SEARCH · Search PubMed

Results for “TOXEMIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

PubMedDate not supplied

[Parameters of blood toxicity in late pregnancy toxemias].

Parameters of blood toxicity (content of medium molecular compounds and paramecia test) have been studied in 41 practically healthy women with normal pregnancy and 151 women with various forms of late toxemia of pregnancy. In late toxemia of pregnancy there is a definite enhancement of blood toxicity, as compared to health controls, the degree of toxicity directly correlating with the severity of toxemia. Blood toxicity parameters in women with primary toxemia of pregnancy are significantly lower than those in women with secondary toxemia, which may be the reason for more severe late toxemia forms in women with extragenital pathology.

Female↗

PubMed1985

[Nephritogenic glycopeptide (nephritogenoside): its existence in the urine of toxemia patients].

Previously we reported that we succeeded in isolating from human full term placenta, glycopeptide which was immunologically the same as nephritogenic glycopeptide (Nephritogenoside) prepared from human renal GBM (glomerular basement membrane). This time to clarify the correlation between the pathology of toxemia and Nephritogenoside, we examined the existence of Nephritogenoside in the urine of toxemia patients. To purify Nephritogenoside from the urine powder of toxemia patients, we use the same procedures (enzyme digestion, Con A affinity column chromatography e.t.c.) as used in purifying Nephritogenoside from human full term placental TrBM (trophoblast basement membrane). In the urine of toxemia patients we clarified the existence of glycopeptide, which had specific affinity with Con A and was immunologically the same as Nephritogenoside. The existence of Nephritogenoside in the urine of toxemia patients further strengthened the possibility of a relationship between Nephritogenoside and the pathology of toxemia.

Electrophoresis↗

PubMed1986

Prolactin in severe toxemia of pregnancy.

Plasma PRL levels were measured in 111 normal pregnant women and in 21 patients with severe toxemia of pregnancy. Twelve of 21 patients with severe toxemia of pregnancy showed high PRL levels in zone A (greater than mean value + 1 S.D. of PRL values in normal pregnancy). These 12 were significantly lower (P less than 0.02) in the Ccre rate, at 70.2 +/- 19.2 ml/min, than 5 toxemia patients (101.4 +/- 26.7 ml/min) in zone B (mean + 1 S.D. approximately mean) and 4 toxemia patients (110.0 +/- 35.3 ml/ml) in zone C (mean approximately mean -1 S.D.). Also, BUN, proteinuria and uric acid levels in zone A patients were higher than in those in zone B and C. However, no correlation was found between PRL levels and mean diastolic and systolic blood pressure. These results suggest that high PRL concentrations in toxemia of pregnancy may be associated with renal dysfunction.

Blood Urea Nitrogen↗

PubMed1989

Placental isoferritin: a new serum marker in toxemia of pregnancy.

The serum concentrations of placental isoferritin and normal ferritin were determined in 20 patients with preeclamptic toxemia of pregnancy and were compared with the level measured in normal pregnant women at the third trimester and in labor at term. The mean serum concentration of placental isoferritin for the women with preeclamptic toxemia was found to be low: 7.5 +/- 23 U/ml compared with 81.6 +/- 89.3 U/ml in normal pregnancy during the third trimester and 54.8 +/- 53 U/ml in term delivery. In comparison, there was no significant difference in the serum levels of normal ferritin in both pregnant women with toxemia and in those without toxemia. These results suggest that placental isoferritin may be a useful marker for preeclamptic toxemia of pregnancy.

Biomarkers↗

PubMed2003

An explanation for the association between specific language impairment and toxemia.

An association between specific language impairment (SLI) and toxemia has been detected in several studies. No clear explanation for this association has been identified to date. However, a number of potential explanations have been offered. These include: (1) toxemia causes fetal anoxia which leads to brain damage; (2) toxemia in the mother is an indication of maternal immune attack on the developing brain; (3) the association between toxemia and SLI is indirect and arises because both are consequences of a common but as yet unknown etiological factor. In this paper we present a fourth possible explanation for the association. That is, that both SLI and toxemia may be the consequence of low circulating levels of essential fatty acids. Evidence supporting this hypothesis is presented and four possible mechanisms underlying the association are discussed.

Brain↗

PubMed1989

Single cause for initiation of labor and toxemia: a hypothesis.

