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Population Attributable Risk (population + attributable_risk)
Selected AbstractsEstimating population attributable risk for hepatitis C seroconversion in injecting drug users in Australia: implications for prevention policy and planningADDICTION, Issue 12 2009Handan Wand ABSTRACT Objective To determine risk factors and estimate their population-level contribution to hepatitis C virus (HCV) burden. Methods Established and potentially modifiable risk factors were estimated using partial population attributable risk (PARp) in a cohort of new injecting drug users (IDUs) in Sydney, Australia. Results A total of 204 hepatitis C seronegative IDUs were recruited through street-based outreach, methadone clinics and needle and syringe programmes (NSPs) and followed-up at 3,6-monthly intervals. A total of 61 HCV seroconversions were observed during the follow-up [overall incidence rate of 45.8 per 100 person-years (95% confidence interval: 35.6,58.8)]. Overall, five potentially modifiable risk factors (sharing needles/syringes, sharing other injecting equipment, assisted injecting, frequency of injection and not being in drug treatment) accounted for approximately 50% of HCV cases observed. Conclusion While sharing needles/syringes or other injecting equipment were associated most strongly with increased risk of HCV infection, the PARp associated with these behaviours was relatively modest (12%) because they are relatively low-prevalence behaviours. Our analyses suggest that more HCV infection could be avoided by changing more common, but less strongly associated behaviours such as assisted injecting or daily injecting. Results suggest that to have a very substantial effect on HCV, a range of risk factors need modifying. The most efficient use of scarce resources in reducing HCV infections will require complex balancing between the PAR for a given risk factor(s), the efficacy of interventions to actually modify the risk factor, and the cost of these interventions. [source] IL23R haplotypes provide a large population attributable risk for Crohn's diseaseINFLAMMATORY BOWEL DISEASES, Issue 9 2008Kent D. Taylor PhD Abstract Background: The IL-23 pathway plays a pivotal role in the development of chronic mucosal inflammation seen in the inflammatory bowel diseases. Multiple studies have now established the contribution of the interleukin 23 receptor gene (IL23R) to Crohn's disease (CD) risk in general and of the IL23R R381Q variant in particular. The aim of this work was to estimate the total contribution of this gene to CD risk test using a haplotype approach. Methods: In all, 763 CD subjects and 254 controls were genotyped for single nucleotide polymorphisms in the IL23R gene using Illumina and ABI methods. Haplotypes were assigned using PHASEv2 and tested for association with CD by chi-square and permutation. Results: Haplotypes with both increased and decreased risk for CD were observed in 2 of the 4 observed blocks (Block 2 H1: 55.4% control, 64% CD, P = 0.019; H2: 64.5% control, 54.4% CD, P = 0.006; Block 3 H1: 55.8% control, 64.4% CD, P = 0.013; H2: 47.0% control, 36.6% CD, P = 0.001). The population attributable risk for these haplotypes was substantially larger than that estimated for the IL23R R381Q variant (Block 2 H1 and block 3 H1 ,20%, compared with ,4% for Block 3 H6, containing the variant). Conclusions: These observations suggest that IL23R makes a substantial contribution to CD susceptibility, larger than that estimated from the population frequency of the R381Q variant. These observations also support the expectation that finding "hits" from genomewide association studies will be but an important chapter in the story of unraveling the genetic contribution to CD, rather than the final chapter that brings clarity to all the plot twists of a complicated story. (Inflamm Bowel Dis 2008) [source] Multimorbidity and Survival in Older Persons with Colorectal CancerJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 12 2006Cary P. Gross MD OBJECTIVES: To ascertain the effect of common chronic conditions on mortality in older persons with colorectal cancer. DESIGN: Retrospective cohort study. SETTING: Population-based cancer registry. PARTICIPANTS: Patients in the Surveillance Epidemiology and End Results,Medicare linked database who were aged 67 and older and had a primary diagnosis of Stage 1 to 3 colorectal cancer during 1993 through 1999. MEASUREMENTS: Chronic conditions were identified using claims data, and vital status was determined from the Medicare enrollment files. After estimating the adjusted hazard ratios for mortality associated with each condition using a Cox model, the population attributable risk (PAR) was calculated for the full sample and by age subgroup. RESULTS: The study sample consisted of 29,733 patients, 88% of whom were white and 55% were female. Approximately 9% of