[Is late toxemia of pregnancy a "salt disease"? Sodium and potassium levels of the body in pregnancy toxemia].
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Female↗
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[Nursing of patients with pregnancy toxemias. Physiopathology of pregnancy toxemia].
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Female↗
[Nursing of patients with pregnancy toxemias. Diagnosis and treatment of pregnancy toxemia].
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[Nursing of patients with pregnancy toxemias. A nursing process for patients with pregnancy toxemia].
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Female↗
[Coagulation-fibrinolysis and kinin-forming systems in toxemia of pregnancy].
The changes in the coagulation-fibrinolytic system and kinin-forming system in toxemia of pregnancy were studied to clarify the relationship between the hemostatic system and severity of toxemia. The results obtained were as follows: 1) Both activity and antigen of antithrombin III (AT-III) and Factor XIII in toxemia of pregnancy were significantly lower than those of normal pregnancy, and became lower as the severity of toxemia increased. In particular, a significant negative correlation was observed between the total score for the gestosis index (G.I) and AT-III activity (r = -0.447, p less than 0.005). These results reveal that AT-III is not only a sensitive indicator of the hypercoagulable state but also a useful indicator of the severity of toxemia. 2) Plasma prekallikrein in toxemia became much lower, and bradykinin in toxemia became much higher than those of normal pregnancy. These results mean that there was not only activation of the coagulo-fibrinolytic system but also activation of the kinin-forming system in toxemia. 3) The plasmin-alpha 2-plasmin inhibitor complex in toxemia was significantly greater than that in normal pregnancy (p less than 0.001), and became very high as the severity of toxemia increased (p less than 0.05). In the mild toxemia group, the plasmin-alpha 2-plasmin inhibitor complex became greater as AT-III decreased and a significant negative correlation was observed (r = -0.59, p less than 0.05), whereas in severe toxemia, the complex did not increase as AT-III decreased and no correlation could be observed. These results show that in toxemia of pregnancy, the coagulation system dominates the fibrinolytic system as severity of toxemia increases.
Antithrombin III↗
[The role of coagulation and fibrinolysis system in pathogenesis of toxemia of pregnancy].
UNLABELLED: It is well known that many pathophysiological findings in toxemia of pregnancy are explained by imbalance of coagulation and fibrinolysis system. The purpose of this study is to elucidate a precise role of coagulation and fibrinolysis system in pathogenesis of toxemia of pregnancy. SUBJECTS AND METHODS: 1) Classification of toxemia of pregnancy. Three hundred and thirty seven of toxemia of pregnancy are classified based on the onset period, and incidence of severity of disease and IUGR, rate of genetic factor of hypertension are compared in each group. 2) Platelet factor 4 (pf4) and beta-thromboglobulin (beta-TG), Fibrinopeptide A (FPA), thrombin-ATIII complex, ATIII fibrinopeptide B beta 15-42, D dimer FDP and plasmin-alpha 2 PI complex are assayed. The levels of PGI2, tissue plasminogen activator (tPA) and thrombomodulin (TM) are measured after venous occlusion. Immunoreactivity and biological activity of TM in urine are analyzed. 3) Aminoacid sequence of TM from normal and toxemia of pregnancy are determined by analyzing cDNA for TM. Moreover, TM are synthesized from recombined DNA and enzymological properties of TM obtained from normal and toxemia of pregnancy are compared. 4) Release of PGI2, tPA and TM by addition of thrombin are observed using monolayer culture of endothelial cells from cord. Enzymological properties of purified placental TM are analyzed. RESULTS: 1) The incidence of severe type, IUGR and the rate of patients who possess genetic factors for hypertension are higher in early onset type, suggesting that hypertension is the predominant characteristics in early onset type and that genetic factors for hypertension are tightly involved. 2) All parameters such as platelets, coagulation and fibrinolysis system are elevated in toxemia of pregnancy compared to those in normal pregnancy. Coagulation index that consists of above parameters is well correlated with clinical index that consists of clinical findings (r = 0.7006, p less than 0.0001). The net increase of PGI2, tPA and TM by venous occlusion are decreased along with severity of toxemia of pregnancy. The potency of production of PGI2 from endothelial cells in maternal omentum is impaired in the severe toxemia of pregnancy. Purified TM in urine from normal pregnancy and toxemia of pregnancy has 63K dalton of single band on SDS-PAGE. However, bioactivity/immunoreactivity ratio of TM in early onset type is lower than those in late onset type, and affinity of TM for thrombin and protein C is decreased in early onset type.(ABSTRACT TRUNCATED AT 400 WORDS)
Amino Acids↗
[Blood coagulation and fibrinolytic studies in patients with toxemia of pregnancy].