A hypothesis is presented that states that the decline in oxygen tension (PO2) in the intervillous space causes both toxemia (preeclampsia-eclampsia) and the initiation of labor. The trophoblast is identified as the monitor of the fetal PO2 and as the source of substances that are released into the maternal circulation stimulating the myometrium, the heart, the vascular smooth muscle, and, perhaps, the brain. In the presence of normal trophoblast the release takes place only when the PO2 in the intervillous space decreases to a level at which the fetus should be expelled from the uterus to avoid intrapartum hypoxia. Near term, the myometrium is the most responsive site to the released substances, and stimulation of the heart and systemic vasculature is observed only infrequently. With release of these substances, intrapartum toxemia results. Toxemia before onset of labor is created by hypoxia of the trophoblast in the presence of a nonresponsive myometrium to materials released. A small placenta, compression of the intervillous space by villous edema, and avulsion of spiral arterioles are the main causes of the premature decline of intervillous space PO2, leading to toxemia. Postpartum toxemia is produced by the retained (extraplacental) trophoblast, perhaps facilitated by the rapid clearance of progesterone.

Animals↗

PubMed1987

Serum concentration of placental proteins (PP5 and PP10) in toxemia of pregnancy as related to intrauterine growth retardation.

Maternal serum concentrations of placental proteins 5 (PP5) and 10 (PP10) were measured by radioimmunoassay in 568 samples obtained from 308 healthy pregnant women and 63 women having toxemia of pregnancy. Below-normal PP5 values were more widely distributed in the mild than in the severe toxemia group, while the incidence of above-normal PP5 values was found only in the severe toxemia group. The incidence of below-normal PP10 values was higher in the severe than in the mild toxemia group. Our study thus suggests that simultaneous measurement of PP5 and PP10 concentrations in maternal serum in toxemia of pregnancy is a useful monitoring technique for predicting progressive pathological change and placental dysfunction related to IUGR.

Female↗

PubMed1988

Maternal toxemia and neonatal germinal matrix hemorrhage in intubated infants less than 1751 g.

Two hundred seventy-two intubated infants who weighed less than 1751 g were enrolled in a clinical trial of phenobarbital prophylaxis of postnatal germinal matrix hemorrhage. The incidence of germinal matrix hemorrhage was 3.1% (one of 32) among infants born to women with toxemia, and 23% (55 of 240) among those born to women without toxemia. The apparent protective effect of toxemia could not be explained by intrauterine growth retardation, mode of delivery, or maternal receipt of any medication. Infants born to toxemic women were less likely than their peers to develop pneumothorax, become acidotic, and to require extensive respiratory assistance. This apparently protective effect of maternal toxemia was not seen in infants born to nontoxemic, hypertensive women. Thus, maternal toxemia, but not hypertension, might reduce the risk of germinal matrix hemorrhage by reducing the occurrence and/or severity of pulmonary and related problems that place infants at high risk of germinal matrix hemorrhage.

Cerebral Hemorrhage↗

PubMed1981

[Hemocoagulatological changes in toxemia of pregnancy--in reference to birth weight (author's transl)].

It is well-known that SFD babies are born of the mothers who had toxemia of pregnancy in many cases. Recently we examined the relation of hemocoagulatological changes in mothers with toxemia to the birth weight of their babies with the intention of investigating the cause of development of SFD babies and obtained some information as follows: 1. The pregnant women with toxemia were significantly lower (p less than 0.01) in platelet count, fibrinogen content, and serum factor XIII value, significantly longer (p less than 0.01) in bleeding time, and significantly higher (p less than 0.01) in serum-urine FDP, platelet ADP aggregation and platelet spreadability than the normal pregnant women. 2. As for the relation of these changes to the birth weight, the value obtained in the SFD baby and that obtained in the AFD baby group were 5.8 +/- 1.5 and 4.5 +/- 1.3 in bleeding time (min), 20.4 +/- 3.17 and 23.4 +/- 4.21 in platelet count x 10(4)/mm3), 296.5 +/- 58.5 and 346.8 +/- 50.4 in fibrinogen content (mg/dl), 1.3 +/- 0.80 and 0.6 +/- 0.63 in urine FDP (microgram/ml), respectively, and the difference between both groups was significant (p less than 0.05) in each of these parameters. The results stated above suggested that toxemia of pregnancy assumed as aspect of chronic DIC and this tendency was stronger in the SFD baby group. From these facts it is considered that a state of chronic DIC in toxemia of pregnancy may be a cause of disturbance in the development of the fetus.

Birth Weight↗

PubMed1978

An experimental study on "replantation toxemia". The effect of hypothermia on an amputated limb.

Hind legs of dogs were amputated at the middle of the thigh and preserved in three different conditions: in ice water, in a refrigerator, and at room temperature. After 6 or 12 hours of ischemia, recirculation was established. The survival rate of the animals was observed and measurement of limb edema, potassium, pH, and lactate in the blood was performed to study the effects of hypothermia on prevention of "replantation toxemia." Cooling of the amputated limb was effective for prevention of toxemia, and the cooling effect was greater in ice water than in a refrigerator. However, when cooled in ice water, some animals died due to toxemia when the time of ischemia was prolonged to 12 hours. In the dead animals, a close relationship was observed between the developement of toxemia and metabolic acidosis due to the increase in lactate.