deaths were attributable to congestive heart failure (CHF; PAR =9.4%, 95% confidence interval (CI) =8.4,10.5%), more than 5% were attributable to chronic obstructive pulmonary disease (COPD; PAR =5.3%, 95% CI=4.7,6.6%), and nearly 4% were attributable to diabetes mellitus (PAR =3.9%, 95% CI=3.1,4.8%). The PAR associated with CHF increased with age, from 6.3% (95% CI=4.4,8.8%) in patients aged 67 to 70 to 14.5% (95% CI=12.0,17.5%) in patients aged 81 to 85. Multiple conditions were common. More than half of the patients who had CHF also had diabetes mellitus or COPD. The PAR associated with CHF alone (4.29%, 95% CI=3.68,4.94%) was similar to the PAR for CHF in combination with diabetes mellitus (3.08, 95% CI=2.60,3.61%) or COPD (3.93, 95% CI=3.41,4.54%). CONCLUSION: A substantial proportion of deaths in older persons with colorectal cancer can be attributed to CHF, diabetes mellitus, and COPD. Multimorbidity is common and exerts a substantial effect on colorectal cancer survival. [source] Apolipoprotein E Genotype and Mortality: Findings from the Cache County StudyJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 6 2005Kathleen M. Hayden PhD Objectives: To evaluate the association between apolipoprotein E (apo E) ,4 and mortality, the population attributable risk for mortality with ,4, and relative contributions of cardiovascular disease (CVD) and Alzheimer's disease (AD). Design: Population-based cohort study. Setting: Community-based. Participants: Permanent residents of Cache County, Utah, aged 65 and older as of January 1, 1995. Measurements: Participants were genotyped at the apo E locus using buccal-swab deoxyribonucleic acid. Cardiovascular health was ascertained using self- or proxy-report interviews at participants' residences. AD was diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, and National Institute of Neurological and Communicative Disorders and Stroke,Alzheimer's Disease and Related Disorders criteria. Utah Department of Vital Statistics quarterly reports were reviewed to identify participants who died. Results: Crude evaluations showed nonsignificantly greater risk of death for ,2/2 (hazard ratio (HR)=1.66, 95% confidence interval (CI)=0.92,2.76) and ,3/4 (HR=1.11, 95% CI=0.97,1.26) genotypes and significantly greater risk for ,4/4 (HR=1.48, 95% CI=1.09,1.96). After adjustment for age, age2, sex, and education, risks increased to 1.98 (95% CI=1.08,3.35), 1.28 (95% CI=1.12,1.46), and 2.02 (95% CI=1.47,2.71), respectively, compared with ,3/3 genotypes. Adjustment for presence of any CVD did not change the risk of death for ,3/4 and ,4/4. Adjustment for AD reduced the risk of death for ,3/4 (HR=1.13, 95% CI=0.99,1.30) and ,4/4 (HR=1.59, 95% CI=1.15,2.14). The population attributable risk of death for ,3/4 and ,4/4 genotypes combined is estimated at 9.6%. Conclusion: These findings suggested that the ,2/2, ,3/4, and ,4/4 genotypes have greater early mortality risks. Further analyses showed that AD partially mediates the association between ,3/4, ,4/4, and death. [source] Association of the VDR Translation Start Site Polymorphism and Fracture Risk in Older Women,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 5 2007Susan P Moffett PhD Abstract We evaluated the association between the VDR translation start site polymorphism and osteoporotic phenotypes among 6698 older white women. Women with the C/C genotype had lower wrist BMD and an increased risk of wrist and all non-spine/low-trauma fractures. The high frequency of this variant confers a population attributable risk that is similar to several established risk factors for fracture. Introduction: The vitamin D receptor (VDR) is a nuclear receptor that regulates bone formation, bone resorption, and calcium homeostasis. A common C to T polymorphism in exon 2 of the VDR gene introduces a new translation start site and a protein that differs in length by three amino acids (T = 427aa, C = 424aa; rs10735810). Materials and Methods: We conducted genetic association analyses of this polymorphism, BMD, and fracture outcomes in a prospective cohort of 6698 white American women ,65 years of age. Incident fractures were confirmed by physician adjudication of radiology reports. There were 2532 incident nontraumatic/nonvertebral fractures during 13.6 yr of follow-up including 509 wrist and 703 hip fractures. Results: Women with the C/C genotype had somewhat lower distal radius BMD compared with those with the T/T genotype (CC = 0.358 g/cm2, CT = 0.361 g/cm2, TT = 0.369 g/cm2, p = 0.003). The C/C genotype was also associated with increased risk of non-spine, low traumatic fractures (HR: 1.18; 95% CI: 1.04, 1.33) and wrist fractures (HR: 1.33; 95% CI: 1.01, 1.75) compared with the T/T genotype in age-adjusted models. Further adjustments for distal radius BMD only slightly attenuated these associations. The VDR polymorphism was not associated with hip fracture. The population attributable