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A method is described for the rapid and quantitative estimation of total amniotic fluid palmitic acid. Palmitic acid and lecithin were measured in 140 samples of amniotic fluid in normal and abnormal pregnancy, and the correlation coefficient between the two parameters was 0.93. It is concluded that amniotic fluid palmitic acid measurements are of value in the prenatal determination of fetal pulmonary maturity.
OBJECTIVES: Morphological lesions in placenta and changed metal distribution through placenta, which were observed in pregnancy exposed to tobacco smoke, could cause alternations in lysosomal enzymes secretion to amniotic fluid. DESIGN: Assessment of total activity and molecular forms of N-beta-D-acetylglucosaminidase in amniotic fluid in pregnancy with oligohydramnios or PROM. MATERIALS AND METHODS: The materials for studies were amniotic fluids collected from pregnancy with oligohydramnios and from pregnancy with PROM. Determination of N-beta-D-acetylglucosaminidase activity was performed with use of sodium salt of 3-crezolosulfthaleinyl-N-beta-D-acetylglucosamide as a substrate (test Boehringer, Niemcy). Creatinine was determined by kinetic method (test of Analco-GBG firm). Protein was determine by Bredford method. NAG-B was assessed after previous thermal NAG-A inactivation in 56 degrees C, for 2 hours and the difference between activity of total form and termostabile form of NAG were assessed. The microsomal and cytosol fractions were separated by ultracentrifugation. RESULTS AND CONCLUSIONS: The statistically significant growth of NAG activity in amniotic fluid in pregnant with oligohydramnios was observed. The cytosol form took over 90% of whole activity. The activity of NAG microsomal fraction was lower in amniotic fluid in women with PROM diagnosis. The positive coleration between NAG-A activity and the Pb level was observed in this group of women as well. In the second group of women with oligohydramnios, the positive coleration between NAG and Cd level, NAG-A and level, NAG-B and Pb level were demonstrated. Obtained results show on damage of placental and foetal membranes cell structure. It could be caused by metal ions cumulation and releasing of molecular N-beta-D-acetylglucosaminase form to amniotic fluid.
The presence of contaminating maternal cells in amniotic fluid is an important, though infrequent, cause of error in karyotyping the fetus. A method of detecting contaminating maternal cells in amniocentesis specimens by determining the HLA phenotype of the cells of amniotic fluid and the mother is described. Tissue typing of 15 amniocentesis specimens was performed, and in 14 cases the fetal origin of the cells was established. In one case, the results of tissue typing suggested maternal cell contamination, though this had not been suspected from chromosome studies of the amniotic fluid cell cultures. Other possible uses for tissue typing of amniotic fluid specimens for prenatal diagnosis are also described.
The prognostic accuracy of spectro photometric examination of the amniotic fluid and of a specific method for the determination of free bilirubin in the amniotic fluid are compared. Amniocentesis was carried out 166 times in 85 sensitized rhesus-negative pregnant women. Spectro photometric examination gave a misleading assessment in 28% of the cases. This applied particularly to Liley's Zone II, in which the presence or absence of haemolytic disease of the newborn was incorrectly predicted in up to 70% of the cases. By contrast, on evaluation of the cases using specific determination of free bilirubin, not a single value obtained after the 34th week of pregnancy led to false assessment of the fetal condition. There is a stong correlation between the extent of fetal damage and the bilirubin content of the amniotic fluid.
Clara cell protein 16 (CC16) is a major immunomodulatory protein produced in the fetal lung. We hypothesized that the mid-trimester amniotic fluid concentration of CC16 would vary according to a +38 CC16 polymorphism in the fetal genome and that increased levels would be an early indicator of subsequent adverse pregnancy outcome. Mid-trimester singleton amniotic fluids from 244 women were assayed for CC16 by ELISA. DNA from fetal cells in 179 amniotic fluids were tested for the A>G polymorphism at position +38 in exon 1 by PCR. Outcome data were obtained from 233 women after completion of laboratory testing. Median CC16 levels were higher in amniotic fluids containing male fetuses than in those with females (p=0.0005). Median amniotic fluid CC16 levels were higher in Hispanics than in Whites and Asians (p<0.05). CC16*G homozygosity was associated with elevated amniotic fluid CC16 concentrations compared to CC16*A homozygotes (p=0.02). Intraamniotic CC16 levels were highest in pregnancies that subsequently resulted in preterm premature rupture of membranes (PPROM) (p=0.01). We conclude that mid-trimester intraamniotic CC16 concentrations vary by gender, ethnicity and fetal CC16 gene polymorphism. Elevated CC16 levels are predictive of subsequent development of PPROM.
