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[Clinical significance of matrix metalloproteinase-9/tissue inhibitors of matrix metalloproteinase -1 imbalance in maternal serum, amniotic fluid, umbilical cord serum in patients with premature rupture of the membranes].

OBJECTIVE: To investigate the roles of matrix metalloproteinase (MMP)-9 and tissue inhibitors of matrix metalloproteinase (TIMP)-1 in maternal serum, amniotic fluid and umbilical cord serum in predicting premature rupture of the membranes (PROM) and chorioamnionitis. METHODS: The levels of MMP-9 and TIMP-1 were detected by enzyme linked immunosorbent assay in maternal serum, amniotic fluid, umbilical cord serum of 58 pregnant women with PROM and 38 women with normal pregnancies. Chorioamnionitis was histopathologically confirmed after delivery. RESULTS: (1) The levels of MMP-9 in maternal serum, umbilical cord serum and amniotic fluid were (141.9 +/- 84.6) ng/L, (138.2 +/- 81.4) ng/L and (85.6 +/- 27.5) ng/L respectively, significantly higher in patients with PROM than those of the control group (P < 0.05, P < 0.05 and P < 0.01 respectively), while the levels of TIMP-1 in maternal serum, amniotic fluid and umbilical cord serum were (378.1 +/- 220.2) ng/L, (44.6 +/- 24.0) ng/L and (257.2 +/- 98.8) ng/L respectively, significantly lower in patients with PROM than those of the control group (P < 0.05, P < 0.05 and P < 0.01 respectively). (2) The longer the duration from rupture of membranes to delivery was, the more serious chorioamnionitis was, and the higher the levels of MMP-9 and the lower the TIMP-1 levels in maternal serum, amniotic fluid, and umbilical cord serum were. (3) The levels of MMP-9 in maternal serum, umbilical cord serum and amniotic fluid were (183.8 +/- 84.7) ng/L, (171.2 +/- 92.9) ng/L and (95.5 +/- 21.1) ng/L respectively, significantly higher in patients with chorioamnionitis than those of non-chorioamnionitis (P < 0.05, P < 0.05 and P < 0.01 respectively), while the levels of TIMP-1 in maternal serum, amniotic fluid and umbilical cord serum were (269.7 +/- 144.4) ng/L, (32.1 +/- 16.6) ng/L and (210.6 +/- 81.9) ng/L respectively, significantly lower in patients with chorioamnionitis than those of non-chorioamnionitis (P < 0.05, P < 0.05 and P < 0.01 respectively). (4) The levels of MMP-9 in maternal serum, umbilical cord serum and amniotic fluid were (234.4 +/- 79.4) ng/L, (222.1 +/- 120.1) ng/L and (108.5 +/- 42.2) ng/L respectively, significantly higher in neonates whose Apgar score < or = 7 than those of neonates whose Apgar score > or = 8 (P < 0.05, P < 0.05 and P < 0.01 respectively), while the levels of TIMP-1 in maternal serum, amniotic fluid and umbilical cord serum were (225.3 +/- 121.7) ng/L, (25.2 +/- 15.8) and (181.7 +/- 135.2) ng/L respectively, significantly lower in neonates whose Apgar score < or = 7 than those of neonates whose Apgar score > or = 8 (P < 0.05, P < 0.05 and P < 0.01 respectively). CONCLUSIONS: It is suggested that preterm PROM is associated with increased MMP-9 and decreased TIMP-1 levels. MMP-9 and TIMP-1 are valuable clinical biological markers for identifying chorioamnionitis and predicting neonates prognosis.

Adult↗

Disposition of ethanol in maternal blood, fetal blood, and amniotic fluid of third-trimester pregnant ewes.

