Laurent Azoulay

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

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Publications (73)501.9 Total impact

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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 · 5.18 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; 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 · 3.12 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; DOI:10.1016/j.amjmed.2014.10.046 · 5.30 Impact Factor
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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; DOI:10.1016/j.juro.2014.11.018 · 3.75 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; DOI:10.2337/dc14-1459 · 8.57 Impact Factor
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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: BackgroundTwo 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.MethodsWe 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.ResultsA 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.ConclusionThe 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 · 4.47 Impact Factor
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    ABSTRACT: Background: Given the conflicting results from observational studies, we assessed whether the use of metformin after a prostate cancer diagnosis is associated with a decreased risk of cancer-specific and all-cause mortality. Methods: This study was conducted linking four databases from the United Kingdom. A cohort of men newly-diagnosed with non-metastatic prostate cancer with a history of treated type 2 diabetes, between April 1, 1998 and December 31, 2009, was followed until October 1, 2012. Nested case-control analyses were performed for cancer-specific mortality and all-cause mortality, where exposure was defined as use of metformin during the time to risk-set. Conditional logistic regression was used to estimate adjusted rate ratios (RRs) of each outcome with 95% confidence intervals (CIs). Results: The cohort consisted of 935 men with prostate cancer and a history of type 2 diabetes. After a mean follow-up of 3.7 years, 258 deaths occurred, including 112 from prostate cancer. Overall, the post-diagnostic use of metformin was not associated with a decreased risk of cancer-specific mortality (RR: 1.09, 95% CI: 0.51-2.33). In a secondary analysis, a cumulative duration ≥ 938 days was associated with an increased risk (RR: 3.20, 95% CI: 1.00-10.24). The post-diagnostic use of metformin was not associated with all-cause mortality (RR: 0.79, 95% CI: 0.50-1.23). Conclusion: The use of metformin after a prostate cancer diagnosis was not associated with an overall decreased risk of cancer-specific and all-cause mortality. Impact: The results of this study do not support a role for metformin in the prevention of prostate cancer outcomes.
    Cancer Epidemiology Biomarkers & Prevention 07/2014; 23(10). DOI:10.1158/1055-9965.EPI-14-0056 · 4.32 Impact Factor
  • Samy Suissa, Laurent Azoulay
    Diabetes Care 07/2014; 37(7):1786-8. DOI:10.2337/dc14-0500 · 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 07/2014; 100(9). DOI:10.1002/bdra.23271 · 2.21 Impact Factor
  • Laurent Azoulay, Oriana Yu, Samy Suissa
    Journal of Clinical Oncology 06/2014; DOI:10.1200/JCO.2014.55.7199 · 17.88 Impact Factor
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    ABSTRACT: Objective Clinical practice guidelines disagree on whether health care professionals should screen women for depression during pregnancy or postpartum. The objective of this systematic review was to determine whether depression screening improves depression outcomes among women during pregnancy or the postpartum period. Methods Searches included the CINAHL, EMBASE, ISI, MEDLINE, and PsycINFO databases through April 1, 2013; manual journal searches; reference list reviews; citation tracking of included articles; and trial registry reviews. RCTs in any language that compared depression outcomes between women during pregnancy or postpartum randomized to undergo depression screening versus women not screened were eligible. Results There were 9,242 unique titles/abstracts and 15 full-text articles reviewed. Only 1 RCT of screening postpartum was included, but none during pregnancy. The eligible postpartum study evaluated screening in mothers in Hong Kong with 2-month-old babies (N = 462) and reported a standardized mean difference for symptoms of depression at 6 months postpartum of 0.34 (95% confidence interval = 0.15 to 0.52, P < 0.001). Standardized mean difference per 44 additional women treated in the intervention trial arm compared to the non-screening arm was approximately 1.8. Risk of bias was high, however, because the status of outcome measures was changed post-hoc and because the reported effect size per woman treated was 6–7 times the effect sizes reported in comparable depression care interventions. Conclusion There is currently no evidence from any well-designed and conducted RCT that screening for depression would benefit women in pregnancy or postpartum. Existing guidelines that recommend depression screening during pregnancy or postpartum should be re-considered.
    Journal of Psychosomatic Research 06/2014; 76(6). DOI:10.1016/j.jpsychores.2014.01.006 · 2.84 Impact Factor
