[Aspects of the therapy of threatened premature labor].
Explore the source record for details and available documents.
Adrenergic beta-Agonists↗
Biomedical subjects
A Conradt
Publications and source records attributed to A Conradt.
[Clinical course of premature and newborn infants of mothers with HELLP syndrome].
The HELLP-syndrome is complicated by a maternal mortality of 3.5% and a perinatal mortality between 9.5 and 60%. It is a variant of severe preeclampsia which includes hemolysis, elevated liver enzymes and low platelets. It is described in the literature that neonates of mothers with HELLP-syndrome show characteristic symptoms especially thrombocytopenia, leukocytopenia and prenatal somatic dystrophy. In this retrospective investigation of 36 preterm and term infants of mothers with HELLP-syndrome we found the following results: 1. Thrombocytopenia was seen in 11% and leucocytopenia in 12% of the analysed cases. Anemia was seen in 10% of the analysed neonates. They needed transfusion of blood. The rate of prenatal somatic dystrophy was increased (58%). 2. Elevated blood pressure was observed in 29% of the neonates within the analysed interval. The time of artificial ventilation of preterm infants with maternal HELLP-syndrome was in 37% extended in comparison with infants without HELLP-syndrome in pregnancy. 3. The perinatal mortality was 8%. All observed infants during delivery and of the neonatal period in our collective survived.
Alanine Transaminase↗
[Pathophysiology and clinical aspects of pre-eclampsia].
From the pre-natal follow-up it was remarkable that cases have been admitted relatively late. Hints to a possible development of preeclampsia could be seen from patients history or the routine check up, for example the registration of edema, fetal growth retardation and oligohydramnios. For early diagnosis of preeclampsia we recommend: Calculation of mean arterial blood pressure or its non-invasive measurement; determination of hematocrit, uric acid and total plasma protein (in particular hemorheologic measurements). Hypomagnesemia in preeclampsia, as described by some authors, was also seen in our cases. The complex symptomatology of preeclampsia could be attributed to a generalised disturbance of microcirculation, which leads to definite reactions of the organs concerned. The microcirculatory failure is caused by vasoconstriction, hemoconcentration, hyperviscosity and hypercoagulation (up to DIC and consumption coagulopathy). The resulting symptoms and syndromes can be: EPH, HELLP, hemolytic-uremic Syndrome, hepato-renal Syndrome, thrombocyte and antithrombin III deficiency etc. The drug of choice for treatment of preeclampsia is magnesium sulfate. Its application is based on long-term clinical experience and new aspects on the physiologic and pharmacologic role of magnesium. The recommendations of the German High Blood Pressure League to use calcium antagonists as a basis in the treatment of high blood pressure can be fulfilled particularly in pregnancy by the physiologic calcium antagonist Mg++. Magnesium sulfate should be given in a dosage of 24-72 g daily. The dose should also be made dependent from urinary output. Further treatment patterns of preeclampsia should be adjusted according to each case. The present results also support our hypothesis that magnesium deficiency (besides predisposing factors) could be responsible for the development of preeclampsia (present model shown in detail). Consequently, the early and long-term substitution of magnesium in pregnancy could help reduce preeclampsia.
Adult↗
[The importance of betamimetics and magnesium for the outcome of pregnancy: I. Reduction of intrauterine growth retardation, premature rupture of membranes and premature birth after supplemental magnesium therapy].