In this study, blood coagulation and fibrinolytic parameters were measured in maternal blood and fetal umbilical cord blood in 200 normal pregnant women and in 46 with severe toxemia of pregnancy (Toxemia), and the relationships between fetal growth and concentrations protein C (PC), antithrombin-III (AT-III) and alpha 2-plasmin inhibitor (alpha 2-PI) were studied. 1. Significant increases in fibrin degradation products (FDP) and in plasminogen (Plg), AT-III and PC were found in maternal blood of Toxemia. A significant increase in AT-III and a decrease in alpha 2-PI and PC were observed in cord blood from these patients. 2. The platelet count (Pl) tended to be low in patients with Toxemia complicated by fetal growth retardation (IUGR). 3. Pl and fibrinogen (Fib) tended to be high in Toxemia complicated by normal fetal growth. 4. PC increased from early pregnancy, and a further increase was observed in the puerperium. 5. The PC concentration correlated with the AT-III but not with the alpha 2-PI concentration in maternal blood. 6. PC in cord blood was lower than that in maternal blood, and was correlated with AT-III and alpha 2-PI. 7. In patients with Toxemia, PC was reduced in both maternal and cord blood, and this correlated with AT-III as well as alpha 2-PI in maternal blood. 8. PC was low in Toxemia complicated by hypertension and proteinuria. These results suggest the involvement of FDP, AT-III, PC and Plg in the pathogenesis of Toxemia, and that the Pl, Fib, FDP and alpha 2-PI concentrations are related to fetal growth. Therefore, the PC and AT-III concentrations appeared to be a useful index for the blood coagulation and fibrinolysis in pregnant women and appeared to be important factors in the degree of Toxemia and IUGR.
Adult↗
[Follow-up study on women suffered from severe toxemia of pregnancy].
We started a special follow-up system for women who had a history of severe toxemic pregnancy in our department since 1975. All medical records from 1956 to 1975 were reviewed and 468 deliveries with such disease were registered at that time. One hundred and ninety five deliveries (186 women) also were added from the prospective point of view until 1985. Among 654 patients, 374 women were available to address. I. The latter 186 women were divided into 7 groups: A1, A2, A3, A4, B1; and B2. The definitions of each group were as follows. A1: primipara with severe toxemia; A2: multipara that had a severe toxemia at the first time and then normal pregnancy (ies); A3: multipara that had a severe toxemia in the first pregnancy and then mild one(s); A4: multipara that repeated severe diseases; A5: multipara that had a severe toxemia and then unclassified type(s) of the disease; B1: multipara that had a normal pregnancy at the first time and then severe toxemia(s); B2: multipara that had a mild toxemia in the first pregnancy and then severe one(s). The percent of each group was 25, 24, 13, 15, 4, 6, and 12% respectively. Those women who had severe toxemia(s) were found to have hypertension, high levels of blood urea nitrogen, hyperhematocritemia, and hyperlipemia from the results of clinical and laboratory data. Consequently, they are a high risk group of atherosclerosis, because hypertension and hyperlipemia are main risk factors of that disease. II. Eighty percent of 374 women who had a history of severe toxemia from 1956 to 1985 was able to be followed up by us until 1987. Those women also were divided into the same groups as described above except A5, and checked up as to hypertension, hyperlipemia, body weight, and so on. The characteristic features were that the group A2 is in a well condition, and that many of group A4 are suffering from various diseases with regard to the remote prognosis. In conclusions, it was suggested that there may be four etiologic causes as to toxemia of pregnancy. The first is a disadaptation during pregnancy, and this seems to consist mainly of pregnancy induced hypertension. The second has various underlying diseases, such as chronic hypertension or renal disease, etc.. The third has a hypertensive trait which is manifested as the pregnancy advances. The fourth is considered to be related to biologic ageing.
Adult↗
[Urinary calcium excretion in toxemia of pregnancy].
