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At least 145 records · Page 8Linked to original sources

[Study on the stereo-architectural changes in human placental villi of toxemia of pregnancy].

Architectural changes in placental villi in clinical types of toxemia of pregnancy which were divided into four groups according to the main maternal symptoms (hypertension: H type, proteinuria: P type, PH type and IUFD) were studied by scanning electron microscopy and computerized image analysis of serial paraffin step sections. Furthermore plastic casts of villous capillaries were compared and changes in endothelial cells of villous capillaries were observed by transmission electron microscopy. 1) Scanning electron microscopy showed characteristic differences between P type cases and H type cases. Terminal villi were markedly reduced in number and showed few branches especially in P type cases, whereas in H type cases slender terminal villi were observed. The surface structure showed rough degenerative microvilli in H type cases and slender long microvilli in P type cases. 2) Average diameters of terminal branches estimated by image analysis were as follows: Normal cases: 24.8 mu, P type: 23.1 mu, H type: 17.9 mu, PH type: 17.7 mu, IUFD: 13.8 mu. The reduction in the number of intermediate villi in cases of toxemia of pregnancy was about 58% of that of normal cases. 3) Plastic casts of villous capillaries emphasized these changes in each type. 4) Swelling of the endothelial cell into the capillary lumen was observed and an increase in the number of filamentous structures in the cytoplasm of endothelial cells was detected by transmission electron microscopy.

Capillaries↗

[Disorders of the hemostasis system in late pregnancy toxemia and their correction].

The coagulation system has been examined in 30 women with late toxemia before and after heparin and trental therapy. Pretreatment fibrinogen levels were elevated and antithrombin III levels were reduced. A hemolysate-calcium mixture showed an increase in coagulation at 8 and 10 minutes of incubation. Staphylococcus agglutination and ethanol tests revealed a significant increase in early PDF and other constituents of the fibrinogen pool. These changes were indicative of prolonged-type disseminated intravascular coagulation in late toxemia. Comprehensive therapy comprising heparin and trental leads to a significant reduction in fibrinogen concentration, alleviation of the hypercoagulatory shift and increase in antithrombin III level. Early PDF and fibrin monomer complexes showed a decline. In addition, the therapy had beneficial effects on the maternal and fetal clinical status.

Adult↗

[Retinochoroidal changes in toxemia of pregnancy with the relation to hypertensive retinopathy and choroidopathy].

Thirty patients who suffered from ocular involvement caused by toxemia of pregnancy were examined ophthalmologically during the nine-year period between 1980 and 1988 at Osaka Medical Center and Research Institute for Maternal and Child Health. The ophthalmoscopic findings were divided into the following five categories: cotton wool patches (CWP), retinal hemorrhages (RH), hard exudates (HE), yellowish opaque foci (YOF) and serous retinal detachments (SRD). Although the first three types of findings were recognized as hypertensive retinopathy (Keith-Wagener III or IV), the last two were recognized as choroidal vascular damage. Based on the frequency of fundus findings, patients were divided into three types: R-type mainly suffered from retinal vascular occlusion (CWP), C-type mainly suffered from choroidal vascular occlusion (YOF, SRD), and R + C-type consisted of mixed vascular occlusion. The maximum systolic blood pressure of C-type patients was significantly lower than that of R-type. The maximum diastolic blood pressure of C-type patients was also significantly lower than those of R-type and R + C-type. There were five C-type cases with systolic blood pressure of less than 160 mmHg in which the choroidal ischemia was concluded not to be hypertensive choroidopathy but a specific alteration characterized by toxemia of pregnancy (hypercoagulopathy).

Adult↗

Retinal detachment in toxemia of pregnancy.

A case of exudative retinal detachment in a 16-year-old Thai woman with toxemia of pregnancy was reported. The patient developed bilateral retinal detachment during toxemia of pregnancy. After termination of pregnancy, the blood pressure returned to normal level, the subretinal fluid reabsorbed and the retina reattached. The visual acuity improved from 6/60 to 6/9 both eyes.

Adolescent↗

[Dopaminergic control of aldosterone and prolactin secretion during normal pregnancy and toxemia of pregnancy].

