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Fetal plasma renin activity (PRA) was measured in 42 pregnancies. Compared to control fetuses, PRA was elevated in three of four hypoxemic fetuses, in two of five with hydrops and in two of five with uropathies. PRA did not change with transfusion in seven alloimmunized fetuses. This study demonstrates PRA in human fetuses and suggests that the renin-angiotensin system can respond to stimuli in fetal life.
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To know the pathophysiological conditions of the fetus as a patient is very important for the determinations of methods of fetal diagnosis and therapy. The mechanisms by which maternal infection triggers the uterine contraction are poorly under stood. Firstly, we investigated the role of maternal endotoxin and heat stress. Studies were carried out in 6 chronically prepared, pregnant goats or sheep at 129 to 137 days gestation. Blood samples were collected for determinations of plasma interleukin-1, PGF2 alpha, cortisol and catecholamines levels from mother and fetus after infusion of 1.0 mg E. Coli endotoxin into the maternal jugular vein. From these animal experiments, it is demonstrated that maternal interleukin-1 PGF2 alpha levels tended to rise, and these endocrinological or interleukin-1 changes induced the uterine contraction during maternal hyperthermia. Recently, diagnostic technique in detections of fetal diseases have undergone a major revolution by the appearance of real-time ultrasound, predictive genetic testing using DNA prove and cordocentesis. Drug therapy and surgical therapy in the fetus have also undergone considerable changes, however, previous attempts at therapy have been generally unsatisfactory and rarely successful. Recently, we performed a new technique for dead fetus removal in utero by selective cesarean in a case of monochorionic monoamniotic twin pregnancy with intrauterine death of one twin at 28 weeks' gestation. The patient was delivered by re-cesarean section at 33 weeks' gestation on five weeks after first surgery was hospitalized for small-for-dates. Ethics in the development of fetal diagnosis and therapy are controversial. We never forget to gain from parents the informed consent.
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We have examined the relationships between maternal connective tissue disease (CTD), fetal and neonatal health, and the presence of specific autoantibodies: antinuclear antibodies (ANA), anti-Ro, antiLa, anti-Sm, anti-RNP, anti-DNA, and anticardiolipin (ACL) in 27 mothers with CTD (Group A), and 10 asymptomatic mothers of babies with complete congenital heart block (CCHB), or cardiac arrhythmias (Group B). Compared to 100 normal pregnant controls, autoantibodies were significantly more common in both Group A (96.3%, p less than 0.0005) and Group B (70%, p less than 0.0005), although the prevalence of autoantibodies in the Group A mothers having abnormal babies compared with those who had normal babies did not differ. Anti-La was present only in mothers with abnormal babies (7 of 17 compared to 0 of 10, p less than 0.025). Anti-La did not occur without anti-Ro, but anti-Ro occurred in 9 mothers without anti-La. Anti-Ro was present in the serum of all mothers of infants with CCHB and occurred alone in 3 of 4 instances. Titers of anti-Ro did not differ between abnormal and normal infants or their mothers. ACL occurred alone in the serum of 10 of 38 mothers, and was present in 7 mothers who had infants with cardiac abnormalities other than CCHB.
BACKGROUND: Embryo-fetal diseases are the consequence of prenatal (progenetic and metagenetic or environmental) and intranatal (of a traumatic, infective, toxic nature) pathological factors. In multiple pregnancies this complex etiopathogenesis also includes an altered didymous embriogenesis. This study aimed to evaluate the pathologies affecting the fetus in multiple pregnancy, a special biological situation leading to the potential onset of severe fetal and neonatal damage. METHODS: The authors studied 205 patients with multiple pregnancies, including 199 bigeminal, 5 trigeminal and 1 quadrigeminal, admitted to the Department B of the Obstetrics and Gynecological Clinic of Turin University between 1989-1999. Possible embyro-fetal damage was examined using a chronological criterion: namely following the development of the multiple fetuses from the zygotic to the neonatal phase. RESULTS: Pregnancies were biamniotic bichorionic in 54% of cases, biamniotic monochorionic in 45% and monochorionic monoamniotic in 1%. There were a total of 154 (79.38%) premature births out of 194 and neonatal birth weight was always SGA (small for gestational age). 66.84% of newborns were LBW (<2500 g) and 7.14% were VLBW (<1500 g). Fetal mortality (2.29%) was higher than early neonatal mortality (1.53%). Perinatal mortality (3.82%) was three times higher than in all neonates from the same period (1.03%). CONCLUSIONS: The severe embryo-fetal and neonatal damage found in multiple pregnancies is a clinical reality that calls for adequate diagnostic and therapeutic measures, and above all specific medical and social prevention to limit maternal pathogenic risks.
Introduction of cordocentesis into clinical practice has made progress in antenatal diagnosis and treatment of congenital (hereditary and acquired) fetal diseases. Cytogenetic, molecular biological, biochemical, and immunological studies of fetal blood have substantial advantages for prenatal diagnosis. Direct administration of blood components and drugs into fetal blood circulation is the treatment of choice in some fetal diseases, severe types of hemolytic disease. Intravascular injection of myorelaxants was shown to greatly favour long-term intrauterine interventions. The potentialities, advances, and prospects of intrauterine surgical correction of fetal developmental disorders are discussed.
We measured five hormones presumably involved in fetal homeostasis in specimens obtained by cordocentesis for clinical indications from 106 fetuses. Norms for atrial natriuretic factor, digoxin-like immunoreactive substance, plasma renin activity, norepinephrine, and epinephrine were derived from fetuses ultimately shown to be free of detectable abnormality. Atrial natriuretic factor, digoxin-like immunoreactive substance, and plasma renin activity were unrelated to umbilical vessel source or gestational age. Digoxin-like immunoreactive substance was directly related to PCO2 (r = 0.63, p = 0.02). Digoxin-like immunoreactive substance level was elevated in all fetal disease states studied except isoimmunization. The level of atrial natriuretic factor was elevated in fetuses with immune hydrops (NS). Norepinephrine and epinephrine levels were higher in the umbilical artery than in the vein (p = 0.05 and 0.006, respectively). There was a significant correlation between norepinephrine and gestational age in normal fetuses (r = 0.7637, p less than 0.025) and between both catecholamines and many of the respiratory blood gas measurements, with pH and PCO2 being the major determinants. Most disease states were associated with an elevated norepinephrine concentration. There was a negative correlation between plasma renin activity and base deficit (p less than 0.0001). Plasma renin activity was elevated in fetuses with idiopathic growth retardation and nonimmune hydrops (p less than 0.05 for each). In summary, fetal homeostasis as reflected by these five hormones was altered by a variety of disorders. With these baseline values the effects of direct or indirect fetal therapy can begin to be studied.
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A study of 103 fetal adrenals obtained from stillborn fetuses and those dying in the neonatal period was performed to assess the significance of definitive cortex cystic change, compact cell change and lipid patterns, and their relationship to other pathological processes. The findings confirm that these changes are more common in intrauterine infection and antepartum hemorrhage and are to a lesser extent complications of prematurity. They also correlate with gestational age. It is proposed that the changes seen are due to the gland being immature.
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A human glial brain cell line derived from a Tay-Sachs disease fetal cerebellum was transformed with SV-40 virus in order to obtain a transformed brain cell line which reflected the characteristics of the disease. It was shown that the transformed TSD cell line maintained an elevated level of GM2 which was similar to that shown by the nontransformed precursor. In addition, the TSD transformed line lacked hexosaminidase A.
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