We studied the effects of caffeine ingestion during pregnancy. A total number of 9,921 healthy pregnant women with a gestational age after 24 weeks were subjected to the study. The women who drank more than 5 cups of coffee per day had a high incidence of impending abortion, premature labor, and fetuses small for gestational age. The heavy coffee drinkers among the pregnant women had high rates of spontaneous abortion, chromosomal abnormality and congenital multi-anomalies. However, we would like to stress that the multiple socioeconomic variables might be more important than any direct effect of caffeine.

We measured FSH and LH concentrations by RIA in 130 cord sera and 213 peripheral sera obtained as serially as possible from 67 infants who were 5-75 days old and were born between the 28th and 42nd gestational weeks. Cord serum FSH and LH (+hCG) levels were 3.9-13.6 mIU/ml and 43.3-88.6 mIU/ml, respectively; they decreased with advancing gestational age. Postnatal FSH levels in male infants maintained low levels (3.7-8.7 mIU/ml). However, those in female infants increased with peak levels (51.8-270.3 mIU/ml) between 11 and 30 days after delivery, and then decreased; the surge was more marked and prolonged in preterm infants than in term infants. Postnatal LH levels in both sexes decreased rapidly after birth, which may be due to a decrease of placental hCG, and thereafter displayed patterns similar to FSH levels. We found a significant sex difference of serum gonadotropin levels in newborn infants and differences between term and preterm infants. Our results suggest that the sex difference of pituitary gonadal function exists and that the function matures during the fetal and neonatal life.

Brain natriuretic peptide (BNP) was increased in many hypertensive subjects. In this study, we have evaluated maternal, umbilical plasma and amniotic fluid BNP and atrial natriuretic peptide (ANP) in 19 normotensive pregnant women and in 35 preeclamptic patients. The maternal plasma and umbilical cord plasma ANP (p < 0.05) and BNP (p < 0.005) levels were significantly higher than those in normal pregnancy. There was no significant correlation among ANP level, BNP level, clinical symptoms and laboratory examinations. It is suggested that ANP and BNP may be rather a sequel to preeclamptic pathophysiological changes, and may not play an important role as the etiological factor of preeclampsia.

Laminin is a large noncollagenous glycoprotein localized in the trophoblast and glomerular basement membrane. We measured laminin levels in maternal serum, umbilical cord serum and amniotic fluid, both from preeclamptic and normal pregnant women, by enzyme immunoassay. The serum laminin levels in the preeclamptic group were significantly (p < 0.05 to p < 0.01) higher than those in the normal pregnant group. It has been suggested that laminin plays an important role in implantation of the placenta during early pregnancy. In this study, the amniotic-fluid laminin level at term was found to be lower than maternal serum laminin. We postulate that laminin may not have an important role in the maintenance of late pregnancy. There was a significant positive correlation between maternal serum laminin levels and serum uric acid levels. There was no significant correlation between maternal serum laminin level and blood pressure, urinary protein concentration, or any other laboratory data. These results suggest that there is damage of glomerular and placental spiral arteries in preeclampsia.

Plasma renin activity , plasma concentratrions of angiotensin 11(AngII), stable metabolites (6-keto-prostaglandin Fla : 6-keto-PGFIa) of prostacyclin (PGI2) and a metabolite (thromboxane B2: TXB2) of thromboxane A2 (TXA2 ) were measured with radioimmunoassay(RIA) in 107 normal pregnancy (control) and 139 preeclamptic patients in 28-41 gestational weeks. PRA and 6-ketoPGFIa were significantly higher and AngII was slightly higher in preeclampsia than in control, and TXB2 was significantly lower in preeclampsia in control. The ratio of 6-keto-PGFIa/TXB2 was significantly lower in preeclampsia than in control. These data suggest that the changes in the renin-angiotensin system may not be primary alterations in preeclampsia. It can be speculated that in preeclampsia the changes in absolute concentrations of 6-keto-PGFIa and TXB2 are less important than the decrease in the ratio of the 6-keto-PGFIa/TXB2. plasma renin activity ; angiotensin II ; prostacyclin ; tromboxane A2; preeclampsia The renin-angiotensin system is known to play an important role in the maintenance of normal blood pressure and it has been shown that women who have, or are destined to develop, preeclampsia show an increased sensitivity to infused angiotensin II (Gant et al. 1976). This effect can be abolished by the administration of prostaglandin E2 or induced by the prior administration of an inhibitor of prostaglandin synthetase (Everetta et al. 1978). It is well established that vasocon-striction in the arteriolar bed, particularly in the uterus and kidney, is a characteristic feature of preeclampsia. Thromboxane A2 (TXA2) and prostacyclin (PGI2) are potent vasoactive compounds. TXA2 causes vasoconstriction and induces platelet aggregation, whereas PGI2 has the opposite properties (Moncada and Vane 1978). Other studies with isolated tissues have shown that there

To clarify the possible role of elevated atrial natriuretic peptide (ANP) in the pathophysiology of preeclapmsia, we measured ANP, renin activity (PRA), angiotensin II (Ang II), TXB2 (a stable metabolite of TXA2) and 6-keto-PGFIa (a stable end product of PGI2) concentrations in the plasma of 19 normal pregnant women and 35 severe preeclamptic patients at term. Plasma ANP levels in the preeclamptic patients (n = 35, 71.5 + 3.8 pg/ml, mean+ s.E.) and also umbilical plasma ANP (n = 35, 83.0± 4.2 pg/ml) were significantly (p <0.01) higher than those of normal pregnant women plasma (n=19, 58.7± 3.7 pg/ml) and umbilical plasma (n =19, 47.6±4.7 pg/ml ). There was a significant (p <0.01) positive correlation between maternal ANP levels and fetal ANP levels (n = 54, r = 0.44). Plasma PRA and 6-keto-PGFIa levels in preeclampsia were significantly (p <0.05) lower than those of normal pregnancy. The ratio of 6-keto-PGFIa/TXB2 in preeclampsia was significantly (p <0.01) lower than that of normal pregnancy as we reported previously. There was no significant correlation between plasma ANP level and plasma PRA, Ang II, plasma TXB2 and 6-keto-PGFI a concentrations. Moreover there was no significant correlation between plasma ANP level and the severity of preeclampsia. These data suggest the possibility of a transplacental crossing of ANP secreted by feto-placental unit, which might be, at least in part, responsible for the high ANP levels observed in preeclampsia. The ANP in preeclampsia is not related directly to hypertension, but it may play a substantial role in the regulation or normalization of blood volume and vascular reactivity.atrial natriuretic peptide ; plasma renin activity ; preeclampsia ; Prostacyclin ; thromboxane A2 Atrial natriuretic peptide (ANP) is a peptide, synthesized and released from

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Using a highly sensitive immunoradiometric assay kit for human TSH, we measured TSH concentrations in unconcentrated amniotic fluids in normal pregnancies and those complicated for example by maternal hyper- and hypothyroidism, and compared them with those in maternal and cord sera. In normal pregnancies the mean concentration of TSH in amniotic fluid samples was 0.129 microU/ml, ranging from 0.065 to 0.278 microU/ml. In patients with premature delivery, the amniotic fluid TSH concentration was higher at 0.218 microU/ml. In four patients with abnormal thyroid function, TSH in amniotic fluid changed in parallel to that in cord serum, and there was a significant positive correlation between the two. No such correlation was observed between the concentrations of TSH in amniotic fluid and maternal serum. These results suggest that TSH in human amniotic fluid reflects fetal rather than maternal thyroid function and that the determination of TSH levels in amniotic fluid is useful in the diagnosis of abnormal thyroid function in fetuses.