[Immunologic elements of pathogenesis of late pregnancy toxemias].
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Principle possibilities of the complex evaluation of the mother-fetus exchange were studied by means of morphological investigations of the human placenta in normality, in vesicular mole, late toxicoses, hemolytic disease of newborns and malformations of the fetus. The investigation of the ratio of the villi of different size, deposition of fibrinoid on their surface, the change of the amount of cytotrophoblastic elements, cells of Kaschenko-Hofbauer and the polymerity of the basic substance are of diagnostic value. The authors propose the basal lamina of the placenta to be included into the scheme of the examination of placenta.
It has been shown that in the ontogenesis of human placenta there occur regular changes in the percentage of the villi of various calibre having different interrelationships between the trophoblast, the connective tissue stroma and the fetal vessel. The changes of the number of chorial villi affected by fibrinoid and containing blood vessels under the trophoblast in late toxicoses of women and the anemic syndrom are analyzed (treated and not treated groups of women suffering from different forms of toxicosis were compared). An increased amount of chorial villi having blood vessels under the trophoblast is noted which is a morphofunctional feature of compensatory-adaptational alterations. Possible ecologo-evolutionary approaches to clearing the biological significance of adaptational changes of morphogenesis of the human placenta in pathological pregnancy are shown by the example of the analysis of morphological peculiarities of the placenta of the dolphin.
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The results of two studies about the course of pregnancy and delivery in adipose women in our hospital are combined and discussed. We found a higher rate of EPH-gestosis in overweight patients. The frequency of Cesarean section was increased. Belated uterine involution post partum is more frequent in adipose women, also the occurrence of urinary tract infections. There is a significant increase in perinatal mortality, mainly due to an increase in still-born. Pneumonia due to aspiration and birth traumata occur more frequently as well and endanger the children.
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A group of 412 infants with birthweights between 501 and 2,500 gm and gestational ages of 36 weeks or less were studied for the influence of both prolonged ruputre of amniotic membranes and maternal hypertension on the incidence of idiopathic respiratory distress syndrome (IRDS). The occurrence of these complications was associated with a significant decrease in the incidence of IRDS only in infants with birthweights between 1,501 and 2,500 gm (37.4% in the no complications group versus 12.8% in the complications group; P less than .01) or gestational ages of 33 to 36 weeks (35.2% in the no complications group versus 13.1% in the complications group; P less than .01). In infants with birthweights of 1,500 gm or less or gestational ages of 32 weeks or less, the specific antecedent complications of pregnancy did not alter the incidence of IRDS. Rupture of the membranes for more than 72 hours had no greater effect on the incidence of IRDS than those lasting 24 to 72 hours.
A simple and noninvasive technique was developed to evaluate the blood perfusion rate within human placenta. The method is based on monitoring the accumulation of the isotope 113mIn in the placental intervillous space using a single detector as a measuring device. The result was expressed as an accumulation index calculated from the tracer appearance curve. The In accumulation index was significantly lower in preeclamptic patients than in the controls, but with a marked overlapping. The In index was significantly correlated with the simultaneously recorded maternal minute volume, 24-hour estrogen excretion and birthweight. No correlation was found with the placental weight or Laakso's perfusion index. Uterine contractions induced a significant decrease in the In index. The authors conclude that the In accumulation index can be used as an objective measure of the placental blood flow.
The influence of chronic intrapregnancy hypoxia caused by mother's diseases (toxemia, gravidarum, hypochromic anemia, diabetes) on the brain of a mature newborn has been investigated. Besides the vast damages of the parieto-occipital cortex, Ammon's horn (entorhinal) motor and insula cortex there were also some damages of the cerebellum and the brain stem cells. The damages of the cells in the brain stem seem to be one of the causes of the abnormal perinatal adaption.