Of 4 905 single pregnancies recorded within a 4 year period (1979-1982) 882 (18%) were risk pregnancies managed with Betamimetics (B); of these 348 (7,1%) had tocolysis (T) and 534 (10,9%) tocolysis and cerclage (T/C). Since the end of 1979 the patients received in addition to the Betamimetic a K-Mg-Vitamin drug (Feto-Longoral) aimed at "Cardioprotection", and since the beginning of 1981 30-40 mval oral Mg daily in the form of Magnesium aspartate (Mg 5-Longoral) to "support tocolysis". The mean age, parity, percentage with Magnesium therapy, the pregnancy outcome using a gestational age limit less than or equal to 36 weeks, the frequency of premature ruptured membranes (PROM) in premature and mature infants as well as the number of intrauterine growth retarded infants (IUR) (less than 10th percentile BPE) were yearly evaluated and compared for both risk collectives T and T/C as well as for the normal collectives (N). While only 2% of the normal collectives had a pregnancy duration of less than or equal to 36 weeks (completed) the figure was five fold in both T and T/C groups, and however was yearly reduced in the T/C group from 11,0% (1979) to 4,9% (1982). The frequency of PROM with premature infants in the T and T/C groups is about 6% (N-collectives about 1%). It is however reduced in the T/C group in 1981 to 2,2% and in 1982 to 1,6%. For mature infants it is N: 17-12% (fluctuating) and B (T + T/C): 22-11% (yearly decreasing). The rate of IUR (less than 10th percentile BPE) in the T and T/C groups in 1979 was 22,2 and 20,5% respectively and in 1980 12,6 and 17,5% respectively. It is further reduced in 1981 to 11,6 and 8,8% respectively and in 1982 to 9,7 and 10,6% respectively (N-collectives between 8,3 and 11,5%). The "weight gain" exceeds the 25th percentile (Hohenauer): 1979 and 1980 for B: 33,1 and 30,2% respectively, and 1981 and 1982 for B: 25,4 and 24,2% respectively (N between 26,5 and 19,5%). The results show that patients with tocolysis--with or without cerclage--have more premature and growth-retarded infants than normal collectives (a sign of more placenta insufficiencies). In the two years where Magnesium was supplemented at 30-40 mval daily, short term pregnancies, the PROM frequency and the IUR rate decreased (statistically evaluated). It could thus be concluded that a relative Magnesium deficiency might have been responsible for a certain percentage of premature births and hypotrophic infants and that better results were obtained after Magnesium substitution.
Adrenergic beta-Agonists↗
[The significance of betamimetics and magnesium for the outcome of pregnancy: II. The role of magnesium in the development of gestosis and fetal hypotrophy].
Of 4905 single pregnancies between 1979 and 1982 the 882 (18.0%) risk pregnancies managed tocolytically with Betamimetics and Magnesium were retrospectively compared with the remaining collective (R) of 4023 (82.0%) patients without management. The tocolysed patients (B/Mg) received Magnesium in addition to Betamimetics: since 1979/1980 a low dose Mg containing drug (Feto-Longoral) aimed at "cardioprotection" (3-6 mval Mg++ daily), and since 1981 to "support tocolysis" 30-40 mval Mg++ daily per os in the form of Mg-aspartate (Mg 5-Longoral). All cases of gestosis (G) in both collectives B/Mg and R were investigated. A normal collective (N) is obtained by subtracting G from R. For all collectives N, G, and B/Mg the following data were compared: mean age, parity, percentage with supplement Mg medication (only the B/Mg collective), the pregnancy outcome with respect to pregnancy duration and the number of intrauterine retarded infants (IUR: less than 10th percentile of the Bavarian Perinatal Evaluation (BPE), less than 25th percentile according to Hohenauer). The number of gestosis in the 882 B/Mg cases is zero. It is 97 (2.0%) in the remaining 4023 patients. The IUR rate (less than 10th perc. BPE) is 9.4% in the 3926 N patients, and is 45.4% in the 97 gestosis patients. The IUR rate is 17.8% in the 398 B/Mg patients of 1979 and 1980 who had received less adjuvant Mg (B/Mg [1]), and it is 10.1% in the 484 B/Mg patients of 1981 and 1982 who had received much higher Magnesium (B/Mg [2]).(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic beta-Agonists↗
[Current concepts in the pathogenesis of gestosis with special reference to magnesium deficiency].
Particular investigations and hints from the literature led to suggest that Magnesium deficiency in pregnancy plays a role in the development of pregnancy-induced hypertension as well as gestosis or pre-eclampsia. The integration of the already known facts about the physiopathology of Magnesium deficiency to those of the pathogenesis of gestosis led to the concept of a gestosis model which is based on Magnesium deficiency. In this way Magnesium deficiency represents the cause of (essential) gestosis. Further investigations should be done in this direction.
Female↗