of cAF. This article is protected by copyright. All rights reserved
    The Journal of Clinical Pharmacology 11/2014; 55(4). DOI:10.1002/jcph.435 · 2.47 Impact Factor
  • Samy Suissa · Laurent Azoulay
    Diabetes Care 10/2014; 37(10):e216. DOI:10.2337/dc14-1075 · 8.57 Impact Factor
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    ABSTRACT: Background: Small cross-sectional studies have suggested that metformin, a first-line oral hypoglycemic agent, may lower thyroid-stimulating hormone (TSH) levels. Our objective was to determine whether the use of metformin monotherapy, when compared with sulfonylurea monotherapy, is associated with an increased risk of low TSH levels (< 0.4 mIU/L) in patients with type 2 diabetes mellitus. Methods: Using the Clinical Practice Research Datalink, we identified patients who began receiving metformin or sulfonylurea monotherapy between Jan. 1, 1988, and Dec. 31, 2012. We assembled 2 subcohorts of patients with treated hypothyroidism or euthyroidism, and followed them until Mar. 31, 2013. We used Cox proportional hazards models to evaluate the association of low TSH levels with metformin monotherapy, compared with sulfonylurea monotherapy, in each subcohort. Results: A total of 5689 patients with treated hypothyroidism and 59 937 euthyroid patients were included in the subcohorts. Among patients with treated hypothyroidism, 495 events of low TSH levels were observed during follow-up (incidence rate 119.7/1000 personyears). In the euthyroid group, 322 events of low TSH levels were observed (incidence rate 4.5/1000 person-years). Compared with sulfonylurea monotherapy, metformin monotherapy was associated with a 55% increased risk of low TSH levels in patients with treated hypothyroidism (incidence rate 79.5/1000 person-years v. 125.2/1000 person-years, adjusted hazard ratio [HR] 1.55, 95% confidence interval [CI] 1.09-2.20), with the highest risk in the 90-180 days after initiation (adjusted HR 2.30, 95% CI 1.005.29). No association was observed in euthyroid patients (adjusted HR 0.97, 95% CI 0.69-1.36). Interpretation: In this longitudinal population-based study, metformin use was associated with an increased incidence of low TSH levels in patients with treated hypothyroidism, but not in euthyroid patients. The clinical consequences of this need further investigation.
    Canadian Medical Association Journal 09/2014; 186(15). DOI:10.1503/cmaj.140688 · 5.81 Impact Factor
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    ABSTRACT: To determine whether the use of incretin-based drugs, including GLP-1 analogs and dipeptidyl peptidase-4 inhibitors, is associated with an increased risk of congestive heart failure (CHF) among patients with type 2 diabetes.
    Diabetes Care 09/2014; 38(2). DOI:10.2337/dc14-1459 · 8.57 Impact Factor
  • Ilan Matok · Laurent Azoulay · Hui Yin · Samy Suissa
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    ABSTRACT: Background: The use of decongestants during the second or third trimesters of pregnancy has been associated with a decreased risk of preterm delivery in two observational studies. This effect may have been subject to immortal time bias, a bias arising from the improper classification of exposure during follow-up. We illustrate this bias by repeating the studies using a different data source. Methods: The United Kingdom Hospital Episodes Statistics and the Clinical Practice Research Datalink databases were linked to identify all live singleton pregnancies among women aged 15 to 45 years between 1997 and 2012. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals of preterm delivery (before 37 weeks of gestation) by considering the use of decongestants during the third trimester as a time-fixed (biased analysis which misclassifies unexposed person-time as exposed person-time) and time-varying exposure (unbiased analysis with proper classification of unexposed person-time). All models were adjusted for maternal age, smoking status, maternal diabetes, maternal hypertension, preeclampsia, and parity. Results: Of the 195,582 singleton deliveries, 10,248 (5.2%) were born preterm. In the time-fixed analysis, the HR of preterm delivery for the use of decongestants was below the null and suggestive of a 46% decreased risk (adjusted HR = 0.54; 95% confidence interval, 0.24-1.20). In contrast, the HR was closer to null (adjusted HR = 0.93 95% confidence interval, 0.42-2.06) when the use of decongestants was treated as a time-varying variable. Conclusion: Studies of drug safety in pregnancy should use the appropriate statistical techniques to avoid immortal time bias, particularly when the exposure occurs at later stages of pregnancy. (C) 2014 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 09/2014; 100(9). DOI:10.1002/bdra.23271 · 2.21 Impact Factor
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    Jonathan Assayag · Michael N. Pollak · Laurent Azoulay