risk (PAR) of the C/C genotype for incident fractures was 6.1%. The PAR for established risk factors for fracture were: low femoral neck BMD (PAR = 16.3%), maternal history of fracture (PAR = 5.1%), low body weight (PAR = 5.3%), corticosteroid use (PAR = 1.3%), and smoking (PAR = 1.6%). Similar PAR results were observed for wrist fractures. Conclusions: The common and potentially functional VDR translation start site polymorphism confers a modestly increased relative risk of fracture among older white women. However, the high frequency of this variant confers a population attributable risk that is similar to or greater than several established risk factors for fracture. [source] Atherosclerosis, dementia, and Alzheimer disease in the Baltimore Longitudinal Study of aging cohortANNALS OF NEUROLOGY, Issue 2 2010Hillary Dolan MA Objective Although it is now accepted that asymptomatic cerebral infarcts are an important cause of dementia in the elderly, the relationship between atherosclerosis per se and dementia is controversial. Specifically, it is unclear whether atherosclerosis can cause the neuritic plaques and neurofibrillary tangles that define Alzheimer neuropathology and whether atherosclerosis, a potentially reversible risk factor, can influence cognition independent of brain infarcts. Methods We examined the relationship between systemic atherosclerosis, Alzheimer type pathology, and dementia in autopsies from 200 participants in the Baltimore Longitudinal Study of Aging, a prospective study of the effect of aging on cognition, 175 of whom had complete body autopsies. Results Using a quantitative analysis of atherosclerosis in the aorta, heart, and intracranial vessels, we found no relationship between the degree of atherosclerosis in any of these systems and the degree of Alzheimer type brain pathology. However, we found that the presence of intracranial but not coronary or aortic atherosclerosis significantly increased the odds of dementia, independent of cerebral infarction. Given the large number of individuals with intracranial atherosclerosis in this cohort (136/200), the population attributable risk of dementia related to intracranial atherosclerosis (independent of infarction) is substantial and potentially reversible. Interpretation Atherosclerosis of the intracranial arteries is an independent and important risk factor for dementia, suggesting potentially reversible pathways unrelated to Alzheimer pathology and stroke through which vascular changes may influence dementia risk. [source] Sequence variants on chromosome 9p21.3 confer risk for atherosclerotic stroke,ANNALS OF NEUROLOGY, Issue 5 2009Andreas Gschwendtner MD Objective Recent studies have identified a major locus for risk for coronary artery disease and myocardial infarction on chromosome 9p21.3. Stroke, in particular, ischemic stroke caused by atherosclerotic disease, shares common mechanisms with myocardial infarction. We investigated whether the 9p21 region contributes to ischemic stroke risk. Methods In an initial screen, 15 single nucleotide polymorphisms (SNPs) covering the critical genetic interval on 9p21 were genotyped in samples from Southern Germany (1,090 cases, 1,244 control subjects) and the United Kingdom (758 cases, 872 control subjects, 3 SNPs). SNPs significantly associated with ischemic stroke or individual stroke subtypes in either of the screening samples were subsequently genotyped in 2,528 additional cases and 2,189 additional control subjects from Europe and North America. Results Genotyping of the screening samples demonstrated associations between seven SNPs and atherosclerotic stroke (all p < 0.05). Analysis of the full sample confirmed associations between six SNPs and atherosclerotic stroke in multivariate analyses controlling for demographic variables, coronary artery disease, myocardial infarction, and vascular risk factors (all p < 0.05). The odds ratios for the lead SNP (rs1537378-C) were similar in the various subsamples with a pooled odds ratio of 1.21 (95% confidence interval, 1.07,1.37) under both fixed- and random-effects models (p = 0.002). The point estimate for the population attributable risk is 20.1% for atherosclerotic stroke. Interpretation The chromosome 9p21.3 region represents a major risk locus for atherosclerotic stroke. The effect of this locus on stroke appears to be independent of its relation to coronary artery disease and other stroke risk factors. Our findings support a broad role of the 9p21 region in arterial disease. Ann Neurol 2009;65:531,539 [source] Quantification of the familial contribution to juvenile idiopathic arthritisARTHRITIS & RHEUMATISM, Issue 8 2010Sampath Prahalad Objective We previously demonstrated that there is familial aggregation of juvenile idiopathic arthritis (JIA). Using a large JIA cohort, we sought to identify additional clusters of JIA cases and to calculate robust estimates of