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Peter von Dadelszen

Bio: Peter von Dadelszen is an academic researcher from King's College London. The author has contributed to research in topics: Pregnancy & Medicine. The author has an hindex of 54, co-authored 329 publications receiving 11617 citations. Previous affiliations of Peter von Dadelszen include Family Research Institute & University of Toronto.


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Journal ArticleDOI
TL;DR: A first step would be to subdivide preeclampsia into early‐onset disease (< 34 + 0 weeks') and late onset disease (> 34 +0 weeks').
Abstract: Preeclampsia is a heterogeneous disorder, and as with other diseases (e.g., type I and type II diabetes), progress in the understanding of this disorder would be assisted greatly if subtypes could be characterized. We suggest that a first step would be to subdivide preeclampsia into early‐onset disease ( 34 + 0 weeks').

700 citations

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TL;DR: This guideline summarizes the quality of the evidence to date and provides a reasonable approach to the diagnosis, evaluation, and treatment of the hypertensive disorders of pregnancy (HDP).
Abstract: Objective: This guideline summarizes the quality of the evidence to date and provides a reasonable approach to the diagnosis, evaluation, and treatment of the hypertensive disorders of pregnancy (HDP). Evidence: The literature reviewed included the original HDP guidelines and their reference lists and an update from 1995. Using key words, Medline was searched for literature published between 1995 and 2007. Articles were restricted to those published in French or English. Recommendations were evaluated using the criteria of the Canadian Task Force on Preventive Health Care (Table 1).

564 citations

Journal ArticleDOI
TL;DR: The quest to effectively predict PE in the first trimester of pregnancy is fueled by the desire to identify women who are at high risk of developing PE, so that necessary measures can be initiated early enough to improve placentation and thus prevent or at least reduce the frequency of its occurrence.

475 citations

Journal ArticleDOI
TL;DR: It is found that less-tight control was associated with a significantly higher frequency of severe maternal hypertension, although no significant between-group differences in the risk of pregnancy loss, high-level neonatal care, or overall maternal complications are found.
Abstract: BACKGROUND The effects of less-tight versus tight control of hypertension on pregnancy complications are unclear METHODS We performed an open, international, multicenter trial involving women at 14 weeks 0 days to 33 weeks 6 days of gestation who had nonproteinuric preexisting or gestational hypertension, office diastolic blood pressure of 90 to 105 mm Hg (or 85 to 105 mm Hg if the woman was taking antihypertensive medications), and a live fetus Women were randomly assigned to less-tight control (target diastolic blood pressure, 100 mm Hg) or tight control (target diastolic blood pressure, 85 mm Hg) The composite primary outcome was pregnancy loss or high-level neonatal care for more than 48 hours during the first 28 postnatal days The secondary outcome was serious maternal complications occurring up to 6 weeks post partum or until hospital discharge, whichever was later RESULTS Included in the analysis were 987 women; 746% had preexisting hypertension The primary-outcome rates were similar among 493 women assigned to less-tight control and 488 women assigned to tight control (314% and 307%, respectively; adjusted odds ratio, 102; 95% confidence interval [CI], 077 to 135), as were the rates of serious maternal complications (37% and 20%, respectively; adjusted odds ratio, 174; 95% CI, 079 to 384), despite a mean diastolic blood pressure that was higher in the less-tight-control group by 46 mm Hg (95% CI, 37 to 54) Severe hypertension (≥160/110 mm Hg) developed in 406% of the women in the less-tight-control group and 275% of the women in the tight-control group (P<0001) CONCLUSIONS We found no significant between-group differences in the risk of pregnancy loss, high-level neonatal care, or overall maternal complications, although less-tight control was associated with a significantly higher frequency of severe maternal hypertension (Funded by the Canadian Institutes of Health Research; CHIPS Current Controlled Trials number, ISRCTN71416914; ClinicalTrialsgov number, NCT01192412) abstr act

420 citations


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01 Mar 2007
TL;DR: An initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI is described.
Abstract: Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

5,467 citations

Journal ArticleDOI
TL;DR: Since 1980, the American College of Cardiology and American Heart Association have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health.
Abstract: Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health. In 2013, the National Heart, Lung, and Blood Institute (NHLBI) Advisory

4,604 citations

Journal ArticleDOI
TL;DR: It is proposed that DNA methylation age measures the cumulative effect of an epigenetic maintenance system, and can be used to address a host of questions in developmental biology, cancer and aging research.
Abstract: It is not yet known whether DNA methylation levels can be used to accurately predict age across a broad spectrum of human tissues and cell types, nor whether the resulting age prediction is a biologically meaningful measure. I developed a multi-tissue predictor of age that allows one to estimate the DNA methylation age of most tissues and cell types. The predictor, which is freely available, was developed using 8,000 samples from 82 Illumina DNA methylation array datasets, encompassing 51 healthy tissues and cell types. I found that DNA methylation age has the following properties: first, it is close to zero for embryonic and induced pluripotent stem cells; second, it correlates with cell passage number; third, it gives rise to a highly heritable measure of age acceleration; and, fourth, it is applicable to chimpanzee tissues. Analysis of 6,000 cancer samples from 32 datasets showed that all of the considered 20 cancer types exhibit significant age acceleration, with an average of 36 years. Low age-acceleration of cancer tissue is associated with a high number of somatic mutations and TP53 mutations, while mutations in steroid receptors greatly accelerate DNA methylation age in breast cancer. Finally, I characterize the 353 CpG sites that together form an aging clock in terms of chromatin states and tissue variance. I propose that DNA methylation age measures the cumulative effect of an epigenetic maintenance system. This novel epigenetic clock can be used to address a host of questions in developmental biology, cancer and aging research.

4,233 citations