BACKGROUND AND AIM OF THE WORK: The high false-positive rate of electronic fetal heart rate monitoring is the major obstacle to the correct prediction and diagnosis of intrapartum fetal distress. Fetal pulse oximetry is a safe and accurate indicator of fetal oxygenation. The aim of this study was to evaluate the clinical use of this technique for the diagnosis of fetal hypoxia and for prevention of fetal metabolic acidosis and asphyxia during labour, in the presence of meconium-stained amniotic fluid with or without abnormal fetal heart rate patterns, using a threshold value of 30% oxygen saturation. METHODS: Fetal blood oxygen saturation levels (SpO2) of 58 term fetuses with non-reassuring fetal status were measured during labour by fetal pulse oximetry. In 35 cases the amniotic fluid was stained with meconium at onset of labour. Mean SpO2 levels at the different stages of labour were matched against fetal heart rate patterns, the amniotic fluid status, and neonatal outcome. The 35 cases with meconium-stained amniotic fluid were compared with a control group of 28 pregnant women at term who had meconium-stained amniotic fluid during labour but were not monitored by pulse oximetry. RESULTS: When the fetal heart rate tracings were abnormal, mean SpO2values were significantly lower in the first 30 minutes of application and in the last 30 minutes of labour or before Cesarean section. Meconium-stained amniotic fluid was associated with lower SpO2values only when fetal heart monitoring showed a "non-reassuring" pattern. No cases were observed with severe neonatal acidosis, with Apgar score <7 at 5 minutes, or with other adverse neonatal events. In patients with meconium-stained amniotic fluid, neonatal outcomes were better in the group monitored by pulse oximetry versus the control group, although the differences were not statistically significant. CONCLUSIONS: Continued monitoring of fetal oxygen saturation combined with fetal heart rate monitoring may improve accuracy in the evaluation of fetal well-being. As a result, labour could be more safely managed in pregnancies with non-reassuring fetal status as measured by conventional methods, especially in the presence of meconium-stained amniotic fluid.
The levels of human placental lactogen (hPL) were measured in maternal blood and amniotic fluid in normal and prolonged pregnancies. Statistical analysis of the hPL levels showed that values rose in both blood and amniotic fluid, reaching maximum levels between Weeks 34 and 36 (6.70 microgram per milliliter in blood serum, 0.85 microgram per milliliter in amniotic fluid). Thereafter, there was a decline, a significant fall occuring between Weeks 40 and 42 and in the prolonged pregnancy group (43 weeks and more) (t = 6.9 and p less than 0.001 in serum levels; t = 3.9 and p less than 0.001 in amniotic fluid levels). There was also a very close correlation (r = 021; p less than 0.005) between maternal blood and amniotic fluid hPL levels in normal pregnancies before labor.
Rat placental lactogen-II (rPL-II) and growth hormone (rGH) in maternal and fetal serum, amniotic fluid, and placental tissue were measured by a homologous radioimmunoassay during the last half of pregnancy. rPL-II appeared first in maternal circulation and the placental tissue on day 11 of pregnancy. The maternal serum rPL-II concentration increased progressively and reached the peak value (684 +/- 76 ng/ml) on day 19, and declined thereafter up to term. rPL-II content in the tissue had a similar pattern to the maternal serum profile of rPL-II, while its concentration in the tissue increased dramatically on day 12 and remained high until day 19. Fetal serum rPL-II was detected on days 17 and 18, though its concentration was much lower (ranged between 3-10 ng/ml) than that of maternal serum. rPL-II in amniotic fluid was also detectable only on days 12-14 of pregnancy, and the peak value on day 13 was 22% of the maternal serum rPL-II concentration. The rGH concentration increased gradually as pregnancy advanced with a decline on the day before parturition. Although rGH in fetal serum increased on day 20 with a decline on the following day, it was slightly detectable in amniotic fluid on the last two days of pregnancy. The molecular profile of rPL-II in amniotic fluid and maternal serum of day 13 pregnant rats were examined by Western blotting. Anti-rPL-II serum detected two proteins with molecular weights (mol wt) of 19.5K and 20.5K in amniotic fluid and one protein with a mol wt of 20.5K in maternal serum under nonreducing conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
The concentration of amniotic fluid glucose, total protein, sodium, potassium, calcium, magnesium and phosphate as well as amniotic fluid osmolality were measured in normal second trimester pregnancies and in second trimester pregnancies complecated by fetal anencephaly or spina bifida. Amniotic fluid glucose concentration was low in anencephaly, while phosphate and total protein were high; calcium concentration and osmolality were slightly elevated with spina bifida. The application of these findings to antenatal diagnosis are discussed.
