Gene/Protein Disease Symptom Drug Enzyme Compound
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The rate of utero-placental blood flow depends on functional components (perfusion pressure and flow resistance within the area of the vascular bed of the placenta), as well as on morphological factors (regressive changes in the placenta). Different primary maternal conditions and diseases may lower the rate of placental flow, leading to placental insufficiency; the highest percentage, by far, of placental dysfunction is found in patients suffering from gestosis. Hypocirculation initially present in cases of EPH gestosis and caused by arteriolar spasms triggers off a vicious circle involving placental infarction and severe reduction in the utero-placental perfusion rate. This in turn leads to fetal hypotrophy, a high rate of premature births and perinatal mortality. Verification of HPL, HCG, alpha-Fetoprotein or E3 in maternal serum and amniotic fluid or urine greatly improved the recording of partial placental functions. Along with ultrasonic biometry, cardiotocography and amnioscopy, these hormonal parameters allow only indirect assessment of the placental function. On the other hand, measurements of the utero-placental flow offers a direct approach. In order to evaluate the placental flow measurements it is imperative to obtain a curve indicating the course over the last third of the pregnancy-in addition to establishing a general normal range. In case of placental insufficiency, it is necessary to determine whether this is due to functional disorders alone, or to more extenisve morphological changes. A placental perfusion test (PPT) was developed in order to make this distinction. Beta2-mimetic treatment is indicated if functional factors predominate, whereby it appears essential to obtain the requisite experimental data for precise quantification of beta-mimetic action.
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PMID:[New aspects in diagnosis and therapy of placental insufficiency. Placental perfusion measurements; placental perfusion test (PPT) and betamimetic long term treatment (clinical and experimental data (authors transl)]. 1 7

Despite scientific advances in obstetrics, maternal mortality is still a serious problem in many countries. This paper analyzes the causes of maternal mortality in Kaplan Hospital since its opening in 1954 up to 1976. 27 women died during this period; total number of deliveries was 63,997. The period was divided into 3: 1954-61, with a mean number of deliveries of 2386 per year; 1962-71, with a mean number of deliveries of 2308 per year; and 1972-76, with a mean number of deliveries of 4244/year. Maternal mortality for the 1st period was 4.9/10,000; in the 2nd, 4.3/10,000 and in the last, 3.0/10,000. Confidence limits based on the Poisson distribution method was used to test for statistical significance. Causes of direct maternal death included: 1) vascular accidents (amniotic fluid embolism and disseminated intravascular clotting) which accounted for almost 1/3 of all cases; 2) infection; 3) EPH gestosis or toxemia of pregnancy; 4) hemorrhage; and 5) anesthesia. Indirect causes of death included cardiac cases, followed by pulmonary embolism, cerebrovascular andirenal diseases, in decreasing order of importance. Older age and parity did not affect incidence of obstetric deaths. This report indicates a definite decline in maternal mortality for the 3 periods. The decline was attributed to liberal use of better antibiotics, emphasis on aseptic techniques, better antenatal care and well-equipped operating theaters. Nevertheless, vascular accidents remain the major direct cause of maternal deaths. Further research should be done on vascular accidents and its prevention; a healthy respect for the use of ceasarian sections may also be helpful in reducing further maternal deaths.
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PMID:Maternal mortality in an Israeli hospital: a review of 23 years. 4 62

Serum, cord blood and amniotic fluid beta2-microglobulin contents were measured from normal pregnancies complicated by EPH gestosis, Rh immunisation and pathological serum levels of HPL and alpha1-fetoprotein. We found no changes in high risk pregnancies from normal serum levels. beta2-microglobulin seems to be no parameter in managing complicated pregnancies and fetal growth retardation.
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PMID:[Serum, cord blood and amniotic fluid concentrations of beta2-microglobulin in patients with normal and complicated pregnancies (author's transl)]. 7 88

The maternal Serum concentrations of beta 1 SP 1, IgM and alpha 2-macroglobulin were determined in relation to the gestation age, using the simple radial immunodiffusion method in 102 non-pathologic pregnancies and 35 pregnancies involving risk factors. To assess the clinical relevance of these determinations, we examined to what extent the changes in concentration of beta 1 SP 1 IgM and alpha 2-macroglobulin would permit a prognostically useful conclusion on the placenta function and foetal condition. All patients with lowered beta 1 SP 1-serum concentrations were examined for their antepartua CTG-evaluation, as well as the type of termination of parturition. The normal distribution for beta 1 SP 1 showed a continuous rise in serum concentration up to the 37th pregnancy week. During the last 3 weeks, beta 1 SP 1 remained almost constant. For the cases with EPH-gestosis and placenta insufficiency, a beta 1 SP 1-concentration below the normal distribution level was found in the large majority of all cases. In diabetes mellitus during gravidity, twin gravidity and MHN, the determination of beta 1 SP 1 is not of any decisive prognostic significance. The maternal serum levels of IgM showed no significant differences when comparing normal pregnancy and risk pregnancy. The serum concentration of alpha 2-macroglobulin increased in both groups of patients with increasing gestation age. Of the three examined protein bodies, we consider beta 1 SP 1 to be a good, additional parameter for the assessment of the trophoblast function.
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PMID:[Comparative examinations of high-molecular maternal serum protein bodies during pregnancy--a contribution to biochemical pregnancy control (author's transl)]. 9 88

