Biomedical subjects
C W Redman
Publications and source records attributed to C W Redman.
Therapy of non-preeclamptic hypertension in pregnancy.
The poor perinatal outcome of pregnant women with chronic hypertension depends on their increased susceptibility to superimposed preeclampsia. There is no direct evidence that this is mediated by hypertension and reduced by antihypertensive treatment. In particular, the arterial lesions of the uteroplacental circulation in preeclampsia also occur in normotensive individuals and would be unusual types of pressure-induced injury. Thus, there is no compelling reason for treating hypertension below a threshold (170/110 mm Hg) above which maternal safety becomes the main concern.
Hypertension in pregnancy: a case discussion.
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Pre-eclampsia in a women with homozygous PiZZ alpha-1 antitrypsin deficiency. Case report.
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Low human fetal heart rate variation in normal pregnancy.
The fetal heart rates of 340 normal singleton pregnancies at 30-33 weeks gestation were screened using a microprocessor system on-line. Eleven fetuses (3.2%) with a heart rate variation less than the 5th centile were identified, of whom 10 were studied longitudinally. At 30-33 weeks the mean minute range of pulse intervals (a measure of fetal heart rate variation) was 31.4 (SE 1.5) ms compared with 51.0 (SE 3.4) ms in a randomly selected control group. The study group continued to have significantly lower fetal heart rate variation than controls on each of three subsequent occasions until delivery. There were no significant differences between the two groups in fetal outcome, which was good. This demonstrates that a small proportion of normal fetuses have consistently low heart rate variation, and helps to define the lower limit of the normal distribution of fetal heart rate variation. After delivery, there were no significant differences between heart rate or its variation between the two groups. We conclude that the lower prenatal heart rate variation in the study group was a consequence of the uterine environment.
Influence of elective preterm delivery on birthweight and head circumference standards.
We calculated new birthweight and head circumference centiles for boys and girls between 24 and 42 weeks' gestation from 20,713 singleton live births at our hospital between 1978 and 1984. Among the 803 babies born at or before 34 weeks' gestation, 28% were delivered electively for fetal problems; they were considerably lighter than babies born after spontaneous preterm labour. In contrast, they showed only a small deficit in head circumference, possibly due to a brain sparing effect in growth retarded infants. Electively delivered preterm infants cause a bias in birthweight and head circumference centiles and we recommend that these babies should be excluded when these centiles are calculated.
Caesarean section dissected, 1978-1983.
Of 32735 singleton births in Oxford in the 6 years 1978-1983, 10% were by caesarean section. In contrast to the national data, no trend in this rate was observed. Repeat caesarean sections accounted for 30% of all sections and the proportion of women who had had a previous caesarean section rose gradually in the hospital population. The other main indications for section were dystocia, fetal distress in labour and breech presentation, which together accounted for a further 45% of all sections. Comparison with caesarean section rates reported from North America shows that repeat sections and sections for dystocia were less frequent in Oxford but the rates for other indications were similar. Dystocia is likely to be a key factor in determining future section rates. Dystocia occurred mainly in primiparae, and was more common with short stature and with increasing gestation and maternal age. For all height, age and gestation groups dystocia was more than twice as frequent in induced as in non-induced labour. This association does not imply a causal relationship, but neither is one excluded.
Urinary albumin excretion in pregnancy.
Urinary albumin excretion during pregnancy has been studied using a sensitive radioimmunoassay. One hundred pregnant women attending a high-risk antenatal clinic and 14 normal pregnant women were investigated serially, during pregnancy and post-partum. The normal subjects showed a small but significant rise in albumin excretion in the third trimester, which was sustained pre-delivery and in the first postnatal week. Twenty-six women were classified as having mild pre-eclampsia and 44 as having chronic hypertension without evidence of superimposed pre-eclampsia. In neither group was there evidence of proteinuria by conventional testing, nor was the median albumin excretion different from normal antenatally; in the first week after delivery a significant increase was observed, but this regressed to normal 6 weeks later. Eight patients developed severe pre-eclampsia, of whom one had evidence of underlying renal disease. Three presented with proteinuria already established. In the remaining five patients, the shift from normal to high albumin excretion occurred rapidly, usually preceded by a rise in uric acid and a decrease in the platelet count. These data suggest that proteinuric pre-eclampsia, as defined by relatively insensitive routine laboratory measurement, is not preceded by a phase of increasing albumin loss which can be detected by more sensitive assays.
Complement activation, circulating protease inhibitors and pregnancy-associated proteins in severe pre-eclampsia.
Circulating protease inhibitors, pregnancy-associated proteins and the split product of complement factor 3 (C3d) were measured in 14 women with severe pre-eclampsia and their matched controls. Only the mean levels of antithrombin III were observed to be significantly lower in pre-eclampsia (P less than 0.02).
Cells bearing class II MHC antigens in the human placenta and amniochorion.
Immunohistological techniques have been used to study the stromal cells of the human placenta in both the chorionic villous mesenchyme and the connective tissue underlying the amnion. Throughout gestation many of these cells express an antigen (3C10) that is found on mononuclear phagocytes but not on dendritic cells or epidermal Langerhans cells. In the first and second trimesters the placental cells also react with a monoclonal antibody (NA1/34) to the human thymocyte antigen (CD1), a lymphocyte differentiation antigen expressed by cortical thymocytes and Langerhans cells; expression of this antigen diminishes as gestation advances. In contrast, an antibody to a different epitope of CD1 (OKT6) does not bind. Class II MHC antigens are not present in the first trimester but are acquired by increasing numbers of placental macrophages from the second trimester onwards. It is possible that the placenta has significant immune functions and that, by term, placental macrophages may be capable of antigen presentation.