The amount of urinary calcium excretion is an useful marker for distinction between patient with preeclampsia and normal pregnancy of chronic hypertension has been reported. This study was performed to investigate the extent and the etiology of decrease in urinary calcium excretion in toxemia of pregnancy. The subjects in this study were 20 patients with severe toxemia of pregnancy (group T) and 20 subjects with normal pregnancy (group N). In these subjects, serum calcium (s-Ca), phosphate (s-Pi) and uric acid (s-UA) and urinary calcium (u-Ca), phosphate (u-Pi) and uric acid (u-UA) were measured. The values of u-Ca and u-Pi in the group T were significantly decreased than the group N (p less than 0.001, p less than 0.01). The values of s-Ca and s-Pi made no distinction between group T and group N. There was significant relationships between u-Ca and, s-UA (r = -0.70), clearance of UA (r-0.82), Ccr (r = 0.64), and FEca: Cca/Ccr (r = 0.87). These results indicated that the decrease of u-Ca was evident in severe toxemia of pregnancy. And the decrease of u-Ca has resulted from increase of tubular reabsorption. The change of u-Ca of patients with toxemia was studied. After the onset of toxemia, u-Ca was decreased rapidly (less than 50 mg/day) and u-Ca was restored to the normal range (more than 100 mg/day) promptly after delivery. The value of u-Ca was over 100 mg/day in the second pregnancy that developed on toxemia of pregnancy among the cases who has severe toxemia in the first pregnancy. However, toxemia of pregnancy have relapsed in the case with low u-Ca excretion of less than 100 mg/day during the second pregnancy.
Calcium↗
[Tubular damage in toxemia of pregnancy using urinary trehalase as a marker].
We proved reversible tubular damage in edema and in toxemia of pregnancy using urinary trehalase as a marker. 1. Urinary trehalase activity in mild toxemia (edema: more than 0.5 kg body weight gain per week) was significantly increased as compared with normal pregnancy (less than 0.5 kg body weight gain per week) (p less than 0.02). Urinary albumin content, however, was not significantly changed with edema. 2. Toxemia of pregnancy showed significantly high urinary trehalase activity, NAG activity and beta 2-MG content as compared with the 3rd trimester of pregnancy. Urinary trehalase activity of severe toxemia was significantly higher than that of mild toxemia. Urinary NAG and beta 2-MG showed similar results to urinary trehalase. On the 5th and 30th puerperal days there was significantly lower trehalase activity than in the 3rd trimester. Urinary beta 2-MG in toxemia was significantly decreased at the 30th puerperal day as compared with the 3rd trimester and 5th puerperal day. However, no significant decrease was observed in urinary NAG. 3. Urinary trehalase activity in superimposed toxemia of pregnancy was significantly increased as compared with the 3rd trimester of pregnancy. However, urinary trehalase activity on the 5th puerperal day was significantly decreased, but was still significantly high. These results show that pregnancy with edema and pure toxemia of pregnancy cause renal tubular damage and this damage is reversible. In the stage of edema, no remarkable glomerular damage, but tubular damage could occur.
Female↗
[Alpha 1 fetoprotein in pre-eclamptic toxemia (author's transl)].
From 1973 to 1975, 287 serum levels of alpha 1 fetoprotein in women with pre-eclamptic toxemia were determined. Pre-eclamptic toxemia was classified according to modified scheme of Goecke and Rippmann. 161 patients had mild pre-eclamptic toxemia (index 1-3), 72 patients had moderate pre-eclamptic toxemia (index 4-6), 54 patients had severe pre-eclamptic toxemia (index 7). In all types of severity of pre-eclamptic toxemia more levels of alpha fetoprotein were lower or higher than the normal levels including the standard deviations. The number of abnormal values rose with an increasing toxemia index. There was no statistically significant difference between too high values and too low values. Significantly more values were above and also below the normal values. Our investigations appear to indicate that the determination of the alpha fetoprotein is not only valuable as screening method for neural tube defects but also of value in the diagnosis and management of pre-eclamptic toxemia. Too high and too low values should not be differentiated but values both above and below the normal levels should be considered.
Adolescent↗
[Vaginal fungi in toxemia of pregnancy (author's transl)].
In order to prevent the transfer of the fungi in maternal vagina into a neonate through transvaginal delivery, we examined the presence of vaginal fungi in the patients with toxemia of pregnancy occurring chiefly from the later stages of pregnancy and made an analysis from the quantitative aspect of fungi (number of colonies produced on Mizuno-Takada medium). The results obtained are as follows: 1) The detection rate of vaginal fungi was evidently so high as 37.1% in toxemia group compared with 27.6% in non-toxemia group (p less than 0.01). And the detection rate of vaginal Candida albicans (hereinafter: C. albicans) also proved to be higher tendency in toxemia group. 2) When the toxemia patients were divided into mild cases and severe ones for comparison, the detection rate of vaginal fungi and that of vaginal C. albicans were both higher in the severe case group. Particularly in the group which had the symptoms of toxemia at the examination time of vaginal fungi there was seen the higher rate. 3) From the quantitative aspect of vaginal fungi it is evident that there were more cases with over 51 colonies in the group showing the symptoms of toxemia at the time of fungi examination than in the group showing no such symptoms at the examination and the group of non-toxemia (p less than 0.01).