We studied reactivity of highly purified pituitary hormones in our human calcitonin (hCT) radioimmunoassay (RIA) which can detect 1 pg of hCT. ACTH at doses of greater than 1 microgram of peptide per RIA tube reacted in the hCT assay, as did beta-endorphin (beta EPH) at a dose of 10 micrograms per tube. No reactivity was observed with comparable concentrations of all other known pituitary hormones. ACTH also reacted at doses greater than 1 microgram per tube with 7 other hCT antisera which recognized differing antigenic determinants in the calcitonin molecule but it was not reactive with 2 antisera against porcine calcitonin or 2 antisera against salmon calcitonin. This slight degree of cross-reactivity of hACTH and beta EPH in the hCT RIA cannot account for the presence of immunoreactive CT in pituitary glands. Nevertheless, antisera used for the localization of peptides must be rigorously tested for the existence of cross-reactivities with other possible substances, especially if such antisera detect the peptide in unexpected tissues.
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PMID:Reactivity of ACTH and synthetic ACTH peptides with antisera to human calcitonin. 23 Feb 60

On healthy individuals fibrin(ogen) split products cannot be demonstrated in the blood. Catabolic products of fibrin and fibrinogen appear in the blood in case of general fibrinolysis, consumption coagulopathy with secondary fibrinolysis as well as local fibrin films with secondary fibrinolysis. The regular routine determination of fibrin(ogen) split products in serum or urine may indicate starting complications of many diseases. The appearance of these split products in case of renal affections indicates acute and active processes on the kidneys themselves; fibrin films appear in case of acute and chronic glomerulonephritis, casting-off crises on renal transplants, EPH gestosis, renal phlebothrombosis, hemolytic-uremic syndrom and occasionally urinary tract infections. The demonstration of fibrin(ogen) split products in serum or urine allows the following conclusions: a) acute and active process on the kidneys themselves; b) HMWS in urine indicate a fibrin film in the kidneys; c) an immediate beginning of an anticoagulation therapy; d) good possibilities to judge the therapeutic effect and by this the further progress of disease.
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PMID:[Fibrin (ogen) Split products of nephropathies]. 23 43

In 130 pregnant women (41 without complications, 40 with prematurity, 49 with EPH-Gestosis) Serumferritin, ferrochelatase (FCH), delta-aminolaevulinic-aciddehydratase (D-ALA-D), porphobilinogendeaminase (PBG-D) as well as hematologic routine parameters were measured. Regarding serumferritin, both uncomplicated and cases with pathologic conditions revealed a significant decrease in group II (28th week of pregnancy) as compared to group I (12th to 28th week of pregnancy). Women with EPH-Gestosis showed the lowest values. Activities of hemesynthesizing enzymes did not show any significant differences, neither between the two groups nor between uncomplicated and pathologic cases. Compared to healthy, non pregnant women; in pregnant women we found a significant increase in D-ALA-D and PBG-D, but a significant decrease in FCH. Enzyme pattern in pregnancy reveals an increased synthesis of porphobilinogen and an increased conversion of porphobilinogen to porphyrin. The low activity of FCH we measured in our study could be a reason for the elevation of free protoporphyrin in the erythrocytes.
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PMID:[Heme synthesis and iron status in pregnancy]. 29 36

Disorders associated with hypertension during pregnancy, which are often linked with oedema and/or proteinuria and are variously termed toxaemia of pregnancy, EPH gestosis, pre-eclampsia, and eclampsia, are of unknown etiology, although they have been known for a long time and many attempts have been made to classify and explain them. In this paper, the author draws attention to the problems of standardizing values for blood pressure, proteinuria, and oedema and of determining their value in the diagnosis of the disorder. Different classification schemes are described and the problems of comparison between them are stressed. The frequency of the hypertensive disorders of pregnancy in different countries and groups at special risk are discussed. Finally, recommendations are made on the types of research and health care needed to combat the problem.
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PMID:Epidemiology of the hypertensive disorders of pregnancy. 31 51

An account is given of some topical aspects relating to immunology of pregnancy, with reference being made to more recent literature. Included are hypothetical considerations on undisturbed embryonic development, the barrier function of the placenta, the ontogenesis of the immune system, immunosuppressive factors of pregnancy serum, the macrophage function of placental cells, pregnancy proteins, and immunological peculiarities of EPH gestosis.
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PMID:[Immunology of pregnancy -- more recent aspects of immunological mother-child relations (author's transl)]. 39 35

In electron microscopic observations on the villous cytotrophoblast in pathologic human placentas we find, besides a general increase of the amount of Langhans cells, significant ultrastructural differences according to the different diseases in pregnancy. Diabetes mellitus: the most striking observations are small, extremely electron dense mitochondria and a lot of intracellular filaments in a hydropic cytoplasm. Rh-incompatibility: according to the stage of placental damage the Langhans cells show a different structure. In light cases we find hydrolic cells with normal mitochondria as well as swollen ones. The plasmalemm shows a lot of foldings and dentations with the syncytium. In serious cases of rh-incompatibility the Langhans cells cover the trophoblastic basal membrane completely. Their electron density is even higher than that of the syncytium. Characteristic lysosomes appear. In the most serious cases the syncytium is completely destroyed and maximal hydropic Langhans cells cover the villi. EPH-gestosis: the Langhans cells show different phases of differentiation, but no other characteristic criteria. The importance of the Langhans cells for the regeneration of the syncytotrophoblast is discussed. Mitochondria and rough endoplasmic reticulum are obviously not formed in the syncytium but they must be regenerated by taking up Langhans cells by syncytial fusion.
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PMID:[The ultrastructure of Langhans cells in pathologic human placentas (author's transl)]. 40 85


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