The disposition of ethanol in maternal arterial blood, fetal arterial blood, and amniotic fluid of nine conscious, cannulated pregnant ewes (128 to 137 days' gestation) was determined for 1-hour maternal intravenous infusion of ethanol, 1 gm/kg maternal body weight. The maternal arterial blood and fetal arterial blood ethanol concentration-time curves were virtually superimposable up to 14 hours. The apparent zero-order ethanol elimination rates for maternal arterial blood and fetal arterial blood were similar. There was a time lag in the transfer of ethanol into amniotic fluid relative to fetal arterial blood, and the peak ethanol concentration in amniotic fluid was significantly lower than the concentrations in maternal arterial blood and fetal arterial blood. The apparent zero-order ethanol elimination rate for amniotic fluid was slower, but not significantly so, compared with the ethanol elimination rates for maternal arterial blood and fetal arterial blood. Ethanol-derived acetaldehyde was found in maternal arterial blood, fetal arterial blood, and amniotic fluid at concentrations at least 1000-fold lower than the respective ethanol concentrations. The data indicate that, for administration of this ethanol dosage regimen to the third-trimester pregnant ewe, there is rapid, bidirectional placental transfer of ethanol; elimination of ethanol from the fetus is regulated primarily by maternal elimination of ethanol; the amniotic fluid may serve as a reservoir for ethanol in utero; and there is appreciable acetaldehyde-metabolizing capacity.

Acetaldehyde↗

Fetal intestinal microvilli in human amniotic fluid.

The intestinal microvilli of fetal origin in human amniotic fluid were purified by Ca2+ precipitation of contaminating organelles followed by differential centrifugation of microvillar membranes. In the purified preparation, the specific activity of the microvillar marker-enzymes maltase and sucrase increased about 77-fold over that in cell-free amniotic fluid. Significant contamination of the purified preparation by endoplasmic reticulum (microsomes) and lysosomes was ruled out on the basis of a low content of the marker enzymes glucose-6-phosphatase (microsomes) and acid phosphatase (lysosomes). Amniotic fluid microvilli contain typical enzymes of the fetal intestine including maltase, sucrase, trehalase, alkaline phosphatase and gamma-glutamyltransferase, and their morphology by electron microscopy resembles that of vesiculated intestinal microvilli. Prenatal detection of genetic diseases due to a deficiency of a protein expressed in these membranes or associated to abnormal microvilli seems feasible.

Acid Phosphatase↗

Interference by endogenous glycerol in an enzymatic assay of phosphatidylglycerol in amniotic fluid.

We investigated the possibility of interference by endogenous glycerol with the enzymatic measurement of phosphatidylglycerol in amniotic fluid. Phosphatidylglycerol is an important indicator of fetal lung maturity. The concentrations of glycerol and phosphatidylglycerol in amniotic fluid were measured by using a coupled enzymatic assay with and without phospholipase D (EC 3.1.4.4). The precision of the assay was acceptable (within-run CV = 1.2%, between-run CV = 4.8%). Endogenous glycerol content was demonstrated to be approximately 10-20 times that of phosphatidylglycerol. This high proportion of endogenous glycerol in amniotic fluid would preclude the accurate enzymatic determination of amniotic fluid phosphatidylglycerol unless the glycerol is first removed. Nor can the actual phosphatidylglycerol concentration be determined by subtracting the endogenous glycerol concentration from the total glycerol, which includes that glycerol derived from phosphatidylglycerol. With a usual range of 9 +/- 7 mumol/L, the error for a given phosphatidylglycerol measurement of +/- 6.6 mumol/L (+/- 2 SD) clearly is too high for this assay to be clinically useful. There was no correlation between concentration of endogenous glycerol or apparent phosphatidylglycerol in amniotic fluid and the lecithin/sphingomyelin ratio of the sample.

Amniotic Fluid↗

Acid- and alkaline phosphatase in amniotic fluid in normal and complicated pregnancy.