Candida albicans↗
[Relationship between coagulation-fibrinolysis kinetics and the severity and predictability of toxemia of pregnancy].
Various attempts have been made in recent years to identify the cause and pathophysiology of toxemia of pregnancy from the standpoint of changes in blood coagulation and fibrinolysis. It is believed that in toxemia of pregnancy, the fibrinolytic process changes as coagulation is augmented. However, definite conclusions about this sequence of events have not yet been reached. This study was designed to analyze the severity of toxemia of pregnancy and to examine the possibility of anticipating its onset from the standpoint of coagulation-fibrinolysis kinetics. The patient population comprised 116 women divided into 4 groups: I) A control group of 10 normal, nonpregnant women; II) Fifty-four normal pregnant women who were followed up from early pregnancy until delivery; III) Twenty-four women who were followed up from early pregnancy until delivery and developed toxemia of pregnancy; and IV) Twenty-eight women with severe toxemia of pregnancy of the pure type who were referred to our institution at the onset of the disease and were treated as inpatients. Intergroup comparison yielded the following results. 1. In group II (normal pregnancy), a significant increase was observed, first in fibrinopeptide B beta and then in fibrinopeptide A, as the pregnancy progressed. This suggested the acceleration of coagulation and fibrinolysis due to pregnancy. 2. In group III (6 of 24 cases developed severe toxemia of pregnancy), AT-III increased, while protein C and hematocrit levels increased relative to those on the normal pregnancy group during the 2nd trimester. Thus, changes in coagulation functions occurred before the onset of toxemia of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
Antithrombin III↗
[Urinary kallikrein quantity and activity of normal pregnant women and toxemia patients in third trimester].
In this study, urinary kallikrein quantity and activity were measured by the kallikrein direct RIA and kininogenase activity with human low molecular weight kininogen in 32 non pregnant healthy women, 20 normal 3rd trimester pregnant women and 18 3rd trimester hypertension type toxemia patients. There was no significant difference in urinary kallikrein quantity between non pregnant women (n = 32, 64.0 +/- 6.3 micrograms/day, mean +/- SE) and normal pregnant women (n = 20, 68.1 +/- 10.1 micrograms/day). There was a significant difference (p less than 0.001) between non pregnant women and toxemia patients (n = 18, 22.5 +/- 3.3 micrograms/day). There was a significant difference (p less than 0.001) between toxemia patients and normal pregnant women. There was a significant difference (p less than 0.05) in urinary kallikrein activity between non pregnant women (n = 32, 496.2 +/- 57.2 micrograms kinin/day) and normal pregnant women (n = 20, 319.5 +/- 48.1 micrograms kinin/day). There was a significant difference (p less than 0.0001) between non pregnant women and toxemia patients (n = 18, 82.6 +/- 13.6 micrograms kinin/day). There was a significant difference (p less than 0.01) between normal pregnant women and toxemia patients. There were no correlation in both urinary kallikrein quantity and activity between severe type toxemia patients (systolic blood pressure greater than or equal to 160mmHg or diastolic blood pressure greater than or equal to 110mmHg) and mild type toxemia patients (160mmHg greater than systolic blood pressure greater than or equal to 140mmHg and 110mmHg greater than diastolic blood pressure greater than or equal to 90mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
HLA antigens-antibodies system and its association with severe toxemia of pregnancy.
