Eclamptic deaths and Baptists.
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Biomedical subjects
Publications and source records attributed to L C Chesley.
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Several reports suggested using the mean arterial blood pressure during the second trimester to predict the future development of preeclampsia. The value of a second-trimester mean arterial blood pressure greater than or equal to 90 mm Hg was reviewed in 39,876 reported cases of preeclampsia and 207 cases of eclampsia. The sensitivity ranged from 0% to 92% and the specificity varied from 53% to 97%. The predictive value of a positive test ranged from 0% to 43% and the predictive value of a negative test ranged from 76% to 98%. The predictive value of a positive test was not greatly higher than the incidence of hypertension in the whole population studied in the majority of the reports. There was a strong association of higher second-trimester mean arterial blood pressure in nulliparous women with eclampsia who had transient hypertension in later gestations and ultimately developed chronic hypertension. The data suggest that one sign of future chronic hypertension, that is, transient hypertension, is often predicted by high second-trimester mean arterial blood pressure, which may have the same significance. We think that if increased second-trimester mean arterial blood pressure levels predict anything, it is transient hypertension rather than preeclampsia-eclampsia.
An analysis has been made of 48 pedigrees selected (ascertained) through an affected mother in the first generation. These pedigrees mainly involve cases of eclampsia which occurred before its recent decline in incidence. The data confirm the genetic determination of susceptibility indicated by published data on eclampsia/preeclampsia. There is a suggestion that the fetal genotype can contribute to susceptibility to eclampsia in its mother, in contrast to previous findings that susceptibility to pre-eclampsia is controlled solely by the maternal genotype. An association between eclampsia and miscarriage is shown in the data. We argue that this suggests that the primary mode of action of the gene(s) involved is to affect the interaction between uterine and placental tissue.
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The purpose of this report was to investigate the potential usefulness of average mean arterial pressure, maximal mean arterial pressure, and maximal diastolic pressure during the second trimester in predicting the development of eclampsia in 207 nulliparas and 20 multiparas with eclampsia. In the nulliparas, both the mean arterial pressure and the maximal mean arterial pressure during the second trimester were greater than or equal to 90 mm Hg in 22% and 34% of the patients, respectively. For the multiparas, the percentages with greater than or equal to 90 mm Hg were 30% and 35%, respectively. Only 8.7% of nulliparas with eclampsia had a maximal diastolic pressure during the second trimester greater than or equal to 80 mm Hg and no patient had a diastolic pressure of greater than or equal to 90 mm Hg. A review of the literature suggests that the mean arterial pressure observed during the second trimester has poor predictive value for future development of preeclampsia-eclampsia. We conclude that there is no correlation between second-trimester blood pressure recordings and subsequent eclampsia.
Our report concerns the incidences of pre-eclampsia and eclampsia in 147 sisters, 248 daughters, 74 granddaughters, and 131 daughters-in-law of women who have had eclampsia. The disorder is highly heritable. We have analysed the data in two ways, firstly, as a single gene condition and, secondly, as a multifactorial condition. The observed incidences fit closely with the single gene model with frequency of the putative gene being 0.25. When Falconer's method of estimating heritabilities of discrete characters is used, estimates of 120% (sisters), 88% (daughters), and 105% (granddaughters)--none significantly different from 100%-are obtained. Insofar as possible, our definition of pre-eclampsia corresponds with EPH in the descriptive classification of the Organisation Gestosis and to 'severe pre-eclampsia' in Nelson's classification. The women were delivered in many different hospitals, however, and many records fail to provide all of the essential information.
For the purpose of clinical management, any woman with an acute rise in blood pressure in the latter half of pregnancy must be regarded as having preeclampsia with the possibility of progression to eclampsia. Unfortunately, such diagnoses have been accepted uncritically in the selection of cases for clinical and laboratory studies of preeclampsia, with inevitably erroneous and contradictory conclusions about the disorder. The diagnosis of mild preeclampsia may be correct in roughly one-half of cases, but others may be latent or frank essential hypertension or any of a variety of renal diseases. In selecting cases for research, the diagnostic errors can be greatly reduced by the exclusion of all multiparas and all primigravidas without abundant proteinuria. The primigravidas should have a reliable history of normality or follow-up studies proving it, be aged 25 or less, and have hyperuricemia. The selection of cases for the study of preeclampsia demands far more rigid criteria for diagnosis than does the diagnosis for clinical management.
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The relation between bodily build and susceptibility to eclampsia has been controversial for nearly two centuries and the issue has been confused by modern studies of women with nonconvulsive hypertensive disorders in whom the diagnosis of preeclampsia is frequently erroneous. The present study is based upon 193 previously nulliparous and 49 multiparous eclamptic women. Sixty-three of the previously nulliparous women were compared with normal controls matched for age, race, parity, clinic, nonclinic, or private status, and as closely as possible with the time of delivery. Eclampsia spares no habitus, but has a slight predilection for underweight women.
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All of 134 women classified as having "functionally severe" rheumatic cardiac disease and surviving pregnancies in 1931 through 1943 have been traced to 1975. Ninety-three percent have died at the exponential rate of 6.3% per year. The women with and without pregnancies following admittance to the series were similar in respect to age at entry, ages in which they lived, and proportionate representation in all but one of five subgroups with extraordinarily high death rates in the first five years of follow-up. Analyses of the data by life tables, average annual death rates, lengths of survival, and average ages at death failed to uncover any evidence for a delayed adverse effect of pregnancy in the whole series or in any of the subgroups. Provided that the patient survives the gestation, the life expectancy is not shortened by pregnancy.
The clinical diagnosis of preeclampsia is often erroneous, for it may be confused with latent hypertension, acute or chronic renal disease, or frank essential hypertension that had abated during much of pregnancy. Eclampsia and "true" preeclampsia run in families with a frequency suggesting that a single recessive gene may be responsible. Eclampsia and "true" preeclampsia do not cause chronic hypertension, whatever their durations. Gestational hypertension is merely hypertension without proteinuria or abnormal edema. It often has been the basis for the diagnosis of mild preeclampsia, although renal biopsy samples almost never show the characteristic lesion in the absence of proteinuria. Gestational hypertension is often a sign of latent hypertension unmasked by pregnancy. Women with gestational hypertension ultimately have a high prevalence of chronic hypertension, whereas all those whose pregnancies are normotensive ultimately have a low prevalence.
The diagnosis of preeclampsia is often erroneous in primigravidas and usually so in multiparas. Gestational hypertension, defined as acute hypertension without proteinuria or abnormal edema, is often misdiagnosed as mild preeclampsia. Several follow-up studies are cited as evidence for the conclusions that (1) eclampsia and "true" preeclampsia seldom if ever cause chronic hypertension in women who otherwise never would have developed it; (2) gestational hypertension often is a sign of latent essential hypertension unmasked by pregnancy, and as such it often portends later chronic hypertension; and (3) normotensive pregnancies indicate a low prevalence of later chronic hypertension, and if it does develop, it usually does so at an age later than the average time of onset.
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