Pharmaceutical Outcomes Programme, Children's and Women's Health Centre of British Columbia, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada. firstname.lastname@example.org
Adverse drug reactions (ADRs) rank as the fifth leading cause of death in the western world. The nature and scope of these ADRs in children are not predictable based on post market surveillance reports that rely heavily on adult drug experience. The genotype-specific approaches to therapy in childhood (GATC) national ADR network was established to identify specific ADRs and to improve drug safety through identification of predictive genomic biomarkers of drug risk.
GATC set out to establish a national network of trained surveillance clinicians in pediatric hospitals across Canada. Surveillance clinicians identified, enrolled, and collected clinical data and biological samples from ADR cases and controls. Surveillance was targeted to three ADRs: anthracycline-induced cardiotoxicity, cisplatin-induced hearing impairment, and codeine-induced mortality in breastfed infants.
The initial surveillance site was established in September 2005, with 10 sites fully operational by 2008. In 3 years, GATC enrolled 1836 ADR cases and 13188 controls. Target numbers were achieved for anthracycline-induced cardiotoxicity. Modified target numbers were nearly attained for cisplatin-induced hearing impairment. Codeine-induced infant mortality in a breastfed infant was discovered by GATC investigators. A case-control study was subsequently conducted.
GATC has demonstrated a model of active and targeted surveillance that builds an important step toward the goal of personalized medicine for children. Effective communication, site-specific solutions and long-term sustainability across the network are critical to maintain participation and productivity. GATC may provide a framework of ADR surveillance that can be adapted by other countries and healthcare systems.
There are very few large scale studies that have examined the association of prostate cancer with alcohol and other beverages. This relationship was examined in a case-control study conducted in 3 geographical areas of Canada [Metropolitan Toronto (Ontario), Montreal (Quebec), and Vancouver (British Columbia)] with 617 incident cases and 637 population controls. Complete history of beverage intake was assessed by a personal interview with reference to a 1-year period prior to diagnosis or interview. In age- and energy-adjusted models for all centers combined, the odds ratio (OR) for the highest quintile of total alcohol intake was 0.89. For alcoholic beverages separately, it was 0.68 for the highest tertile of beer, 1.12 for wine and 0.86 for liquor. The decreasing trend was significant for beer intake. The results were only significant for British Columbia out of all the 3 centers studied. Whereas coffee and cola intake was not associated with prostate cancer, a decrease in risk was observed with tea intake of more than 500 g per day (OR 0.70). Our results do not support a positive association between total alcohol, coffee and prostate cancer.
To study the association between alcohol consumption and risk of benign proliferative epithelial disorders (BPED) of the breast (conditions which are thought to have premalignant potential).
The study was undertaken within the 56,537 women in the Canadian National Breast Screening Study (NBSS) who completed self-administered dietary questionnaires. (The NBSS is a randomized controlled trial of screening for breast cancer in women aged 40-59 years at recruitment.)
The study subjects were the 657 women in the dietary cohort who were diagnosed with biopsy-confirmed incident BPED. For comparative purposes, a subcohort consisting of a random sample of 5681 women was selected from the full dietary cohort. After exclusions for various reasons, the analyses were based on 557 cases and 5028 non-cases.
When compared to non-drinkers, rate ratios (95% CI) for those consuming > 0 and 10 and 20 and 30 g day(-1) were 0.35 (0.27-0.45), 0.26 (0.18-0.39), 0.29 (0.18-0.48), and 0.23 (0.13-0.40), respectively (the associated P value for the trend was 0.089). Similar findings were obtained from analyses conducted separately in the screened and control arms of the NBSS, in premenopausal and postmenopausal women, and for non-atypical and atypical forms of BPED, and there was little difference between the results for screen-detected and interval-detected BPED.
Alcohol consumption was associated with a non-dose-dependent reduction in risk of BPED.
Despite warnings to abstain from alcohol, American women who are or could become pregnant still drink. This study evaluates whether women who consume alcohol are at an increased risk of recognizing pregnancy later than women who do not, adjusting for confounding factors that have been associated with alcohol consumption during pregnancy.
The sample included 863 control women from a multisite case-control study conducted from 1996 to 2002 in the United States and Canada. Telephone interviews were conducted with mothers by trained nurse interviewers who administered standardized questionnaires on demographic and reproductive factors, and pregnancy exposures.
Alcohol consumption was classified as none (42.0%), occasional (31.9%), regular (15.6%), and heavy (10.5%). Time to recognition of pregnancy was calculated as the date pregnancy was suspected minus the last menstrual period date (median: 31 days; range: 7-227 days). Unadjusted Cox proportional hazard models found that regular drinkers, but not heavy drinkers, had a significantly higher risk of recognizing pregnancy later than non-drinkers. However, this association went away after adjustment for demographic factors. Among women with unplanned pregnancies, heavy alcohol intake was associated with a 45% increased hazard ratio, compared to 0.80 for women with planned pregnancies; however, this finding was not statistically significant.
While time to pregnancy recognition did not vary among drinkers and non-drinkers, results from this study reiterate previous findings that pregnant women consume alcohol, and that drinkers share social and demographic characteristics that could be used to target public health interventions.