the relative risk (RR) of JIA in the siblings and cousins of JIA probands. We also estimated the population attributable risk (PAR) of familial factors in JIA. Methods A probabilistic record-linking analysis was performed by matching the records of 862 patients with JIA with the records of ,7 million individuals in the Utah Population Database (UPDB), a computerized genealogic database. For each patient, 5 control subjects matched for birth year and sex were selected from the UPDB. Specialized software was used to test for familial aggregation of disease, to estimate the magnitude of familial risks, and to identify families at high risk of disease. Results We identified 22 founders who had significantly more descendants with JIA than expected (5,13 descendants; P values ranged from <0.0001 to <0.008). The PAR of familial factors for JIA was ,13%. The RR of JIA in the siblings of patients was significantly increased (11.6, 95% confidence interval [95% CI] 4.9,27.5, P < 2.59 × 10,8). The RR of JIA in first cousins was also increased (5.82, 95% CI 2.5,13.8, P < 6.07 × 10,5). Conclusion We have identified the largest sets of JIA pedigrees described to date. Approximately 13% of cases of JIA can be attributed to familial factors. Siblings and first cousins of probands with JIA have an increased risk of JIA. The observed decline in the magnitude of risk between siblings and cousins suggests that JIA is influenced by shared genetic factors. [source] Heritability of vasculopathy, autoimmune disease, and fibrosis in systemic sclerosis: A population-based studyARTHRITIS & RHEUMATISM, Issue 7 2010Tracy Frech Objective To investigate the familiality of systemic sclerosis (SSc) in relation to Raynaud's phenomenon (RP) (a marker of vasculopathy), other autoimmune inflammatory disease, and fibrotic interstitial lung disease (ILD). Methods A genealogic resource, the Utah Population Database (UPDB), was used to test heritability of RP, other autoimmune disease, and ILD. Diseases were defined by International Classification of Diseases, Ninth Revision codes and identified from statewide discharge data, the University of Utah Health Science Center Enterprise Data Warehouse, and death certificates and were linked to the UPDB for analysis. Familial standardized incidence ratio (FSIR), relative risks (RRs) to first-, second-, third-, and fourth-degree relatives for SSc, RP, other autoimmune disease, and ILD (with 95% confidence intervals [95% CIs]), and population attributable risk (PAR) were calculated. Results A software kinship analysis tool was used to analyze 1,037 unique SSc patients. Fifty SSc families had significant FSIRs, ranging from 2.07 to 17.60. The adjusted PAR was ,8%. The RRs were significant for other autoimmune disease in the first-degree relatives (2.49 [95% CI 1.99,3.41], P = 2.42 × 10,15) and second-degree relatives (1.48 [95% CI 1.34,2.39], P = 0.002), for RP in first-degree relatives (6.38 [95% CI 3.44,11.83], P = 4.04 × 10,9) and second-degree relatives (2.39 [95% CI 1.21,4.74], P = 0.012), and for ILD in first-degree relatives (1.53 [95% CI 1.04,2.26], P = 0.03), third-degree relatives (1.47 [95% CI 1.18,1.82], P = 0.0004), and fourth-degree relatives (1.2 [95% CI 1.06,1.35], P = 0.004). Conclusion These data suggest that SSc pedigrees include more RP, autoimmune inflammatory disease, and ILD than would be expected by chance. In SSc pedigrees, genetic predisposition to vasculopathy is the most frequent risk among first-degree relatives. [source] Are common symptoms in childhood associated with chronic widespread body pain in adulthood?: Results from the 1958 british birth cohort studyARTHRITIS & RHEUMATISM, Issue 5 2007Gareth T. Jones Objective Studies have shown that common symptoms in childhood predict the onset of chronic widespread pain in the short term. However, it is unknown whether this association persists into adulthood. The aim of the current study was to examine, prospectively, whether children with common symptoms experience an increased risk of chronic widespread pain as adults. Methods Information on vomiting/bilious attacks, abdominal pain, and headaches/migraine was collected on 10,453 7-year-old children, by maternal report. Similar data were gathered when the children were ages 11 years and 16 years. Body pain at age 45 years was assessed by postal questionnaire. Poisson regression was used to examine chronic widespread pain in relation to childhood symptom reporting. Results Of the 10,453 subjects on whom data were obtained when they were children, 7,470 participated at age 45 years (71.5%). Children with multiple symptoms at age 7 years experienced a 50% increased risk of chronic widespread pain (relative risk 1.5 [95% confidence interval 1.03, 2.3]). This relationship persisted after adjustment for sex, recent psychological distress, and childhood and current socioeconomic status, and after excluding children with major