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    ABSTRACT: Background Recent observational studies have produced conflicting results with respect to beta-blocker use after prostate cancer diagnosis and mortality outcomes. Objective To determine whether post-diagnostic use of beta-blockers is associated with prostate cancer mortality and all-cause mortality. Patients and methods A cohort of 6270 men newly-diagnosed with non-metastatic prostate cancer between 1st April 1998, and 31st December 2009, followed until 1st October 2012, was identified using large population-based electronic databases from the United Kingdom. Time-dependent Cox proportional hazards models were used to estimate adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of mortality outcomes associated with post-diagnostic use of beta-blockers. Secondary analyses were performed to examine the independent effects of non-selective beta-blockers, as well as cumulative duration of use. Results During a mean follow-up time of 3.8 years (standard deviation: 2.7 years), 1761 deaths occurred, including 715 from prostate cancer. Post-diagnostic use of beta-blockers was not associated with a decreased risk of prostate cancer mortality (HR: 0.97, 95% CI: 0.72–1.31) and all-cause mortality (HR: 0.97, 95% CI: 0.81–1.16). There was no statistically significant association for non-selective beta-blockers (prostate cancer mortality, HR: 1.05, 95% CI: 0.72–1.53 and all-cause mortality, HR: 0.94, 95% CI: 0.74–1.18), and no statistically significant trends of cumulative duration of use for both mortality outcomes. Conclusion The use of beta blockers, including those of the non-selective type, was not associated with a decreased risk of prostate cancer and all-cause mortality.
    European Journal of Cancer 09/2014; 50(16). DOI:10.1016/j.ejca.2014.08.006 · 4.82 Impact Factor
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    ABSTRACT: Background Two studies have reported statistically significant associations between the use of cardiac glycosides (CGs) and an increased risk of lung cancer. However, these studies had a number of methodological limitations. Thus, the objective of this study was to assess this association in a large population-based cohort of patients. Methods We used the United Kingdom Clinical Practice Research Datalink (CPRD) to identify a cohort of patients, at least 40 years of age, newly-diagnosed with heart failure, or supra-ventricular arrhythmia. A nested case–control analysis was conducted where each incident case of lung cancer identified during follow-up was randomly matched with up to 10 controls. Exposure to CGs was assessed in terms of ever use, cumulative duration of use and cumulative dose. Rate ratios (RRs) with 95% confidence intervals (CIs) were estimated using conditional logistic regression after adjusting for potential confounders. Results A total of 129,002 patients were included, and followed for a mean (SD) of 4.7 (3.8) years. During follow-up, 1237 patients were newly-diagnosed with lung cancer. Overall, ever use of CGs was not associated with an increased risk of lung cancer when compared to never use (RR = 1.09, 95% CI: 0.94-1.26). In addition, no dose–response relationship was observed in terms of cumulative duration of use and cumulative dose with all RRs around the null value across quartile categories. Conclusion The results of this large population-based study indicate that the use of CGs is not associated with an increased risk of lung cancer.
    BMC Cancer 08/2014; 14(1):573. DOI:10.1186/1471-2407-14-573 · 3.32 Impact Factor
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    ABSTRACT: The aim of this study is to determine whether the use of cardiac glycosides (CGs), drugs used in the treatment of congestive heart failure (CHF) and supra-ventricular arrhythmia, is associated with an increased risk of breast cancer. A cohort of 53,454 women newly diagnosed with CHF or supra-ventricular arrhythmia between January 1, 1988 and December 31, 2010, followed until December 31, 2012, was identified using the United Kingdom Clinical Practice Research Datalink. A nested case-control analysis was performed, where all incident cases of breast cancer occurring during follow-up were identified and matched with up to 10 controls on age, cohort entry date, and duration of follow-up. Conditional logistic regression models were used to estimate adjusted odds ratios (ORs) with 95 % confidence intervals (CIs) of incident breast cancer associated with the use of CGs, along with measures of cumulative duration of use and dose. All analyses considered a one year lag period prior to the event, necessary for latency considerations and to minimize detection bias. The 898 breast cancer cases diagnosed beyond one year of follow-up were matched to 8,940 controls. Overall, use of CGs was not associated with an increased risk of breast cancer when compared to non-use (OR 1.07, 95 % CI 0.90-1.26). Furthermore, the risk did not vary with cumulative duration of use or cumulative dose. The findings of this large population-based study indicate that the use of CGs is not associated with an increased risk of breast cancer. This should provide reassurance to physicians and patients using these drugs.
    Breast Cancer Research and Treatment 07/2014; 146(3). DOI:10.1007/s10549-014-3058-8 · 4.20 Impact Factor

Publication Stats

1k Citations
558.61 Total Impact Points

Institutions

  • 2011–2015
    • Lady Davis Institute for Medical Research
      • Centre for Clinical Epidemiology (CCE)
      Montréal, Quebec, Canada
  • 2009–2014
    • McGill University
      • • Department of Oncology
      • • Department of Epidemiology, Biostatistics and Occupational Health
      Montréal, Quebec, Canada
  • 2011–2013
    • Jewish General Hospital
      Montréal, Quebec, Canada
  • 2008
    • CHU Sainte-Justine
      Montréal, Quebec, Canada
  • 2005–2008
    • Université de Montréal
      • • Center for Mathematical Research
      • • Faculty of Pharmacy
      Montréal, Quebec, Canada