Amputation, Surgical↗

PubMed1976

Placental lesions in experimental toxemia in the rabbit.

Unlike the normal human placenta, the normal rabbit placenta, near term, is essentially free of such stigmas of aging as infarcts and syncytial knots. When experimental toxemia is produced in the pregnant rabbit by ligating the terminal aorta to a specific degree of stricture, placental lesions resembling those found in human toxemia are observed; namely, diffuse congestion, old and recent infarcts, and syncytial knots. All the treated animals who exhibited anatomical and clinical signs of toxemia presented, in association, obvious placental lesions; there were, however, some animals which showed infarct but no other signs of toxemia.

Animals↗

PubMed1977

Experimental toxemia in the pregnant primate.

In order to develop a model for the study of eclamptogenic toxemia, a series of experiments were carried out on 31 female baboons. In Group 1, consisting of 10 animals, metal clips were placed around the uterine arteries in order to partially occlude them, and the ovarian vessels were transected. The animals were subsequently mated. Nine developed hypertension and proteinuria, and one aborted. The renal lesions in these animals were indistinguishable from those described in human toxemia. Group 2 consisted of three of the 10 baboons from Group 1, which became pregnant a second time. They again developed hypertension and proteinuria. In Group 3, three baboons at 100 days of gestation were treated as in Group 1 with similar results. Groups 4 and 5 served as pregnant (3) and nonpregnant (15) controls. It is concluded that a toxemia model has been developed in a subhuman primate. This model will prove useful in the further study of eclamptogenic toxemia.

Animals↗

PubMed1978

Studies on lipoperoxide of normal pregnant women and of patients with toxemia of pregnancy.

1. Serum lipoperoxide was determined by the method of Yagi et al. (Yagi, K., Nishigaki, I. and Ohama, H. (1968) Jap. J. Vitamin 37, 105) for 22 cases of non-pregnant women, 24 cases of 1st trimester of pregnancy (1-12 weeks), 39 cases of 2nd trimester of pregnancy (13-26 weeks), 58 cases of 3rd trimester of pregnancy (27-40 weeks), and 30 cases of toxemia of pregnancy (27-40 weeks). Remarkable increases of lipoperoxide were observed at 2nd and 3rd trimester of pregnancy compared with non-pregnant women, and the increase in toxemia of pregnancy was more remarkable than that at 3rd trimester of pregnancy. In umbilical cord blood a higher level of lipoperoxide was observed in patients with toxemia of pregnancy than in normal pregnant women. 2. The total TBA value determined by extracting the serum-lipids with chloroform and methanol solution showed a similar tendency to the above. 3. Those showing TBA-reaction by the analysis of lipids with thin-layer chromatography were the fractions of cholesterol ester, triglyceride and phospholipid. While triglyceride fraction showed a marked increase of TBA value during pregnancy and in toxemia of pregnancy.

Female↗

PubMed1987

Theory of the etiology of human toxemia of pregnancy: fetal hyperinsulinemia as a compensatory response to decreased uterine blood flow.

Toxemia of pregnancy is a perplexing clinical problem that has defied accurate elucidation of its etiology because the disorder does not occur in undisturbed lower mammalian species that are currently used as animal models of reproductive physiology. We propose that toxemia of pregnancy occurs as the end stage human fetal-placental unit response to decreased maternal uterine blood flow, and that this fetal-placental unit response may be unique to the human species. The human fetus increases insulin secretion in response to progressive intrauterine asphyxia, which may result in decreased fetal-placental prostacyclin production (a vasodilator and inhibitor of platelet aggregation) and increased fetal-placental thromboxane A2 production (a vasoconstrictor). This could result in increased uteroplacental perfusion pressure, maternal hypertension, and increased maternal platelet aggregation. We also suggest that women who develop idiopathic toxemia of pregnancy are at increased risk for adult onset diabetes later on in life because they have a mild derangement in glucose-insulin homeostasis during their reproductive years that results in increased uterine vascular damage, that leads to decreased uterine blood flow, and ultimately the fetal hyperinsulinemia-prostaglandin pressor release mechanism. Therefore, prevention of toxemia may be possible by correction of mild derangements in glucose-insulin receptor homeostasis before conception occurs.

Female↗

PubMed2001

A study of intravaginal misoprostol for induction of labor in toxemia of pregnancy.

