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Sökning: WFRF:(Richiardi Lorenzo)

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11.
  • Richiardi, Lorenzo (författare)
  • New evidence on germ-cell testicular cancer aetiology
  • 2004
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Testicular cancer has been increasing in incidence for at least 50 years in many populations, but its etiology remains elusive. We investigated several prenatal and postnatal factors in association with germ-cell testicular cancer risk. Moreover, we evaluated recent trends in testicular cancer incidence in Northern European countries. Using data from birth records and from the Swedish Cancer Register, we carried out a casecontrol study of 628 cases and 2,309 controls. We aimed at investigating the association between perinatal characteristics and testicular cancer, and assessing potential etiological heterogeneity between seminomas and nonseminomas, the two major histological groups of testicular cancer. Gestational duration was inversely associated with testicular cancer risk, whereas men with both high and low birth weight had an excess risk, indicating that intrauterine environment affects the risk of testicular cancer. Seminomas and nonseminomas seemed to have similar risk patterns. Data from the first study were linked to the Swedish Military Service Conscription Register, which contains information on a medical examination that is mandatory in Sweden for the purpose of military service. The linkage permitted us to get information on body size at two different points in life on 371 cases and 1,238 controls. We found that height at eighteen years old is directly associated with testicular cancer risk. The association persisted after adjusting for perinatal characteristics, suggesting that both foetal life and later periods in life, such as childhood and adolescence, are important time windows for determining lifetime risk for testicular cancer. A case-control study, including 3,051 cases and 9,007 controls born in Sweden after 1940, was carried out using data from the Multi-Generation Register and the Swedish Cancer Register. We obtained information on number and gender of first-degree relatives of all study subjects. We found that both low birth order and having few siblings is associated with an increased risk of testicular cancer. Since sibship size is correlated with birth order, we performed stratified analyses to disentangle between the effects of the two variables, and found that sibship size is a more important factor. We interpret that these findings are explained by an association between parental fertility and risk of testicular cancer in the offspring. Data from the Multi -Generation Register and the Cancer Register were also used to investigate the fertility status before and after diagnosis of testicular cancer. Fecundity and the likelihood of fathering dizygotic twins, which is decreased among subfertile subjects, were used as independent measures of fertility of 4,592 cases and 12,154 controls, born in Sweden in 1916 onwards. Prior to diagnosis cases had a decreased number of children, with a lower frequency of dizygotic twinning, indicating that testicular cancer patients have an increased frequency of fertility problems before diagnosis. After diagnosis cases fathered twins more often than controls, probably reflecting an increased use of assisted reproduction techniques. Finally, the occurrence patterns of testicular cancer in eight Northern European countries were evaluated using data from national Cancer Registries, We found that the incidence of seminomas and nonseminomas is still increasing in all countries analyzed, with the possible exception of Denmark. Moreover, we found that, in Scandinavian countries, the increasing trend is a birth cohort phenomenon also in recent cohorts.
12.
  • Sonnenschein-van der Voort, Agnes M. M, et al. (författare)
  • Preterm birth, infant weight gain, and childhood asthma risk: A meta-analysis of 147,000 European children
  • 2014
  • Ingår i: Journal of Allergy and Clinical Immunology. - Elsevier. - 0091-6749. ; 133:5, s. 1317-1329
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Preterm birth, low birth weight, and infant catch-up growth seem associated with an increased risk of respiratory diseases in later life, but individual studies showed conflicting results. Objectives: We performed an individual participant data meta-analysis for 147,252 children of 31 birth cohort studies to determine the associations of birth and infant growth characteristics with the risks of preschool wheezing (1-4 years) and school-age asthma (5-10 years). Methods: First, we performed an adjusted 1-stage random-effect meta-analysis to assess the combined associations of gestational age, birth weight, and infant weight gain with childhood asthma. Second, we performed an adjusted 2-stage random-effect meta-analysis to assess the associations of preterm birth (gestational age less than 37 weeks) and low birth weight (less than 2500 g) with childhood asthma outcomes. Results: Younger gestational age at birth and higher infant weight gain were independently associated with higher risks of preschool wheezing and school-age asthma (P less than. 05). The inverse associations of birth weight with childhood asthma were explained by gestational age at birth. Compared with term-born children with normal infant weight gain, we observed the highest risks of school-age asthma in children born preterm with high infant weight gain (odds ratio [OR], 4.47; 95% CI, 2.58-7.76). Preterm birth was positively associated with an increased risk of preschool wheezing (pooled odds ratio [pOR], 1.34; 95% CI, 1.25-1.43) and school-age asthma (pOR, 1.40; 95% CI, 1.18-1.67) independent of birth weight. Weaker effect estimates were observed for the associations of low birth weight adjusted for gestational age at birth with preschool wheezing (pOR, 1.10; 95% CI, 1.00-1.21) and school-age asthma (pOR, 1.13; 95% CI, 1.01-1.27). Conclusion: Younger gestational age at birth and higher infant weight gain were associated with childhood asthma outcomes. The associations of lower birth weight with childhood asthma were largely explained by gestational age at birth.
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13.