171 samples of amniotic fluid were obtained by abdominal amniocentesis from 67 women with complicated pregnancies (isoimmunization, diabetes mellitus or toxaemia). The levels of heat-labile alkaline phosphatase (HLAP), heat-stable alkaline phosphatase (HSAP) and acid phosphatase (AcP) were determined and compared to the enzyme levels in 179 samples from women with normal pregnancies of corresponding gestational ages. HLAP showed two "peaks" of activity, one in the 5th-22nd week and the other at term. HSAP and AcP showed increased activity at term. HSAP was decreased (p less than 0.01) in isoimmunization between the 36th and 40th week. 11 cases of toxaemia with placental insufficiency showed no differences in the levels of HLAP and HSAP compared with normal pregnancy. AcP showed no differences between normal and complicated pregnancy. Samples contaminated by blood showed no significant increase in the acid- and alkaline phosphatase levels. Samples contaminated by meconium showed a complex pattern. Some samples had normal enzyme levels, some had high levels of HLAP only and some had high levels of HSAP and AcP. The origin of the enzymes is not known with certainty. HSAP in amniotic fluid is most likely not of placental but intestinal origin. Determinations of acid- and alkaline phosphatase in amniotic fluid seem to be of little values in the clinical management of complicated pregnancy.

Acid Phosphatase↗

Early amniocentesis: effect of removing a reduced volume of amniotic fluid on pregnancy outcome.

In mid-trimester amniocentesis (MTA), 12-15 ml of amniotic fluid is aspirated for cytogenetic analysis. When a similar volume of amniotic fluid is removed by early amniocentesis (EA), it represents a significant proportion of the total amniotic fluid volume in the first trimester. The fluid depletion, which may persist for 7 to 10 days, is considered to impair development of fetal lungs and extremities and, possibly, contribute towards procedure-related congenital abnormalities and miscarriages. By only removing 7 ml of amniotic fluid, we have demonstrated a total miscarriage rate (3.8 per cent) comparable with previous large studies (Table V), a low incidence of respiratory difficulties at birth (2.7 per cent) and a low incidence of fixed flexion deformities (1.6 per cent), at the expense of a small increase in the incidence of culture failure (2.2 per cent).

Abortion, Spontaneous↗

Improved thin-layer chromatography of disaturated phosphatidylcholine in amniotic fluid.

We describe an indirect test of fetal lung maturity: the quantitation of disaturated phosphatidylcholine in amniotic fluid. The lipids in samples of amniotic fluid from 172 patients were reacted with osmium tetroxide, and disaturated phosphatidylcholine was then isolated by thin-layer chromatography. Interfering substances were retained by a pre-adsorbent layer. The charred disaturated phosphatidylcholine, quantitated by densitometry, was compared to standard dipalmitoyl phosphatidylcholine. Both within-run and between-run coefficients of variation were about 10%. Blood and meconium do not interfere. Six infants developed respiratory distress when disaturated phosphatidylcholine concentrations of amniotic fluid drawn within 72 h of delivery were less than 5.5 mg/L. A concurrently determined lecithin/sphingomyelin ratio falsely predicted lung maturity in one of these. In seven other samples for which lecithin/sphingomyelin ratios suggested lung immaturity but disaturated phosphatidyl-choline predicted maturity, none of the infants developed respiratory distress. In normal pregnancies, measurement of disaturated phosphatidylcholine in amniotic fluid appears to be a better predictor of fetal lung maturity than is measurement of the lecithin/sphingomyelin ratio. Further studies are needed to determine if this analysis is a better predictor in diabetic pregnancies.

Amniotic Fluid↗

Alpha1-antitrypsin in amniotic fluid and cord blood of preterm infants with the respiratory distress syndrome.