illnesses that might have explained early symptom reporting. A similar relationship with symptoms at ages 11 and 16 years was observed, although this was not associated with additional risk compared with that found with the presence of symptoms at age 7 years. However, despite a modest increase in risk, the presence of multiple symptoms at early ages was uncommon (<1.5%), and therefore, the associated population attributable risk was low (<1%). Conclusion Multiple common symptoms in childhood are associated with an increased risk of chronic widespread pain in adulthood. However, the magnitude of this increased risk is modest, and reports of multiple symptoms in childhood are uncommon. Thus the "early pain pathway" phenomenon is applicable only to a small proportion of individuals with chronic widespread pain. [source] Environmental factors, parental atopy and atopic eczema in primary-school children: a cross-sectional study in TaiwanBRITISH JOURNAL OF DERMATOLOGY, Issue 6 2007Y-L. Lee Summary Background, Parental atopy and environmental exposure are recognized risk factors for atopic eczema (AE) in childhood. However, the relative contributions of specific risk factors and the overall contributions of hereditary and environmental exposure remain unexplored. Objectives, To identify risk factors, estimate the population attributable risk (PAR) of environmental exposure, and compare the AE data for boys vs. girls in primary-school children. Methods, During a February to June 2001 cross-sectional, Taiwan-based questionnaire survey, we investigated 23 980 children from 22 primary schools, all located within 1 km of an air-monitoring station. Results, The 12-month prevalence of AE was reported as 6·1% in boys and 4·9% in girls. In both sexes, the risk of AE was strongly associated with parental atopy and perceived ambient air pollution. The presence of cockroaches [odds ratio (OR) 1·18, 95% confidence interval (CI) 1·00,1·40] and visible mould on walls at home (OR 1·46, 95% CI 1·22,1·70) were also significantly related to AE for girls; however, only visible mould on walls (and not the presence of cockroaches) at home was related to AE for boys (OR 1·40, 95% CI 1·18,1·66). While mutually adjusted models were applied, we found adjusted ORs and PARs were similar in boys and girls in hereditary and outdoor environmental factors. The PAR of indoor environmental factors was higher in girls (8·4%) than in boys (5·5%). There was no interaction between parental atopy and environmental factors. Conclusions, Parental atopy contributed more to AE than indoor or outdoor environmental factors. Girls may be more susceptible to indoor environmental factors than boys. [source] Unraveling the genetics of exfoliation glaucomaACTA OPHTHALMOLOGICA, Issue 2008F JONASSON Purpose To give an account of our recent discovery (2007) of the association of lysyl oxidase like 1 (LOXL1) sequence variants and exfoliation glaucoma (XFG) as well as later replications in other populations. Methods We did a genome-wide association study on open angle glaucoma cases and controls using the Illumina 300 chip. This chip includes probes for 317.000 single , nucleotide polymorphisms (SNPs), that tag, as highly correlated surrogates about 80% of the 2.1 million known common SNPs in the Caucasian genome. For diagnosis of exfoliation syndrome a peripheral band or central shield of exfoliative material on the anterior lens capsule was required. Results When we had done 195 open angle glaucoma cases high genome wide significance was achieved on chromosome 15q24.1 an association later found to be confined to XFG only. This SNP (rs2165241T) was located in the first intron of the LOXL1 gene. We then added 11 correlated SNPs that are not on the Illumina chip and found that two non-synonymous variants in the first exon of LOXL1 can jointly account for all the observed association (R141L, OR 2.5; G153D, OR 20.1). Combined the variants explained 99% of the population attributable risk for exfoliation glaucoma. Conclusion These findings have now largely been confirmed in numerous American, Asian, Australian and European studies, and in all instances do these polymorphisms in the LOXL1 gene confer risk to XFG. LOXL1 is cross linking enzyme responsible for elastin polymer deposition in ocular tissue. The LOXL1 discovery is the first big hit in the search for genetic background for exfoliation glaucoma. These findings may soon influence monitoring of glaucoma suspects in the clinic targeting persons with the high risk haplotypes. [source] S03.3: Interaction effects and population attributable risks for smoking and alcohol on laryngeal cancer and its subsites: a case-control studyBIOMETRICAL JOURNAL, Issue S1 2004Heribert Ramroth No abstract is available for this article. [source] In this issue: Biotechnology Journal 9/2010BIOTECHNOLOGY JOURNAL, Issue 9 2010Article first published online: 10 SEP 2010 Linking