  • Stemann Larsen, Pernille, et al. (författare)
  • Pregnancy and Birth Cohort Resources in Europe: a Large Opportunity for Aetiological Child Health Research
  • 2013
  • Ingår i: Paediatric and Perinatal Epidemiology. - Wiley-Blackwell. - 0269-5022. ; 27:4, s. 393-414
  • Forskningsöversikt (övrigt vetenskapligt)abstract
    • Background During the past 25 years, many pregnancy and birth cohorts have been established. Each cohort provides unique opportunities for examining associations of early-life exposures with child development and health. However, to fully exploit the large amount of available resources and to facilitate cross-cohort collaboration, it is necessary to have accessible information on each cohort and its individual characteristics. The aim of this work was to provide an overview of European pregnancy and birth cohorts registered in a freely accessible database located at http://www.birthcohorts.net. Methods European pregnancy and birth cohorts initiated in 1980 or later with at least 300 mother-child pairs enrolled during pregnancy or at birth, and with postnatal data, were eligible for inclusion. Eligible cohorts were invited to provide information on the data and biological samples collected, as well as the timing of data collection. Results In total, 70 cohorts were identified. Of these, 56 fulfilled the inclusion criteria encompassing a total of more than 500000 live-born European children. The cohorts represented 19 countries with the majority of cohorts located in Northern and Western Europe. Some cohorts were general with multiple aims, whilst others focused on specific health or exposure-related research questions. Conclusion This work demonstrates a great potential for cross-cohort collaboration addressing important aspects of child health. The web site, http://www.birthcohorts.net, proved to be a useful tool for accessing information on European pregnancy and birth cohorts and their characteristics.
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14.
  • Zugna, Daniela, et al. (författare)
  • Mortality Rate in Children Born to Mothers and Fathers With Celiac Disease : A Nationwide Cohort Study
  • 2013
  • Ingår i: American Journal of Epidemiology. - Oxford University Press. - 0002-9262. ; 177:12, s. 1348-1355
  • Tidskriftsartikel (refereegranskat)abstract
    • Celiac disease (CD) is associated with increased mortality rate and adverse pregnancy outcome, but little is known about offspring mortality rate. In this nationwide retrospective cohort study, we identified persons whose biopsy-verified CD was diagnosed in Sweden in 19692008. We compared mortality rates in children born to mothers with and without CD (n 16,121 vs. n 61,782) and children born to fathers with and without CD (n 9,289 vs. n 32,984). Median age of offspring at end of follow-up was 28.7 (range, 16.739.7) years. We also examined mortality rates in children born to mothers with undiagnosed CD (later CD diagnosis; n 12,919) and diagnosed CD (n 3,202) to determine if intrauterine exposures associated with CD could affect offspring mortality rate. We estimated hazard ratios for death by using Cox regression. Death rates were independent of maternal CD (60 deaths per 100,000 person-years in children of mothers with CD, vs. 54 in controls) and paternal CD (53 deaths per 100,000 person-years in children of fathers with CD, vs. 53 in controls). Corresponding adjusted hazard ratios were 1.09 (95 confidence interval: 0.95, 1.26) for maternal CD and 1.02 (95 confidence interval: 0.85, 1.23) for paternal CD. Death rates were similar in children born to mothers with undiagnosed CD and in children whose mothers had diagnosed CD during pregnancy. Parental CD does not seem to influence mortality rate in offspring, which suggests that neither genetic influences of CD nor intrauterine conditions have adverse effects on offspring mortality rate.
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15.
  • Zugna, Daniela, et al. (författare)
  • Risk of Congenital Malformations Among Offspring of Mothers and Fathers With Celiac Disease : A Nationwide Cohort Study
  • 2014
  • Ingår i: Clinical Gastroenterology and Hepatology. - Elsevier. - 1542-3565. ; 12:7, s. 1108-
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND & AIMS: Many patients with celiac disease experience malabsorption, weight loss, and anemia; undiagnosed celiac disease during pregnancy has been linked with adverse outcomes. Studies of celiac disease and congenital malformations in offspring have been underpowered. We investigated the risk of congenital malformations among the offspring of parents with celiac disease. METHODS: We performed a nationwide cohort study of data from linked health care registers in Sweden from 1973 through 2009. We collected histopathology data from 28 pathology departments in Sweden to identify individuals with celiac disease (based on the presence of villous atrophy). We estimated the risks of malformations in the offspring of mothers and fathers with and without celiac disease. Logistic regression was used to estimate adjusted prevalence odds ratios (aPORs) with 95% confidence intervals (CIs). RESULTS: Among 11,382 offspring of mothers with celiac disease, there were 672 cases (5.9%) of malformation compared with 2098 cases (5.1%) among 40,922 offspring of mothers without celiac disease. Similarly, 352 (5.9%) of 6002 offspring of fathers with celiac disease and 1009 (5.1%) of 19,600 offspring of fathers without celiac disease had a malformation. In adjusted analyses, the offspring of mothers or fathers with celiac disease had a slightly increased risk of having children with malformations (for those with mothers with celiac disease: aPOR, 1.15; 95% CI, 1.05-1.26; for those with fathers with celiac disease: aPOR, 1.14; 95% CI, 1.00-1.29). However, these excess risks decreased or vanished entirely when we restricted our data to births since 2000 (for those with mothers with celiac disease: aPOR, 1.11; and 95% CI, 0.79-1.56; for those with fathers with celiac disease: aPOR, 1.01; 95% CI, 0.81-1.26). CONCLUSIONS: In a nationwide study, we found an increased risk for malformation among the offspring of mothers or fathers with celiac disease. However, the excess risk is small; the upper limits of the CIs for malformation indicate a 29% maximum relative increase.
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