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Nicholas J Wald

Publications and source records attributed to Nicholas J Wald.

29 records · Page 2Linked to original sources
PubMed2003

Antenatal screening for Down's syndrome with the quadruple test.

Second trimester screening for Down's syndrome is widely practised throughout the world. We assessed the performance of antenatal serum screening for Down's syndrome with the quadruple test in 46193 pregnancies from 14 hospitals over 5 years. Women who screened positive (risk > or =1 in 300) were offered diagnostic amniocentesis or chorionic villus sampling. Of 88 observed Down's syndrome pregnancies, 71 (81%) had a positive screening result (81% detection rate, 95% CI 72-89), and of 46105 unaffected pregnancies, 3200 tested positive (7% false-positive rate). These results show that the quadruple test is a better method of screening for Down's syndrome than use of maternal age alone (51% detection rate, 14% false-positive rate) and is more effective than other second trimester screening tests. Therefore, we conclude that the quadruple test should be the test of choice in second trimester screening for Down's syndrome.

Down Syndrome↗
PubMed2003

Combining nuchal translucency and serum markers in prenatal screening for Down syndrome in twin pregnancies.

A method is described to combine the ultrasound marker nuchal translucency (NT) with serum markers so that they can be used together in prenatal screening for Down syndrome in twin pregnancies. For monochorionic twin pregnancies (taken as monozygous), the two fetus-specific NT measurements are averaged before risk is calculated and before the contribution of the serum markers is incorporated. For dichorionic twin pregnancies (taken as dizygous), the risk for each fetus based on the individual NT measurements is calculated, the two fetus-specific risks are added together, and then the contribution of the serum markers is incorporated. In this way, all the screening markers can be used in combination to produce a pregnancy-specific "pseudo-risk", rather than a fetus-specific pseudo-risk. We refer to pseudo-risk because in the absence of sufficient data on the screening markers in affected twin pregnancies, a true risk estimate cannot be calculated. Tentative estimates are given of screening performance in twins using NT, the combined test (NT with first-trimester serum markers), and the integrated test (NT with first- and second-trimester serum markers), all interpreted with maternal age.

Biomarkers↗
PubMed2002

The underlying risk of death after myocardial infarction in the absence of treatment.

BACKGROUND: The underlying risk of death in the absence of treatment after a myocardial infarction (MI) is poorly documented. METHODS: Analysis of 23 published studies in which 14 211 patients were followed prospectively after MI; 6817 deaths were recorded. We restricted the analysis to studies in which follow-up was completed by 1980 to quantify the underlying risk in the absence of effective treatments. RESULTS: After a first MI, on average, 23% of patients died before reaching the hospital and another 13% died during hospital admission; these rates increased with age. After hospital discharge cardiovascular mortality was approximately 10% in the first year and 5% per year thereafter, rates that were unrelated to age or sex. The yearly death rate of 5% persisted indefinitely; after 15 years, cumulative cardiovascular mortality was 70%. After a subsequent MI, 33% of patients died before reaching the hospital, and 20% died in hospital. After discharge, cardiovascular mortality was approximately 20% in the first year and 10% per year thereafter, rates again unrelated to age and sex. Approximately a third of all heart disease deaths occurred minutes after the first MI, a sixth during the first hospitalization, and half after a subsequent MI, which could occur many years after the first. CONCLUSIONS: In persons with a history of MI, cardiovascular mortality in the absence of treatment is high-5% per year after a first MI and 10% per year after a subsequent MI, persisting for many years and probably for the rest of a person's life. The high mortality rate emphasizes the need to ensure that everyone who has had an MI, even years previously, receives effective preventive treatment.

Cardiovascular Diseases↗
PubMed2002

Influence of maternal smoking on the birth prevalence of Down syndrome and on second trimester screening performance.

OBJECTIVES: To determine the influence of maternal smoking on the birth prevalence of Down syndrome and on second trimester screening performance. METHODS: First, a meta-analysis of cohort and case-control studies was performed to estimate the effect of maternal smoking on the live birth prevalence of Down syndrome. Then, data from 8779 women screened using the quadruple test (alphafetoprotein (AFP), unconjugated estriol (uE(3)), human chorionic gonadotrophin (free beta-hCG), and inhibin-A levels with maternal age) were used to determine the effect of smoking on the serum markers. A Monte Carlo simulation was used to assess the impact of adjusting for smoking status on screening performance. RESULTS: The relative risk of Down syndrome in smokers (versus non-smokers) was 0.95 (95% confidence interval (CI) 0.87 to 1.03). Serum marker levels were determined as multiples of the median for non-smokers of the same gestational age and adjusted for maternal weight (MoM). The MoM values for AFP were 5% higher (95% CI 2-7%), uE(3) 4% lower (95% CI 2-5%), free beta-hCG 20% lower (95% CI 17-23%) and inhibin-A 62% higher (95% CI 57-67%) in smokers compared with non-smokers. Adjusting marker levels for smoking resulted in less than a 1 percentage point increase in the detection rate for a 5% false positive rate with the double, triple or quadruple tests. CONCLUSIONS: There is no evidence of an association between the birth prevalence of Down syndrome and maternal smoking. The case for adjusting screening marker levels for smoking is not compelling. But if smoking data are collected routinely adjustment could be made and this would yield similar detection and false positive rates in smokers and non-smokers.

Biomarkers↗
PubMed2002

Endometrial thickness as a test for endometrial cancer in women with postmenopausal vaginal bleeding.

OBJECTIVE: To assess the value of endometrial thickness measurement as a test for endometrial cancer in postmenopausal women with vaginal bleeding (symptomatic women). DATA SOURCES: We conducted a literature search using the MEDLINE database from 1991 to 1997, and the key words "vaginal ultrasonography" and "endometrial thickness measurement." The review was limited to original research reports written in English, concerning symptomatic women having vaginal ultrasonography before a diagnostic test and not receiving tamoxifen. STUDY SELECTION: A total of 48 studies were identified. A questionnaire was sent to the corresponding author of each paper requesting supplementary information. Data were included in our analysis if the corresponding author was able to supply information on the median endometrial thickness in unaffected symptomatic women and the endometrial thickness values in affected women. Nine studies were thus included in our meta-analysis, representing 3483 women without endometrial cancer and 330 women with endometrial cancer. TABULATION, INTEGRATION, AND RESULTS: The median endometrial thickness in women with endometrial cancer was 3.7 times that in unaffected women at the same center, and with the same menopausal status and same hormone replacement therapy use category. The detection rate was 63% (95% confidence interval 58, 69) for a 10% false-positive rate, or 96% (95% confidence interval 94, 98) for a 50% false-positive rate. CONCLUSION: Endometrial thickness measurement in symptomatic women does not reduce the need for invasive diagnostic testing because 4% of the endometrial cancers would still be missed with a false-positive rate as high as 50%.

Endometrial Neoplasms↗
PubMedDate not supplied

Environmental tobacco smoke and ischemic heart disease.

Cohort and case control studies show a 30% excess risk of ischemic heart disease in nonsmokers whose spouses smoke compared with that in nonsmokers whose spouses do not smoke. There is a nonlinear dose-response; the excess risk from actively smoking 20 cigarettes/day is only 80%. Large cohort studies of active smoking support the nonliner dose-response (the excess risk in smokers of 5 cigarettes/day is about 50%). Animal studies show a pronounced vascular effect of environmental tobacco smoke. In experimental studies passive and active smoking have similar effects on platelet aggregation. The collective evidence supports a significant effect of low dose tobacco smoke exposure in causing ischaemic heart disease.

Animals↗