obesity and colorectal cancer Sung and Bae, Biotechnol. J. 2010, 5, 930,941 Obesity is known as one of the most closely related risk factors of colorectal cancer (CRC). However, due to the complicated nature of the diet, it has been very difficult to provide clear explanations and molecular mechanisms for the role of dietary components in carcinogenesis. Nutrigenomics has become a powerful tool to study the relationships between food components and genes. It includes nutrigenetics (dealing with genetic variations related to phenotypic changes in response to diet), nutritional epigenomics and nutritional transcriptomics/proteomics/metabolomics. This review summarizes data on genes, proteins and metabolites that are related to either obesity or CRC and candidate molecules that may link obesity and CRC. The application of bioinformatics helps to perform large-scale network analysis to study cause-effect relationships between dietary components and CRC in the future. Hepatoprotective effects of oleuropein Kim et al., Biotechnol. J. 2010, 5, 950,960 Oleuropein, an active constituent of olive leaf, has a variety of pharmacological activities associated with its capacity to scavenge reactive oxygen species and has a protective effect against non-alcoholic fatty liver disease (NAFLD) in vivo. To gain insights into the molecular mechanisms of its hepatoprotective action the group of Taesun Park (Seoul, Korea) fed mice with a high fat diet supplemented with oleuropein. Then, liver tissue was subjected to DNA microarray analysis. Oleuropein in high fat diet reduced the mRNA level of regulators of hepatic fatty acid uptake and transport. The expression of a number of genes involved in oxidative stress responses, detoxification of lipid peroxidation products and proinflammatory cytokine genes were reduced, while highly regulated transcription factors were implicated in the lipogenesis, inflammation, insulin resistance and fibrosis, underlying the multifactorial effect of oleuropein on NAFLD. Genetic variations in obesity and diabetes Varma et al., Biotechnol. J. 2010, 5, 942,949 Obesity is a state of metabolic deregulation and a leading cause for development of type 2 diabetes, which are complex polygenic diseases. Here, authors from the National Centre of Toxicological Research at the FDA (Jefferson, Arizona, USA) used a data mining approach to evaluate the role of carbohydrate metabolic pathway genes in the development of obesity and type 2 diabetes. Data from public databases were used to map the position of these genes to known quantitative trait loci (QTL) and to find sequence and structural genetic variants such as single nucleotide polymorphisms (SNPs). The results demonstrated that a majority of carbohydrate metabolic pathways genes are associated with QTL for obesity and many for type 2 diabetes. This data mining approach can establish a strategy for interpreting an individual's risk factor for disease development, instead of population attributable risks. [source] General obstetrics: Preterm birth and multiple pregnancy in European countries participating in the PERISTAT projectBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 5 2006B Blondel Objective, To compare rates of preterm birth among multiple births in European countries, to estimate their contribution to overall preterm birth rates and to explore factors which could explain differences between preterm birth rates. Design, Analyses of data from vital statistics, birth registers or national samples of births. Setting, Eleven member states of the European Union. Population, All live births or representative samples of births at national or regional level for the year 2000 or most recent year. Methods, Description of rates of preterm birth before 37 and 32 weeks, estimation of population attributable risks (PAR), study of associations between preterm birth rates in multiples and singletons and nonspontaneous labour using Spearman's rank correlation coefficient. Main outcome measures, Preterm birth rates, PAR, proportions of deliveries with nonspontaneous onset (caesarean sections before labour or induction of labour). Results, The proportion of multiple births before 37 weeks varied from 68.4% in Austria to 42.2% in the Republic of Ireland. In half of the countries, over 20% of all preterm births were attributable to multiple births. A strong association was found between the proportions of births before 37 weeks among multiple and singleton births (r= 0.81; P < 0.001). An association was observed between the rates of preterm birth and the proportions of deliveries with nonspontaneous onset among twins. Conclusions, Wide variations in rates of preterm births and deliveries with nonspontaneous onset were found between countries, suggesting marked differences in clinical practice which could have long-term implications for the health of children from multiple births. [source] | ||||||||||