HLA antigens and antibodies were investigated in order to study the relationship between severe toxemia of pregnancy (toxemia) and the HLA system, which is in a close relationship with the immune response. The frequencies of 8 HLA-A antigens, 21 HLA-B antigens, 10 HLA-DR antigens and 4 HLA-MT antigens were determined in 21 patients with toxemia and their husbands and some of their children, 45 fertile couples without a history of abnormal pregnancy and 206 healthy adult controls (DR were in 106 controls). Sera from toxemias and normal pregnant women in the 3rd. trimester and postpartum intra-uterine blood in women with normal deliveries were tested for Warm-T and Warm-B cell antibody against 30 panel lymphocytes. Results obtained were as follows: In toxemic couples there is a much higher incidence of HLA-DR and MT sharing between wives and husbands, mothers and children. In those sera with toxemias, there is a higher incidence of Warm-T antibody and a lower incidence of Warm-B antibody compared with those with a normal pregnancy. From the immunogenetic point of view, when the HLA-DR X MT locus of a certain fetus is homozygous, the mother tends to manifest toxemia. These results indicated that matching of HLA-DR X MT loci in parents possibly plays a role in causing severe toxemia, and genetic prediction of its onset and prognosis can be carried out through HLA typing.
Female↗
[Studies on platelet function in toxemia of pregnancy].
This study evaluated the role of platelets in the pathogenesis of toxemia. The findings were: (1) Thrombocytopenia and macrothrombocytosis are characteristic of toxemia. (2) ADP induced platelet aggregation increases during pregnancy, but decreases in severe toxemia significantly. (3) beta-thromboglobulin levels in both plasma and urine rise during pregnancy, and are significantly high in toxemia, especially in a severe type. (4) The plasma TxB2/6-keto-PGF1 alpha ratio markedly increase in severe toxemia due to the increase in the amount of TxB2. And in the IInd trimester, the ratio in the toxemia onset group in which toxemic pregnancy occurred in the IIIrd trimester showed a significantly higher value than the control group. These findings suggest that, in toxemic patients, platelets are in a hyperactive state and there is rapid turnover caused by selective consumption in organs such as the kidneys and placenta, and that platelet aggregation decreases due to the relative increase in the number of exhausted platelets as the toxemic state is impending. Furthermore, the TxA2/PGI2 balance shifts to TxA2 dominant and measurement of the plasma TxB2/6-keto-PGF1 alpha ratio was considered to help prediction of toxemia in the latter term of pregnancy.
6-Ketoprostaglandin F1 alpha↗
Diet-related toxemia in pregnancy. I. Fat, fatty acids, and cholesterol.
Toxemia in pregnancy (preeclampsia)is characteristerized by a combination of at least two of the following clinical symptoms: hypertension, edema, and proteinuria. In three successive trials over three consecutive years, the dietary intake of a selected number of young pregnant women attending a Maternal and Infant Care Program at Tuskegee Institute were evaluated for total lipids, individual fatty acids, and cholesterol. Women with toxemia or with any of the individual symptoms were identified and women without toxemia or these symptoms served as controls. Results were variable from repetition to repetition in all but the toxemia group and the edema group. The consumption of total lipids and cholesterol was significantly greater in all three trials by both the toxemia and edema groups. Also, total saturated, monounsaturated, and polyunsaturated fatty acids were eaten in greater amounts. The greatest differences were in palmitic acid, stearic acid, oleic acid, and linoleic acid. The proportion of unsaturated fatty acids consumed in all groups was very low. All differences could be attributed primarily to breakfast and dinner meals and were found in the milk, meat, and egg food groups. Although satistical correlations were found between lipid intake and toxemia of pregnancy any specific relationship between the two is still unclear.
Adolescent↗
Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study.
Toxemia was induced in 13 of 20 pregnant ewes by the stress of a change in environment and food deprivation late in pregnancy. Of the toxemic ewes, eight developed prominent neurological findings with convulsions, motor weakness, and blindness, whereas five ewes developed azotemia without neurological signs. Proteinuria and azotemia occurred in all but one of the toxemic animals. Seven animals did not develop clinical or laboratory evidence of toxemia. Hypertension did not occur with the onset of toxemia but all toxemic animals showed glomerular changes by light and electron microscopy. These abnormalities, which were similar to those seen in human preeclampsia, included endothelial cell swelling, focal reduplication of the basement membrane, and fusion of the epithelial cell foot processes. The toxemia could not be attributed to changes in hematocrit, plasma glucose, Na, Cl, CO(2), K, Ca, fibrinogen, arterial pH, lactate, or pyruvate concentrations. Cardiac output fell only in ewes with prominent neurological signs. Plasma renin rose strikingly in animals developing toxemia, without change in substrate concentration. In contrast to human and other species, sheep uterus and amniotic fluid contained no detectable quantities of renin. Thus in response to stress the pregnant ewe develops a toxemia which in the absence of hypertension has clinical and pathological similarities to human preeclampsia.
Adrenal Glands↗