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    ABSTRACT: To determine whether the use of incretin based drugs, compared with sulfonylureas, is associated with an increased risk of acute pancreatitis. Population based cohort study. 680 general practices in the United Kingdom contributing to the Clinical Practice Research Datalink. From 1 January 2007 to 31 March 2012, 20 748 new users of incretin based drugs were compared with 51 712 users of sulfonylureas and followed up until 31 March 2013. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals for acute pancreatitis in users of incretin based drugs compared with users of sulfonylureas. Models were adjusted for tenths of high dimensional propensity score (hdPS). The crude incidence rate for acute pancreatitis was 1.45 per 1000 patients per year (95% confidence interval 0.99 to 2.11) for incretin based drug users and 1.47 (1.23 to 1.76) for sulfonylurea users. The rate of acute pancreatitis associated with the use of incretin based drugs was not increased (hdPS adjusted hazard ratio: 1.00, 95% confidence interval 0.59 to 1.70) relative to sulfonylurea use. Compared with use of sulfonylureas, the use of incretin based drugs is not associated with an increased risk of acute pancreatitis. While this study is reassuring, it does not preclude a modest increased risk, and thus additional studies are needed to confirm these findings.
    BMJ (online) 04/2014; 348:g2780. DOI:10.1136/bmj.g2780 · 16.38 Impact Factor
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    ABSTRACT: Platinum-based chemotherapy regimens are frequently used in patients with triple-negative breast cancer (TNBC). The aim of the current study was to assess whether or not platinum-based chemotherapy is associated with an increased time to progression when compared with non-platinum-based regimens in TNBC and non-TNBC. A retrospective analysis was conducted within a cohort of patients with metastatic breast cancer who received platinum-based chemotherapy at a single institution. Data were collected for up to three lines of treatment for metastatic disease. Time to progression was determined for platinum-based chemotherapy and non-platinum-based regimens for each line of treatment. Adjusted hazard ratios (HRs), together with 95% confidence intervals (CIs) were estimated comparing the time to progression associated with the use of platinum-based chemotherapy versus non-platinum-based regimens. A total of 159 patients were included in the analysis, with 58 diagnosed with TNBC. Among the patients with TNBC, compared with non-platinum-based chemotherapy, no correlation was identified between platinum-based chemotherapy and an improved time to progression [first line: HR, 0.97 (95% CI, 0.40-2.35); second line: HR, 0.91 (95% CI, 0.42-2.01); and third line: HR, 2.83 (95% CI, 0.73-11.03)]. By contrast, patients with non-TNBC appeared to improve with non-platinum-based chemotherapy [first line: HR, 2.57 (95% CI, 1.11-5.99); second line: HR, 1.91 (95% CI, 1.00-3.63); and third line: HR, 1.08 (95% CI, 0.53-2.18)]. Although the present study was limited by the sample size and its observational nature, the results indicated that platinum-based chemotherapy does not offer a discernible or distinct advantage compared with standard regimens in patients with TNBC, and is perhaps less efficacious in patients with non-TNBC.
    Oncology letters 03/2014; 7(3):866-870. DOI:10.3892/ol.2014.1782 · 0.99 Impact Factor
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    ABSTRACT: The aim of this study was to determine whether type 2 diabetes is associated with the incidence of prostate cancer mortality and all-cause mortality. This study was conducted by linking four databases from the United Kingdom: the National Cancer Data Repository, the Clinical Practice Research Datalink, the Hospital Episodes Statistics database, and the Office for National Statistics database. The cohort consisted of men newly diagnosed with non-metastatic prostate cancer between 1 April 1998 and 31 December 2009, followed until 1 October 2012. Cox proportional hazard models were used to estimate adjusted hazard ratios with 95 % confidence intervals (CIs) of prostate cancer mortality and all-cause mortality comparing patients with to without type 2 diabetes. All models were adjusted for a number of potential confounders, which included excessive alcohol use, smoking, comorbidities, and prostate cancer-related variables. The cohort consisted of 11,920 patients, which included 1,132 (9.5 %) with preexisting type 2 diabetes. During a mean follow-up of 4.7 (SD 3.0) years, there were 3,605 deaths (incidence rate: 6.4 %/year) including 1,792 from prostate cancer (incidence rate: 3.3 %/year). Type 2 diabetes was associated with a 23 % increased risk of prostate cancer mortality (HR 1.23, 95 % CI 1.04-1.46) and a 25 % increased risk in all-cause mortality (HR 1.25, 95 % CI 1.11-1.40). The results of this large population-based study indicate that type 2 diabetes is associated with an increased risk of prostate cancer mortality and all-cause mortality, which may signal an association between hyperinsulinemia or other diabetes-associated metabolic derangements and cancer aggressivity.
    Cancer Causes and Control 01/2014; 25(3). DOI:10.1007/s10552-013-0334-6 · 3.20 Impact Factor

Publication Stats

773 Citations
501.90 Total Impact Points

Institutions

  • 2011–2014
    • Lady Davis Institute for Medical Research
      • Centre for Clinical Epidemiology (CCE)
      Montréal, Quebec, Canada
  • 2010–2014
    • McGill University
      • • Department of Oncology
      • • Centre for Clinical Epidemiology and Community Studies
      Montréal, Quebec, Canada
  • 2010–2013
    • Jewish General Hospital
      Montréal, Quebec, Canada
  • 2012
    • Centre Georges-François Leclerc
      Dijon, Bourgogne, France
  • 2005–2008
    • Université de Montréal
      • Faculty of Pharmacy
      Montréal, Quebec, Canada