To investigate the dopaminergic regulation of plasma aldosterone and prolactin secretion during the third trimester of pregnancy, the following experiments were performed. All patients gave informed consent before entering the study. Fourteen non-pregnant women, 22 normal pregnant women and 9 patients with severe toxemia of pregnancy (Gestosis Index; 4-6) during the 32nd-41st weeks of gestation, and 8 puerperal women were received 10mg of metoclopramide (MCP) i.v. as a bolus. Plasma aldosterone concentrations were measured sequentially according to time course. The aldosterone levels in maternal vein and umbilical cord vessels at delivery in 10 term-pregnant women were compared. In addition, changes in plasma aldosterone, estradiol, progesterone and hCG levels after placental delivery were observed in 5 normal pregnant women. Plasma aldosterone concentrations increased gradually throughout normal pregnancy, and peak values in the third trimester were approximately seven times as great as those in the non-pregnant state. The aldosterone responses (net increase) to MCP in normal pregnancy were markedly greater than those in the other three groups. Plasma basal aldosterone levels and their responses to MCP in toxemia of pregnancy were significantly lower than in normal pregnancy. Plasma basal prolactin levels and their responses to MCP during pregnancy and puerperium were significantly greater than those in non-pregnancy. The aldosterone levels were significantly greater in umbilical veins and artery than in maternal peripheral veins. Plasma aldosterone, estradiol, progesterone and hCG concentrations declined rapidly soon after removal of the placenta. The significant correlation between plasma aldosterone and the other three hormones was found in terms of the rate of disappearance from the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗

[State of the immune system of the fetus and newborn infant in late pregnancy toxemias].

Histologic and morphometric studies were performed on lymphoid organs of fetuses and neonates from mothers with late gestosis. The thymuses were found to be mature with minimal signs of activation if the mothers had edema, first-degree nephropathy, or second- to third-degree nephropathy of less than 2 weeks in duration. In cases of longer-lasting nephropathy of degree 2 or 3, the thymuses were often retarded in their development, had considerable structural abnormalities and reduced weight, decreased lymphocytes numbers in the cortex and medulla, contracted lobes, and elevated numbers of Hassall's bodies. Prolonged severe toxemia led, in some instances, to diminished thymic activity, as documented by calcification of these bodies. A feature of the fetal thymic response to maternal toxemia was the absence of accidental transformation with its typical phasic changes. In the peripheral lymphoid organs, stimulation of the humoral arm of immunity was clearly observed.

Female↗

Liver disease in toxemia of pregnancy.

This study reviews liver disease in toxemia of pregnancy based on 102 cases submitted to the Armed Forces Institute of Pathology. The common clinical features were right upper quadrant and epigastric pain, nausea, vomiting, and elevation of the serum transaminases. Jaundice occasionally developed. These occurred in severe preeclampsia or eclampsia and their cause was usually recognized. However, hepatic symptoms and signs did result in inappropriate diagnoses and misdirected therapy. Such confusion occurred when these were the initial problems confronting the clinician in women presenting with advanced toxemia due to poor prenatal care. They were also likely to be misleading when other more classic parameters, such as blood pressure and proteinuria, were only midly abnormal. Central nervous system complications were the common cause of death but liver disease could be partially or wholly responsible. Extensive periportal lesions, hepatic hematomas, spontaneous rupture, and infarction all contributed to hepatic injury and to morbidity. Fibrin deposition, hemorrhage, or both in the periportal areas was characteristic of the histopathology. Scanning electron microscopy validated this spectrum of change. A toxemic vasculopathy related to severe vasospasm in the hepatic arterial circulation may be responsible.

Eclampsia↗

Experimental toxemia of pregnancy in the monkey, with a preliminary report on renin and aldosterone.

Experimental toxemia of pregnancy was induced in 8 pregnant monkeys (Macacamulatta) by reducing the abdomiinal aorta to one-third of its original diameter during the last month of gestation. It was characterized by hypertension and proteinuria. In the kidney, light and electron microscopy and immunofluorescence revealed findings similar to those in human toxemia. Focal necrosis in the liver and diffuse hemorrhagic infarctions in the placenta were also observed. Plasma renin activity and aldosterone levels, as determined in blood from the uterine vein, were elevated. None of these changes were found in 4 control animals.

Aldosterone↗

[Acute choriocapillaris occlusion in pregnancy and puerperium. Toxemias, thrombotic microangiopathies].