The essential EPH-gestosis seems to have multiple aetiological factors and the disease develops already a long time before the appearance of the classical symptoms. The disturbed renal function is the main point among secondary pathological effects as the damaged placenta, the disseminated coagulation, the glomerular endotheliosis, the increased retention of water and sodium with increased arterial responsiveness. It may be that this reduced reversible renal function is of extra-renal origin. As predisposing factors were discussed the reduced uteroplacental circulation with the release of still unknown pressor substances or decreased inactivation of pressor amines, the uterorenal reflex mechanism, the disturbed homeostasis of the body fluids and the vegetativ-hypothalamic crisis etc. But other factors may also be participate on this disease as immunological and hormonal aspects, especially the renin-angiotensin-aldosteron-system and prostaglandins. To find out the aetiological factors we should examine the disease at the beginning in comparison with normal pregnancy. These factors must explain why the true EPH-gestosis appears mainly during the first pregnancy and frequently in twins and so on.
The determination of the frequency of the histological severity of cellular, predominantly leukocytic infiltration in the fetal membranes and umbilical cord and its dependence upon the time of rupture of the membranes, the transmission, and the EPH gestosis yielded the following results: (1) Cellular infiltration of the decidua, the severity of which ranged from low to high, was observed in almost 90 percent of the placentae included in this investigation, with infiltration being not detected in only about 10 percent. (2) There was observed a continuous decrease in the frequency of low- and high-severity infiltration in the fetal membrane layers toward the choriodecidual space, so that high-severity infiltration of the amnion could be detected in about 3 percent only. (3) The percentages of infiltrates detected were roughly 13 percent in the umbilical vein wall and only 8 percent in the umbilical arterial walls. (4) Cellular infiltration of the umbilical vein may be observed significantly more frequently in those cases in which the time from the rupture of the membranes to the delivery of placenta is longer than three hours than in cases where this time is shorter than three hours. (5) In the case of transmission the frequency of cellular infiltration of the amnion and umbilical vein wall is significantly higher than in the cases of normal gestations. (6) High-severity forms of cellular infiltration of the umbilical vein and arteries are significantly more frequent in the case of EPH gestosis than low-severity forms. (7) The differences in frequency of cellular infiltration in fetal membrane layers and umbilical vessel walls not mentioned under (4) through (6) above are not significant for different times between the rupture of the membranes and the delivery of placenta, transmission, and EPH gestosis. (8) Hypoxidosis and chemotaxis due to acidification of the amniotic fluid rather than bacterial infection are considered to be the causes of cellular infiltration in the majority of cases of increases in time between the rupture of the membranes and the delivery of placenta, transmission, and EPH gestosis.
In the serum of 145 women between the 34th and 42nd weeks of pregnancy, 209 radioimmunological determinations of human placental lactogen were made, using the Pharmacia, Uppsala, Sweden, HCS Phadebas Test. Following the determination of normal HPL levels in late pregnancy, the HPL values of high-risk pregnancies were investigated in relation to normal values and compared with the clinical pattern. A satisfactory relation was found between low HPL levels and fetal growth retardation. To some extent the HPL data can also be used in monitoring severe EPH-gestosis and postmaturity. Light cases of gestosis and pregnancies involving Rh-incompatibility do not affect HPL production. The clinical findings regarding HPL levels should not be overestimated in attempting to diagnose placental insufficiency.
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The relations between the maternal and foetal organisms during pregnancy are partly very complicated and remain inexplicable. Blastocyst, trophoblast, embryo and foetus have membrane antigens at a very early stage, and the immunocompetence of the foetus develops already during the second third of the pregnancy period. Many non-specific factors are involved in preventing the castingoff reaction of the foetal organism. The trophoblastic tissue is probably of central importance. The focal point of interest in trophoblast tissue research is probably the testing of the local action of HCG and HPL and perhaps also AFP, as well as the question whether cellular and nuclear fusions occur in the region of the syncytiotrophoblasts and the decidual base, or if leucocyte antibodies can block the HLA antigens or the trophoblastic surface.