Total protein, alpha1-antitrypsin, and alpha2-macroglobulin were measured on amniotic fluid in 125 pregnancies between 11 and 42 weeks' gestation, and on the cord blood of 66 newborn infants. Amniotic fluid surface active material was assessed by the foam stability test. Amniotic fluid alpha1-antitrypsin is linearly and directly related to amniotic fluid total protein (r = 0.703, p less than 0.001). The cord alpha1-antitrypsin is also linearly related to cord total protein. Intrapartum complications are associated with a significant lowering of the cord alpha1-antitrypsin. Infants with a negative foam stability test had RDS regardless of the amniotic fluid alpha1-antitrypsin. The cord blood alpha1-antitrypsin value did not appear to be related to amniotic fluid surface active material. There were 23 infants with cord alpha1-antitrypsin of less than 0.2 gm/dl and with an intermediate or positive foam stability test; 19 of them had respiratory difficulties of varying severity. It is conceivable that infants, in spite of apparent adequate prenatal lung surfactant, develop respiratory disturbances on the basis of pulmonary fluid and protein transudation and/or reduction or inhibition of pulmonary surfactant incident to intrapartum complications.

Amniotic Fluid↗

Amniotic fluid tumor necrosis factor-alpha is a marker for the prediction of early-onset neonatal sepsis in preterm labor.

BACKGROUND: Our purpose was to determine whether amniotic fluid concentrations of tumor necrosis factor-alpha are of value in the prediction of early-onset neonatal sepsis (proven or suspected) in patients with preterm labor and intact membranes. METHODS: The relationship between amniotic fluid tumor necrosis factor-alpha concentrations and early-onset neonatal sepsis was examined in 59 consecutive patients with preterm labor and intact membranes who delivered preterm neonates within 72 h after transabdominal amniocentesis. Early-onset neonatal sepsis was defined either as the presence of a positive blood culture or as suspected sepsis within 72 h of delivery. Tumor necrosis factor-alpha was determined by enzyme-linked immunosorbent assays. RESULTS: Patients delivering neonates with early-onset neonatal sepsis had significantly higher median amniotic fluid TNF-alpha concentrations than patients delivering neonates without early-onset neonatal sepsis (p < 0.0005). An amniotic fluid tumor necrosis factor-alpha concentration > or =41 pg/ml had a sensitivity of 82% (23/29) and specificity of 79% (38/48) in the prediction of early-onset neonatal sepsis. Multiple logistic regression indicated that elevated amniotic fluid tumor necrosis factor-alpha (> or =41 pg/ml) was the only independent predictor of early-onset neonatal sepsis (odds ratio 12.9, 95% confidence interval 1.3-125.3, p=0.01) after correction for known confounding variables. CONCLUSIONS: (1) Amniotic fluid tumor necrosis factor-alpha is a marker for the prediction of early-onset neonatal sepsis in patients with preterm labor and intact membranes. (2) Amniotic fluid tumor necrosis factor-alpha is a better independent predictor of early-onset neonatal sepsis than placental histologic finding or amniotic fluid culture.

Adult↗

Factor IX and prothrombin in amniotic fluid and fetal plasma: constraints on prenatal diagnosis of hemophilia B and evidence of proteolysis.

Potential limitations of prenatal diagnosis of hemophilia B, as compared to hemophilia A, include (1) occurrence of far more frequent defects with abnormal circulating antigen, (2) lower levels of factor IX in fetal plasma at 16 to 20 weeks gestation, and (3) the presence of factor IX antigen in amniotic fluid. In addition, proteolysis could occur, especially with amniotic fluid contamination of fetal plasma. A sensitive polyclonal immunoradiometric assay for factor IX antigen was used to characterize the range of levels in amniotic fluids and fetal plasma samples. To assess for altered forms, factor IX species were compared to those of a homologous clotting factor, prothrombin. Fourteen postmortem abortus blood samples from fetuses of 14 to 23 weeks gestation had factor IX antigen levels that averaged 5.1 U/dL and ranged from 1.7 to 15 U/dL. Amniotic fluid factor IX antigen averaged 2.9 U/dL, with a range from 1.4 to 8.5 U/dL in 19 separate amniocentesis samples. Thus, in a male fetus at risk of hemophilia B and with a low circulating level of gene product, mixture of fetal plasma with amniotic fluid could severely limit prenatal diagnosis, assuming that the amniotic fluid factor IX is of maternal origin. Despite rapid processing of amniotic fluid samples, the prothrombin was extensively cleaved, suggesting that it had been activated in vivo. On gel electrophoresis of amniotic fluid samples, however, factor IX was only minimally cleaved. In the postmortem fetal blood specimens, prothrombin was partially cleaved. On crossed-immunoelectrophoresis, fetal plasma prothrombin showed decreased migration in calcium, compared to EDTA, indicative of mature gamma-glutamyl carboxylation. The latter presumably resulted from fetal hepatic synthesis.