Six cases of gravidic toxemia (4) and thrombotic thrombocytopenic purpura (Moschowitz's disease) in puerperium with choriocapillaris occlusion, were examined. At the acute stage, the vision is improved, ophthalmoscopy of the fundus revealed cystlike bullous exudative subretinal with retinal detachment, yellowish spots (of retinal pigment epithelium) and often minimal localized arteriolar narrowing. The evolution included retina application pigmentary disturbances and Elschnig's spots. Fluorescein angiography showed delayed filling of the capillaris and dye leakage in the subretinal space (first hypofluorescence and late hyperfluorescence). There are various stages of ischaemic involvement but in all cases visual symptoms may be due to central obstructive choroidopathy with delayed filling and occlusion. The retinal detachment in toxemia or Moschowitz disease in pregnancy in secondary to microcirculatory choroidal damage (short ciliary vessels essentially) with rupture of blood retinal barrier. Other constatations are made in disseminated intravascular coagulation, periarteritis nodosa, accelerated nephrosclerosis, hemolytic uremic syndrome in puerperium, and these suggested possible relationship between the various conditions.

Choroid↗

True pregnancy toxemia (preeclampsia) in the guinea pig (Cavia porcellus).

In this study, normal nonpregnant, normal full-term pregnant, fasting ketotic and spontaneous pregnancy toxemic guinea pigs were compared to define the mechanism of this disease. In addition to conventional clinical, laboratory and pathologic studies, arterial blood pressure (thoracic and abdominal aortic) measurements and angiography were used. The results showed that in spontaneous cases of pregnancy toxemia, there is an aortic compression just caudal to the renal arteries. This compression reduced the aortic diameter by 22% of prerenal level as compared to 10% for fasting ketotic and normal pregnant guinea pigs. The aortic compression also resulted in a 30% postcompression reduction in blood pressure. No pressure differences were seen in the other groups. The postulated etiology for true toxemia of pregnancy in guinea pigs is, therefore, similar to that of man where aortic compression produces uterine ischemia and the resultant syndrome.

Alkaline Phosphatase↗

Prevalence of elevated blood pressure in a village community with a high incidence of toxemia of pregnancy.

Blood pressure measurements were recorded in 95% of the men and 97% of the women aged 30 to 59 years in a small Israeli village populated by Jews of Kurdish origin and in which a high incidence of toxemia of pregnancy was previously observed. The prevalence of hypertension in the men, as well as in the women, was significantly higher in all age groups studied than in a sample of the general population. These findings support the hypothesis that toxemia of pregnancy is an expression of a preexisting hypertensive state rather than an etiological factor in the development of later hypertension in women.

Adult↗

[A typical case of DIC precipitated by cesarean section done for severe toxemia of pregnancy and a follow up laboratory study of the progress of DIC].

A typical case of DIC presumably precipitated by cesarean section done for severe toxemia of pregnancy is reported. A laboratory study followed up the progress of DIC, especially of the drop in the consumptive platelet count and fibrinogen level as a result of excessive blood clotting. In this case the patient was a 29-year-old nulliparous gravida 1 who developed severe toxemia at 29 weeks and underwent a cesarean section for fetal distress at 33 weeks, although the baby died immediately after birth. On the following day of operation slight bleeding from the operative wound occurred and she had pertinent laboratory tests, which yielded a platelet count of 81,000/mm3, plasma fibrinogen level of 200mg/dl and FDP of 160 micrograms/ml and led to a diagnosis of DIC. While placing her on replacement and adjunctive therapies the laboratory tests were performed serially, which permitted a close follow-up observation of the subsequent progress of DIC with the detection of lowered platelet counts and fibrinogen levels as administration of Heparin resulted in an increase in the amount of bleeding, FOY, 800mg/day, was instituted and following this treatment the DIC disappeared.

Adult↗

Morphology of fetal placental stem arteries in hypertensive disorders ('toxemia') of pregnancy.

Morphological features of 3rd order, fetal stem arteries of placentae from 50 'toxemic' patients, including all types, i.e., those with pre-eclampsia, essential hypertension, and chronic renal disease, were compared with similar arteries in 50 placentae of normal pregnancies. Striking changes of the arterial wall and subtle but definite alterations in the surrounding stroma were observed in the fetal arteries from hypertensive pregnancies. The earliest mural alteration consisted of endothelial proliferation which narrowed the lumen. This was followed by proliferation of subendothelial and smooth muscle cells probably derived from the medial layer. In the media, the proliferating smooth muscle cells were affected by vacuolation and other degenerative processes. Of the above changes the intimal and medial alterations were present in 38 placentae of toxemic patients, whereas some of these features were found only in 6 cases of the control group. Other lesions of the fetal stem arteries (i.e. thrombi and arteritis) were observed less commonly. Moreover, smooth muscle cells that usually are scattered in the villous stroma in normal placentae, in toxemic patients were more numerous and tended to form bridges between the fetal arteries. On the basis of the present observations, it may be concluded that several lumen-narrowing alterations affect the fetal arteries of the placentae in toxemia of pregnancy. Whereas these undoubtedly contribute to the 'placental insufficiency' commonly found in this group of diseases, they probably represent a reaction to a more basic and as yet not identified factor(s) that may be operational in 'toxemia' of pregnancy.