OBJECTIVE: To compare the efficacy and complications of intravaginal misoprostol for induction of labor in patients with and without toxemia of pregnancy. METHODS: Forty-two patients with toxemia of pregnancy (group 1) and 59 women at term without toxemia (group 2) with Bishop scores of < or = 6 were treated with 50 microg intravaginal misoprostol given four times at 4-h intervals. Labor and neonatal outcomes, and any complications, were recorded. Mann-Whitney U-, Student's t- and chi(2)-tests were used for statistical analyses. P < or = 0.05 was considered significant. RESULTS: The rates of vaginal delivery were 73.8% and 84.6%, oxytocin augmentation were 4.8% and 5.1% and the mean insertion to delivery times were 12.5 and 13.8 h in group 1 and 2, respectively, with no significant differences between the groups. Neonatal outcomes, rates of uterine contraction abnormalities and gastrointestinal symptoms were similar in both groups. CONCLUSIONS: Intravaginal misoprostol is an equally effective and safe method of induction of labor in patients with toxemia of pregnancy and in normal pregnant women.

Administration, Intravaginal↗

PubMed1988

Coagulation-fibrinolytic and kinin-forming systems in toxemia of pregnancy.

The relationship between the hemostatic system and the severity of toxemia was studied in 78 pregnant women with toxemia. The activities of plasma antithrombin III (AT-III), prekallikrein, plasminogen, alpha 2-plasmin inhibitor and factor XIII were determined using the chromogenic substrate and fluorescent methods. The antigens of both AT-III and factor XIII were determined by the single radial immunodiffusion method. Plasma bradykinin was determined by radioimmunoassay. The main results obtained were as follows. Both activities of AT-III and plasma prekallikrein decreased as the gestosis index increased (p less than 0.001), and a significant negative correlation was observed between the total score of the gestosis index and AT-III (r = -0.447, p less than 0.005) or plasma prekallikrein (r = -0.434, p less than 0.005). The levels of plasminogen, alpha 2-plasmin inhibitor and factor XIII decreased and plasma bradykinin increased in toxemia. Among the various factors, plasma AT-III and prekallikrein were the most sensitive indicators of the severity of toxemia.

Antigens↗

PubMed1976

The differential diagnosis between preeclamptic toxemia and glomerulonephritis in patients with proteinuria during pregnancy.

The renal biopsies from 123 patients who presented with proteinuria during pregnancy have been reviewed. Forty-seven showed glomerulonephritis that could be diagnosed on morphological grounds or on a clear-cut history of urine abnormalities before pregnancy. Fifty of the remaining 76 had been followed after pregnancy. In these 50 patients, a retrospective diagnosis of glomerulonephritis or preeclamptic toxemia was based on the persistence or disappearance of proteinuria and/or hematuria three or more months after pregnancy. Among 22 in whom a biopsy diagnosis of "pure" preeclamptic toxemia had been made, 19 showed disappearance of urine abnormalities after pregnancy, thus confirming the biopsy diagnosis. A retrospective analysis showed focal and segmental glomeris group but none in the preeclamptic toxemia group. Other differences could not be defined without quantitative evaluation; however, the glomeruli appeared to be more cellular in the glomerulonephritis group. The presence of IgA, IgG, IgM, Complement, and fibrin was not of value in distinguishing glomerulonephritis from preeclamptic toxemia.

Arteries↗

PubMed1988

Triglycerides and apoproteins in toxemia of pregnancy.

In order to clarify the mechanism of hypertriglyceridemia caused by toxemia of pregnancy, apoprotein B, CII, CIII, and E in serum were determined by single radial immunodiffusion, and apoprotein CIII0, CII, CIII1 and CIII2 in very low density lipoprotein (VLDL) fractionated by ultracentrifugation were quantified by analytical isoelectric focusing. The increase in triglycerides in toxemia of pregnancy was estimated in VLDL and low density lipoprotein (LDL), mainly in VLDL. In contrast to the increase in triglycerides, apoprotein B and E, believed to interact with LDL receptors on cell membranes, remained unchanged from levels in normal pregnancy. The lack of correlation between triglycerides and these apoproteins may be related to the increase in triglyceride in VLDL. In toxemia of pregnancy, the relative amounts of apoprotein CII, an activator of lipoprotein lipase, and CIII, an inhibitor of lipoprotein lipase, in serum were similar to those in normal pregnancy, but those in VLDL decreased significantly. This finding suggests that the increase in triglyceride in VLDL was caused by inhibition of VLDL to LDL catabolism. These results suggest that one of the factors which causes hypertriglyceridemia in toxemia of pregnancy is impaired removal of triglyceride, in LDL fraction, but mainly in VLDL fraction.

Adult↗