Amniotic Fluid↗

Prenatal diagnosis of the fragile X syndrome: possible end of the experimental phase for amniotic fluid.

We have had experience with 260 prenatal diagnosis cases for the fragile X syndrome [fra(X)]; amniotic fluid was received in 230. There was a documented family history of fra(X) in 148 amniotic fluid cases. Our sample includes 91 males. Eleven were correctly identified as fra(X)-positive and 2 were false-negative. Eight of 57 females were fra(X) positive and one was a false-negative. CVS were received in 21 cases with a family history of fra(X), and there were 2 positive results in females and 3 false-negative results in males which were ultimately detected by means of molecular analysis or a subsequent amniotic fluid specimen. RFLPs were utilized in 29 cases (amniotic fluid and CVS); RFLPs identified 2 false-negative cytogenetic results in CVS. Two male fetuses were found to have a high probability of being affected by means of RFLPs, but on the basis of prenatal and postnatal negative fra(X) cytogenetic results and subsequent normal growth and development, they are either unaffected transmitting males or are double recombinants. Three female fetuses were also found to be cytogenetically negative in CVS but had a 90%, 93%, and 99% probability of being affected by RFLPs. On the basis of the data, it can be concluded: 1. Amniotic fluid experience is adequate to eliminate the "experimental" designation providing the limitations are understood and an experienced laboratory is involved. 2. Chorionic villus cells for cytogenetic analysis should still be considered experimental. 3. Negative results with CVS should be confirmed by molecular methods and/or by cytogenetic analysis of another tissue. 4. Multiple approaches can maximize reliability of fra(X) prenatal diagnosis.

Amniocentesis↗

Relative amounts of sialic acid and fucose of amniotic fluid glycoconjugates in relation to pregnancy age.

The present knowledge concerning the glycan structures and role of glycoconjugates derived from amniotic fluid is fragmentary and mainly focuses on the individual glycoproteins. The question has arisen as whether the general glycosylation pattern of amniotic fluid glycoconjugates can change with the progression of a normal pregnancy. In the present work we have described the dynamic, quantitative alterations in relative amounts of sialic acid and fucose linked by a variety of anomeric linkages to subterminal oligosaccharide structures of amniotic fluid glycoconjugates in relation to pregnancy age. The analysis was performed in the following groups of amniotic fluids derived from normal pregnancy by lectin dotting method: "2nd trimester" (14-19 weeks), "3rd trimester" (29-37 weeks), "perinatal period" (38-40 weeks) , "delivery at term" (39-41 weeks) and "post date pregnancy" (41-43 weeks). In the "3rd trimester" the amniotic fluid glycoconjugates contained higher relative amounts of glycans terminated by alpha2-6-linked sialic acid (p < 0.00002) and by alpha1-6 innermost fucose (p < 0.000001) than those in the 2nd trimester. In contrast, they showed the lower relative amount of fucose linked alpha1-3 (p < 0.02). At the perinatal period the relative amount of alpha2-6-linked sialic acid increased (p < 0.03), and it then decreased during delivery (p < 0.02) to the level found in the "3rd trimester" group. In the post date pregnancy all parameters studied increased. The sialyl- and fucosyl-glycotopes of the amniotic fluid glycoconjugates may play an critical role in growth and tissue remodeling of the foetus, as well as may might reflect maturation of a foetus. Additionally, a determination of the glycotope expressions might be helpful in prenatal diagnosis as predictor factors for well being of mother and child.