Immunology of the placenta.
The central issues of the immunology of the placenta are poorly defined. As an allograft its success almost certainly depends on the absence of transplantation antigens from syncytiotrophoblast. The placenta is an imperfect immune barrier between mother and fetus. Rhesus isoimmunization is one well-known consequence but maternal graft-versus-host disease is another, although much rarer. The placenta performs an important function by transferring maternal IgG to the fetus and filters out potentially harmful cytotoxic antibodies. However, autoantibodies may, in rare circumstances, cause passively acquired fetal autoimmune disease. Direct maternal immune attack on the placenta is not a clear pathological entity but may occur with placental villitis and pemphigoid gestationis; and may contribute to recurrent abortion of unknown aetiology or to pre-eclampsia.
Immunological disorders of human pregnancy.
Three types of disorders of human pregnancy with a possible immune etiology have been discussed. Pre-eclampsia and recurrent abortion may result from a failure of a maternal immunoregulatory response to trophoblast but the evidence is incomplete and circumstantial. There are several fetal problems which may arise because of transfer of maternal allo-, iso-, or autoantibodies to the fetus. Third, maternal graft-versus-fetal-host disease occurs rarely and may present in a delayed and incomplete way as severe combined immunodeficiency.
Evidence for a novel HLA antigen found on human extravillous trophoblast and a choriocarcinoma cell line.
We describe the characterization of a novel HLA Class I molecule, which we have isolated from chorionic cytotrophoblast cell membranes, and from a trophoblast-derived choriocarcinoma cell line, BeWo; classical HLA Class I antigens are not expressed on these cells. This antigen is an electrophoretically non-polymorphic glycoprotein of approximately 40,000 molecular weight, which is found in association with beta 2 microglobulin, and which is detected by monoclonal antibodies recognizing monomorphic determinants of HLA Class I. Elucidation of the nature and origin of this molecule may provide valuable information regarding the immune barrier that exists between mother and fetus.
Overview of randomised trials of diuretics in pregnancy.
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Characterization and localization of HLA antigens on hydatidiform mole.
Frozen sections of three specimens of hydatidiform mole were stained with monoclonal antibodies to HLA Class I and Class II antigens by means of an indirect immunoperoxidase technique. Class I (HLA A, B, C) antigens were detected on proliferating extravillous trophoblast and on villous stromal cells but not on quiescent villous trophoblast. Trophoblast Class I antigen was detected with four different antibodies to monomorphic determinants but not with antibodies to the appropriate polymorphic HLA A or B type. Stromal cells were reactive with all Class I antibodies. Class II (HLA DR) antigens were not detected on any molar tissue. The expression of HLA antigens by molar tissue is similar to that of the normal first-trimester human placenta.
Immunohistological and biochemical evidence for a role for hyaluronic acid in the growth and development of the placenta.
A monoclonal antibody, designated NDOG1, has been used to stain a series of human and monkey placentae as well as several adult human tissues using immunoperoxidase techniques. In early placentae, NDOG1 was found to stain extracellular material associated with proliferating, extravillous cytotrophoblast cell columns and with the cytotrophoblast shell at the feto-maternal junction. The immunohistology suggests that NDOG1 antigen may be secreted by the anchoring cytotrophoblast into the immediately adjacent maternal tissues. NDOG1 antibody also shows extracellular staining in the stroma of early human placentae and reacted with the apical villous syncytiotrophoblast plasma membrane throughout pregnancy. Biochemical experiments demonstrated that extracts of this latter membrane contained NDOG1 antigenic activity which was susceptible to digestion with bovine testicular hyaluronidase. Hyaluronic acid was the only glycosaminoglycan found in this membrane, thereby implying a reaction between NDOG1 antibody and hyaluronic acid. Whilst no such direct interaction could be demonstrated in vitro, NDOG1 was shown to compete with two other antibodies which themselves demonstrated specificity for hyaluronic acid. The proposed identity between the NDOG1 antigen and hyaluronic acid is discussed particularly in terms of placentation where the distribution of NDOG1 staining may confirm the role of hyaluronic acid in providing an open matrix structure during stages of cell proliferation, migration and invasion.
Maternal cell-mediated immunity to the fetus in human pregnancy.
Cell-mediated sensitisation of the mother to her fetus is not a regular event in human pregnancy, and the role of suppressor cells and blocking antibodies in preventing this sensitisation is unresolved. There is as yet little evidence to support the hypothesis that maternal immune recognition of the fetus is essential for the success of the pregnancy. Further progress in this area will depend on systematic investigations of the development of specific maternal humoral and cell-mediated responses to the fetus throughout gestation, and whether a deficiency of these responses results in the failure of the pregnancy.
Improvements in the registration and analysis of fetal heart rate records at the bedside.
A microprocessor system is described for on-line analysis of the fetal heart rate detected by conventional Doppler systems. A brief account is given of the instrumentation and program structure. The system has been tested by analysing normal and abnormal antenatal fetal heart rate records. Pulse Doppler with autocorrelation measurement of the fetal pulse interval reduced the signal loss in clinical practice by a factor of 10, to an average of 2.1% in 629 records from uncomplicated pregnancies. Yet it is still necessary to identify signal loss, because it occasionally rises to unacceptable levels in association with fetal movements or hiccups. Medium-term measures of fetal heart rate variation (within 16-0.1 cycles/min) varied with gestational age, but were a better index of fetal well-being than longer-term measures. The application of the system to fetal monitoring is illustrated.