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Biomedical subjects

E B Hook

Publications and source records attributed to E B Hook.

At least 55 records · Page 3Linked to original sources
PubMed1995

The natural history of Down syndrome conceptuses diagnosed prenatally that are not electively terminated.

The pregnancy outcomes on cases of Down syndrome diagnosed prenatally in which the mother did not elect termination were evaluated in data reported to a comprehensive Register of Down syndrome for England and Wales for 1989-94. In the 168 cases in which placental biopsy was not used, the overall rate of spontaneous loss was 35%, but this figure masks considerable heterogeneity by gestational stage at ascertainment. Data on ages at diagnostic procedure and on pregnancy termination enabled a more precise survival analysis. The loss rates were approximately 50% for those fetuses ascertained at 15-17 completed wk, 43% at 18 wk, 31% at 19 wk, 25% at 20 wk, and then a leveling off at approximately 20%-25% for fetuses ascertained at 21-28 completed wk. For fetuses ascertained prior to 18 wk, there was no evidence that maternal age was associated with fetal loss, consistent with earlier reports. At 18 wk and after, however, maternal age was on the average approximately 3 years greater in fetuses that were lost. Comparison of successive gestational birth cohorts provided no evidence in these 168 cases that the diagnostic procedure itself had any effect on loss or that selective ascertainment of mothers in risk of loss had any effect on the results. In contrast, in the 21 cases in which placental biopsy had been undertaken, the overall loss rates were not only higher when appropriate comparisons could be made, but there was some evidence for selective ascertainment and/or procedure-associated losses.(ABSTRACT TRUNCATED AT 250 WORDS)

Abortion, Spontaneous↗
PubMed1994

The imprecision in rates of Down syndrome by 1-year maternal age intervals: a critical analysis of rates used in biochemical screening.

Current algorithms to determine eligibility for prenatal cytogenetic diagnostic services depend critically on the accuracy and precision of the underlying rates of cytogenetic abnormality used in the calculations. We examine the maternal age-specific rates of Down syndrome livebirths in eight studies of European-origin populations, pooled rates from which are widely used for baseline calculations in biochemical screening. These studies vary significantly in such factors as methods of ascertainment of cases, likelihood of complete ascertainment, and methods of correction, if any, for underascertainment. Restriction of analysis to those two studies among the eight whose methods suggest the greatest likelihood of complete ascertainment for Down syndrome generates rates significantly higher than those in widespread use. Confidence intervals about previously reported and currently derived rates indicate that even with large-scale data, there is considerable residual uncertainty in derived rates.

Adolescent↗
PubMed1994

Cardiovascular birth defects and prenatal exposure to female sex hormones: a reevaluation of data reanalysis from a large prospective study.

In data of the U.S. Collaborative Perinatal Study (CPS), the Drug Epidemiology Unit (DEU) reported a relative risk of about 2.3 between maternal female sex hormone exposure during months 1 to 4 of pregnancy and cardiovascular malformation in infants (Heinonen et al., '77a N. Engl. J. Med., 296:67-70). Wiseman and Dodds-Smith ('84, Teratology, 30:359-370) reexamined the original CPS data and found the DEU had made some errors in classification of exposure and disease. Also they challenged the classification of cases as "exposed" in those born to mothers who received the compounds outside the day 19 to 50 window of cardiovascular embryogenesis. Wiseman and Dodds-Smith stated that their reanalysis "clearly showed that there was [in the data used by the DEU] no statistically significant association between exposure in the critical organogenic period of pregnancy and cardiac malformation in offspring." They did not undertake any statistical analysis, but their reanalysis resulted in a wide-spread nonacceptance of the association reported by the DEU. The study reported here reclassified the cases of the original DEU study in accord with the implications of the Wiseman and Dodds-Smith reanalysis of exposure and disease. After this reclassification, an effect magnitude measure of association, the relative risk rose from 2.33 to 2.48 and remained nominally significant statistically at the .05 level. Thus, if anything, the quantitative consequences of the Wiseman and Dodds-Smith review of the data, when applied in an unbiased manner, result in an increase in the measure of effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMed1993

Effect of variation in probability of ascertainment by sources ("variable catchability") upon "capture-recapture" estimates of prevalence.