Adolescent↗

Influence of fetal gender on the concentration of interleukin-1 receptor antagonist in amniotic fluid and in newborn urine.

IL-1 receptor antagonist (IL-1ra) is a cytokine that blocks the effects of IL-1 by binding to IL-1 receptors without inducing signal transduction. Amniotic fluid contains high concentrations of IL-1ra. The purpose of this study was 1) to analyze whether factors related to the mother or the fetus influence amniotic fluid IL-1ra concentration, and 2) to study whether the fetus is a source of IL-1ra. Two hundred two specimens of amniotic fluid, as well as 21 urine samples from newborn infants, were analyzed. Women carrying a female fetus had a higher concentration of amniotic fluid IL-1ra than those carrying a male fetus (female 136.4 +/- 6.1 micrograms/L, n = 83; male 74.7 +/- 3.7 micrograms/L, n = 119; p < 0.0001, unpaired two-sided t test). Length of gestation, presence or absence of labor signs, or elevated IL-1 beta in amniotic fluid did not affect the concentration of IL-1ra in amniotic fluid. Urine of infants taken during the first 48 h of life contained a high concentration of IL-1ra (91.1 +/- 17.5 micrograms/L). The urinary IL-1ra concentration was higher in female newborns than in male newborns (females 124.0 +/- 25.2 micrograms/L, n = 11; males 54.9 +/- 19.1 micrograms/L, n = 10; p = 0.04). We conclude that 1) the concentration of IL-1ra in amniotic fluid and newborn urine is dependent on the gender of the fetus and of the newborn and 2) fetal urine is a major source of amniotic fluid IL-1ra.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗

Insulin levels in amniotic fluid of normal and abnormal pregnancies.

The normal level of insulin in amniotic fluid between the 13th and 42nd weeks of pregnancy was determined by means of 988 single analyses in individual healthy women. Insulin passes into the amniotic fluid via the fetal urine, and its level does not depend on fetal gender. Between the 13th and 25th weeks of gestation, the insulin level increases by an average of 1.3 to 5.1 microU/ml. From the 27th to the 42nd weeks, an increase of 6 to 9.1 microU/ml is observed. In the same period, the 97th percentile rises from 11.2 to 18 microU/ml. In 543 patients with pregnancy disorders, lower levels of insulin in amniotic fluid were observed in intrauterine fetal death, placental insufficiency, fetal growth retardation, and malformations. Elevated levels of insulin were observed in rhesus disease. In the treatment of pregnant women with betamimetics and glucocorticoids, the mean amniotic fluid insulin level rose to more than double the normal values.

Adrenergic beta-Agonists↗

Clara cell protein in human amniotic fluid: a potential marker of fetal lung growth.

Clara cell protein (CC16) is a 16-kD protein secreted at the surface of respiratory airways by nonciliated bronchial and bronchiolar cells, including Clara cells. Using the same immunoassay as that recently developed for CC16 in lung lavage, we have measured CC16 in amniotic fluid samples from 100 normal fetuses and 51 fetuses with various pathologies. Ouchterlony immunodiffusion analysis showed a complete identity between CC16 in amniotic fluid and the protein in lung lavages of adults. CC16 was detectable in amniotic fluid from about the 15th wk of pregnancy, then progressively increased until delivery, with a tendency to reach a plateau after the 30th wk. Between the 15th and the 39th wk of pregnancy, the concentration of CC16 in amniotic fluid increased on average 25 times. The sex of the fetus did not influence the concentration of CC16 in amniotic fluid. Compared with expected values, levels of CC16 in amniotic fluid were on average not significantly altered in cases of spina bifida (n = 9), anencephaly (n = 7), and trisomy 21 (n = 6). In contrast, CC16 was on average significantly decreased in cases of diaphragmatic hernia (n = 6), trisomy 18 (n = 14), Turner syndrome (n = 4), and diabetic pregnancy (n = 5). In cases of diaphragmatic hernia, a relation emerged between the concentration of CC16 in amniotic fluid and both the weight of the lungs and the survivorship of the fetuses. The time course of CC16 in amniotic fluid during normal pregnancy and its reduction in pathologies associated with lung hypoplasia suggest that CC16 in amniotic fluid might serve as a marker of bronchial epithelium growth.