Arteries↗

Proteolysis and antiproteolysis associated with toxemia of pregnancy.

Ten pregnancy toxemia patients, 10 pregnant patients with essential arterial hypertension and 12 normal pregnant women were studied between the weeks 37 and 40 of gestation. From them blood samples were obtained 24 hours before and 24 hours and three months after the delivery. In these samples proteolytic (P) and antiproteolytic (AP) activities and alpha-1-antitrypsin (A1-AT) concentration were determined. The P and the AP were measured by hydrolysis of BAPNA, and the A1-AT by radial immunodiffusion. The most interesting results were observed 24 hours before the delivery. Toxemic patients presented increase of P and AP, and hypertensive patients diminution of A1-AT when compared with normal controls. These results demonstrated that in toxemia and essential hypertension during pregnancy maladjustments in mechanisms of serum proteolysis and antiproteolysis, perhaps related with the activation of complement, clotting and circulating immune complexes formation systems, exist.

Blood Proteins↗

Uterine, placental, renal biopsies, and fibrin deposits in toxemia of pregnancy.

Histopathologic lesions of toxemia of pregnancy found in 46 first trimester-induced abortions and 82 women with kidney biopsies are reviewed and discussed. Decidual arteriolar vasospasm and degeneration, syncytial trophoblastic degeneration, and chorionic villous fibrin deposits characterize the early toxemic changes of the uterus and placenta. Pure toxemic glomerular, arteriolar, tubular, and juxtaglomerular alterations were present in about 40% of the kidney biopsies. Others had arteriolar nephrosclerosis, chronic glomerulonephritis or both. Two women had renovascular hypertension. Excessive vascular permeability predisposed to fibrinogen leakage and fibrin deposits. The mechanisms of preclinical toxemia of pregnancy and clinical preeclampsia are considered in view of these biopsy observations.

Female↗

Toxemia of pregnancy. Part II. Immunofluorescent studies with placental connective tissue antisera: the possibility of characteristic lesions.

Seventeen placentas from term gestation complicated by toxemia of pregnancy and 17 normal controls were tested by the fluorescent antibody technic. Antisera to normal placental connective tissue and toxemic placental connective tissue were used. The antisera were obtained by the injection into rabbits of placental extracts rich in connective tissue elements from normal and toxemic placentas. The antitoxemic antisera, after absorption with soluble sonic fraction of normal placentas, stained the following elements exclusively in 14 of the 17 placentas: part of the syncytial knots, fibrillar elements in the adventitia of blood vessels, and amorphous deposition of connective tissue. In each of the remaining three placentas at least two of the lesions were observed. The observation of bright fluorescence in part of the syncytiotrophoblasts and the syncytial knots in toxemic placentas led to the suggestion that they arise late in pregnancy during the disease. The thin fibrillar elements and the amorphous deposition of connective tissue were documented in the various developmental stages in toxemic and normal placentas as well. These findings established possible characteristic lesions in the placenta of pregnancies complicated by toxemia.

Adolescent↗

[Does a preventive treatment of pregnancy toxemia exist: the role of aspirin].

After studying the risk factors of eclamptic toxemia, the author describes the various methods of prevention proposed. A salt-free diet has no effect. Increased intake of zinc or magnesium has no impact. Calcium (600 to 2,000 mg/d) may reduce the incidence of toxemia among teenagers from 27.9% to 4%. Low dose aspirin appears to be equally effective. Cod liver oil is currently being tested.

Aspirin↗

[Immunologic aspects on the etiology of pregnancy toxemia].

Since 70 years ago, the possibility that the etiology of Gravidic Toxemia is inmunologic has been studied. Several researchers agree in the disminution of the levels of IgG with no modifications on the levels of complement fractions. The determination of IgA, IgM, IgC, C3 and C4 was made on fifteen pacients with gravidic toxemia and fifteen pacients that presented no complicated pregnancy. The results are the same as the reported facts like disminution of IgG, it was observed also, a disminution on the complement fractions C3 and C4. The research let us stabblish the posibility of a sikness caused by immune complexs having as an antigenic stimulations the trofoblast.

Adult↗