Capture-recapture methods in epidemiology analyze data from overlapping lists of cases from various sources of ascertainment to generate estimates of missing cases and the total affected. Applications of these methods usually recognize the possibility of, and attempt to adjust for, nonindependent ascertainment by the various sources used. However, separate from the issue of dependencies between sources is the complexity of within source variation in probability of ascertainment of cases, e.g., variation in ascertainment by population subgroups, such as socioeconomic classes, races, or other subdivisions. The authors present a general approach to this issue for the two-source case that takes account of not only biases that arise from such "variable catchability" within sources but also the separate complexity of dependencies between sources. A general formula, (K - delta)/(K + delta), is derived that allows simultaneous calculation of the effects of variable catchability, delta, and source dependencies, delta, upon the accuracy of the two-source estimate. The effect of variable catchability upon accuracy and applications to data by race on the neurodegenerative disorder, Huntington's disease, are presented. In the latter analysis, multiple different two-source estimates of prevalence were made, considering each source versus all others pooled. Most of the likely bias was found to be due to source dependencies; variable catchability contributed relatively little bias. Multiple poolings of all but one source may prove a generally efficient method for overcoming the problem of likely variable catchability, at least when there are data from many distinct sources.

Bias↗
PubMed1993

Representative and misrepresentative associations of birth defects in livebirths. Conditions under which relative risks greater than unity in livebirths necessarily imply relative risks greater than unity in all conceptuses.

One may express the relative risk of defect in all conceptuses, r(def), as a function of the relative risk of defect in livebirths, r(def,lb), and in embryonic and fetal deaths, r(def,efd), as r(def) = C(lb)r(def,lb) + C(efd)r(def,efd), where C(lb) and C(efd) are coefficients defined in terms of conceptus and defect viability and lethality. If the relative risk of birth defect in livebirths, r(def,lb), is greater than unity, but the relative risk of defect in all conceptuses, r(def), is equal to or less than unity (or the reverse pattern holds), then the relative risk of defects in livebirths may be said to be "distorting" or "misrepresentative" because it does not reflect the nature of the association in all conceptuses. The authors define and present an explicit expression for a boundary upon the relative risk of defect in livebirths. If the relative risk of defect in livebirths is (validly) greater than this boundary value, then the relative risk in all conceptuses must be greater than unity and the observed relative risk of defect in births is "representative" and not distorting. The authors show that the boundary value is equal to 1/C(lb), where C(lb) is a simple function of the lethality of all unexposed conceptuses, the lethality of unexposed conceptuses with defect, and the relative risk of any embryonic and fetal death. Tables of the boundary relative risk for various values of these variables are presented. Over a very wide range of reference variables, a (valid) relative risk of defect in livebirths of 3.5 or greater implies a positive association with defect in all (recognized) conceptuses in the population studied.

Congenital Abnormalities↗
PubMed1993

Relation of the crude relative risk of a disorder to relative risks in strata of a "susceptible" variable.

If tau d is the relative risk of a disorder in the entire population, and tau d,i is the relative risk of the disorder in i = 1, ... m strata, then one may show readily that tau d = sigma ci tau d,i, where ci is the product of two terms tau i, the risk ratio of being in the ith stratum, and pi,unexp d, the proportion of those with the disorder and unexposed who are in the ith stratum. This formulation is of primary interest in epidemiology when relative risks are available on one or only some strata of a variable that itself may be affected by exposure (what one may define as a "susceptible" covariate) such as mortality or hospitalization. Although relative risks within strata of such a variable may be of some intrinsic clinical interest, only the risk ratio unstratified on such a variate may be pertinent to a causal effect (unlike the case for nonsusceptible variables such as sex, age, etc). In some instances, as for birth defects, one may have data from a few strata or only one (for example, livebirths) of a susceptible covariate (for example, conceptus viability). But one may still be able to draw useful inferences about tau d, the risk ratio in the entire population, because if tau d,i > or = 1/ci (or k/ci), one may conclude that tau d is, at least, greater than 1.0 (or k). Similarly, a study of a disorder limited to hospitalized cases and controls may enable investigators to infer, using the same criterion, a positive association in the entire population despite the presence of hospitalization bias of the type described by Berkson.

Abortion, Spontaneous↗
PubMed1993

Alpha-fetoprotein: a biomarker for pregnancy outcome.

Beginning in 1977, numerous studies have reported an association between high levels of maternal serum alpha-fetoprotein, measured in early pregnancy, and low birthweight and perinatal death. It has been suggested, however, that these findings may be explained by bias. We reviewed 21 studies and found that they were unanimous in reporting this association and that the association cannot be explained by any of the proposed biases. Comparing women whose alpha-fetoprotein levels were 2.5 times the median or more with all other women, the highest relative risk of fetal death was 21.0, with a 95% confidence interval of 8.4-52.2, and the lowest relative risk of fetal death was 4.4, with a 95% confidence interval of 2.8-7.0. For low birthweight (< 2,500 grams), the highest relative risk was 6.4 (95% confidence interval = 3.1-13.1) and the lowest relative risk was 1.9 (95% confidence interval = 1.5-2.5).

Biomarkers↗