Evidence and Risk Assessment Division, Centre for Chronic Disease Prevention and Control, Public Health Agency of Canada, 120 Colonnade Road, AL 6701A, Ottawa, Ontario, Canada. Jinfu_Hu@phac-aspc.gc.ca
Epidemiologic studies have reported that moderate alcohol consumption is inversely associated with the risk of renal cell carcinoma (RCC), but sex-specific results are inconsistent. The present study examines the association between alcohol intake and the risk of RCC among men and women.
Mailed questionnaires were completed by 1138 newly diagnosed, histologically confirmed RCC cases and 5039 population controls between 1994 and 1997 in eight Canadian provinces. A food frequency questionnaire provided data on eating habits and alcohol consumption 2 years before data collection. Other information included socio-economic status, lifestyle habits, alcohol use, and diet. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived through unconditional logistic regression.
Total alcohol intake was inversely associated with RCC in men and in women; the OR for the highest intake group (> or =22.3 g/day among men and > or =7.9 g/day among women) versus the non-drinkers was 0.7 (95% CI, 0.5-0.9) for both sexes. Analysis of menopausal status produced ORs for the highest intake group versus the non-drinkers of 1.2 (95% CI, 0.7-2.1) among premenopausal women and 0.6 (95% CI, 0.4-0.9) among postmenopausal women. Smoking and obesity were not important effect modifiers.
Moderate alcohol consumption may be associated with a decreased risk of RCC in men and in women (mainly postmenopausal women).
Alcohol, tobacco and coffee consumption and the risk of pancreatic cancer: results from the Canadian Enhanced Surveillance System case-control project. Canadian Cancer Registries Epidemiology Research Group.
The relationship between alcohol, tobacco and coffee consumption and pancreatic cancer was investigated using population-based case-control data obtained from eight Canadian provinces. Our findings are based on analyses performed on 583 histologically confirmed pancreatic cancer cases and 4813 controls. Questionnaire data were obtained directly from 76% of the cases. Male subjects with 35 or more cigarette pack-years had an increased risk of developing pancreatic cancer relative to never smokers (OR= 1.46, 95% CI 1.00-2.14). Similarly, women reporting at least 23 cigarette pack-years of smoking had an odds ratio of 1.84 (95% CI 1.25-2.69). For the most part, consumption of total alcohol, wine, liquor and beer was not associated with pancreatic cancer. Coffee drinking was not related to pancreatic cancer. More work is needed to clarify the role of these and other potentially modifiable risk factors as a means to reduce the incidence of this disease for which treatment results remain disappointing.
To evaluate cardiovascular disease risk in First Nation youth with and without type 2 diabetes mellitus (T2DM) or obesity by comparing pro- and anti-inflammatory adipokines, markers of oxidative stress and the plasma phospholipid fatty acid profile.
Self-declared First Nation youth (12-15 yr) with T2DM (n = 24) as well as age-, gender-, and body mass index-matched controls (obese group; n = 19) and unmatched controls (control group; n = 34) were recruited from a pediatric diabetes clinic.
Plasma tumor necrosis factor-alpha, ultrasensitive C-reactive protein, resistin, and total antioxidant status were not different among the three groups. Plasma total leptin, soluble leptin receptor, and free leptin were significantly higher in the T2DM group than the control group (p
Department of Ophthalmology, University of Manitoba, Winnipeg, Canada and the Department of Ophthalmology and Visual Sciences, University of Toronto, Toronto, Canada.. Electronic address: email@example.com.
A study of 105 patients with childhood malignant germ-cell tumors (MGCT) and 639 community controls was conducted utilizing a large epidemiologic database collected by the Childrens Cancer Group from 25 member institutions in the United States and Canada. This study was designed to explore the risk factors of this malignancy whose etiology remains poorly understood. A structured, self-administered questionnaire was used to collect exposure information, and data were analyzed using an unconditional logistic regression model with adjustment for relevant confounders. Consistent with the findings from studies of adult MGCT, gestational age was associated inversely with risk of MGCT, with a 70 to 75 percent reduction in risk for children born at term compared with those born pre-term. Parental, particularly maternal, self-reported exposure to chemicals or solvents (odds ratio [OR] = 4.6, 95 percent confidence interval [CI] = 1.9-11.3) and OR = 2.2, CI = 1.1-4.7 for maternal and paternal exposure, respectively) and plastic or resin fumes (OR = 12.0, CI = 1.9-75.0 [maternal] and OR = 2.5, CI = 1.0-6.5 [paternal]) were associated with elevated risk of MGCT. New findings, not reported previously, include a positive relationship of MGCT risk with birthweight and prolonged breastfeeding, an inverse association between MGCT risk and number of cigarettes smoked by the mother during pregnancy, and a 3.1-fold increased risk (CI = 1.5-6.6) associated with maternal urinary infections during index pregnancy. Although these findings need confirmation from future studies, they suggest a potential influence of in utero exposure to maternal endogenous hormones, parental environmental exposures, and maternal diseases during pregnancy in the development of childhood MGCT.