Amniotic Fluid↗

Removal of a component interfering with phosphatidylglycerol estimation in the "Helena" system for amniotic fluid phospholipids.

A simple " prechromatography " step removes a component of amniotic fluid ("pseudo PG") that otherwise co-chromatographs with phosphatidylglycerol in the system for amniotic fluid analysis developed by Touchstone et al. (Lipids 15: 61-62, 1980) and incorporated into the Helena "Fetal-Tek" kit. The final positions of the major phospholipids are practically unchanged but the faster migrating, more neutral components are swept into a tight band near the solvent front, providing improved general resolution. The resulting change in the ratio of "phosphatidylglycerol" to sphingomyelin ("PG"/S) is as much as 0.5 for some specimens, but no change is seen for others. In 20% of the 73 cases examined, including four of the six fluids associated with respiratory distress syndrome, the PG initially reported was found to be "pseudo PG" and was completely removed by the prechromatography step. This step produces a negligible decrease in the lecithin to sphingomyelin (L/S) ratio in amniotic fluid.

Amniotic Fluid↗

Obstetric and perinatal outcome of pregnancies with term labour and meconium-stained amniotic fluid.

The purpose of this study was to evaluate the meconium staining of amniotic fluid (AF) in term of fetal distress, meconium aspiration syndrome, and perinatal morbidity and mortality. In a prospective study at Princess Badeea Teaching Hospital from April to November 1999, women with a singleton cephalic pregnancy of completed 37-42 weeks and with no pre-defined risk factor were recruited into the study. Study patients comprised 390 (10%) patients with meconium and 400 patients as controls but with clear amniotic fluid. Virtually meconium staining of the amniotic fluid was significantly associated with poor neonatal outcome in all outcomes measures assessed. Perinatal mortality increased from 2 per 1000 births with clear AF to 10 per 1000 with meconium (P<0.001). Other adverse outcomes also increased; e. g., severe fetal acidemia, Apgar score < or = 3 at 1 min and 5 min, and meconium aspiration syndrome. Delivery by cesarean section also increased with meconium from 7-14% (P<0.001). We concluded that meconium in the amniotic fluids associated with an obstetric hazard and significantly increase risks of adverse neonatal outcomes. Women with thin meconium in the presence of normal fetal heart rate can be safely managed at the clinical level. Mod-thick meconium alone should alert the obstetrician to a high risk fetal condition. Continuous fetal heart rate monitoring during labour and reassurance of fetal well-being by acid-base assessment were most significant factors in the reduction of meconium aspiration syndrome.

Adult↗

Improved one-dimensional thin-layer chromatography of phospholipids in amniotic fluid.

With this extraction procedure and chromatographic method, six amniotic fluid phospholipids [phosphatidylcholine (lecithin), sphingomyelin, phosphatidylinositol, phosphatidylserine, phosphatidylethanolamine, and phosphatidylglycerol] are completely resolved in less than 70 min from the time the specimen is received. The mobile phase (chloroform/petroleum ether/methanol/acetic acid, 5/3/1.6/1, by vol) is used with commercially available 7.5 X 10 cm silica-gel plates. The phospholipids are made visible by immersing the plate in cupric acetate/phosphoric acid. Lecithin/sphingomyelin (L/S) ratios are determined densitometrically. Rf values are well reproducible for both samples and standards, as are L/S ratios, and the method is simple and inexpensive. The relation between L/S ratios (for 100 specimens of amniotic fluid measured by this method) and fetal status is consistent with other reports. We confirm phosphatidylglycerol to be a sensitive indicator of fetal lung maturity: when it was detectable in amniotic fluid, the newborn invariably showed no symptoms of the respiratory distress syndrome.

Amniotic Fluid↗