Amniotic fluid was obtained from 180 patients by amniocentesis at 16-22 weeks of gestation and assayed for the levels of interleukin (IL)-6, IL-8, leukocyte elastase (LE), and glucose. Ten of cases had clinical symptoms, such as uterine contraction, genital bleeding, and cervical ripening, and the other 170 were assessed for fetal chromosomal features. Four of the ten cases with uterine contraction developed abortion, while 10 of those screened had findings of fetal chromosomal anomalies, and 7 cases then underwent induced abortion artificially. In the cases of abortion, levels of IL-6, IL-8 and LE were higher than in the samples from the 160 pregnant women without clinical symptoms and a normal karyotype, while glucose in amniotic fluid was lower. Of 6 cases with clinical symptoms, but not developing abortion, 4 developed preterm labor, and in these IL-6 and IL-8 also were significantly elevated, with LE being slight high compared to normal. The results suggest that IL-6, IL-8, LE, and glucose in amniotic fluid at early second trimester can be used as markers of severe infection in the uterus, and with the first two being particularly sensitive.
BACKGROUND: The purpose of this study was to examine (1) the association between amniotic fluid volume (AFV) and sonographically detected fetal structural anomalies, and (2) the effectiveness of using abnormal AFV as a screening test prior to patient referral for a targeted ultrasound. MATERIAL/METHODS: For singleton pregnancies in the 2nd and 3rd trimester frequencies of individual anomalies and odds ratios were calculated for each category of amniotic fluid volume relative to the frequency of anomalies with normal volume. The anomaly detection rate and frequency of referral for targeted ultrasound on the basis of abnormal amniotic fluid volume were calculated. RESULTS: 15,959 (92.0%) of patients had normal amniotic fluid volume, 537 (3.1%) decreased, 544 (3.1%) increased, 167 (1.0%) oligohydramnios, and 141 (0.8%) polyhydramnios. There were 365 (2.1%) fetuses with major structural anomalies. 1.8% of patients with normal AFV had anomalies. Anomalies were significantly more frequent in all categories of abnormal fluid: decreased (3.2%, OR 1.74, 95% CI 1.06-2.86), increased (5.7%, OR 3.22, 95% CI 2.2-4.71), oligohydramnios (9.0%, OR 5.26, 95% CI 3.09-9.05), and polyhydramnios (5.7%, OR 3.21, 95% CI 1.56-6.6). Referral for targeted ultrasound based on any abnormal AFV volume compared to only oligohydramnios or polyhydramnios increased the overall anomaly detection rate by nearly three-fold (19.5% vs. 6.3%), with minimal changes in the number of referrals per anomaly detected (13.4 vs. CONCLUSIONS: Referral for targeted ultrasound in the presence of even minor abnormalities of amniotic fluid would significantly improve anomaly detection with minimal increase in referrals.
Reported are the concentrations of beta-endorphin, beta-lipotropin, and adrenocorticotropic hormone (ACTH) in the amniotic fluid and plasma of 40 healthy pregnant women at different stages of gestation. Moreover, the amniotic fluid levels of the three peptides were evaluated in 20 other pregnant women affected by different pathologic conditions (Cooley's disease, gestosis, diabetes, placental insufficiency, etc.). A silicic acid extraction procedure was performed on the samples. Each extract was subjected to Sephadex G-75 column chromatography, and the two fractions corresponding to beta-lipotropin and beta-endorphin were collected, freeze-dried, and assayed by two specific radioimmunoassays. Levels of ACTH were measured by radioimmunoassay directly on the extracts. Levels of beta-endorphin in amniotic fluid showed the highest values in the first trimester (173 +/- 30 fmol/ml, mean +/- SEM) but were significantly decreased in the second (75.2 +/- 14) and third trimesters (14.3 +/- 1.8). An inverse trend characterized plasma levels of beta-endorphin, which showed a progressive increase from the first trimester to term (10.4 +/- 11.1). Amniotic fluid levels of beta-lipotropin remained stable during the first (48.6 +/- 6.3) and second (54.6 +/- 11.1) trimesters, but decreased significantly in the third trimester (17.9 +/- 2.3). The plasma concentrations of beta-lipotropin showed the highest levels in the first trimester (10.9 +/- 0.9), and decreased significantly at term (8.9 +/- 1.3). Last, amniotic fluid levels of ACTH decreased from 55.3 +/- 4.75 fmol/ml in the first trimester to 12.5 +/- 1.16 in the second trimester, and rose again in the third trimester to 34.4 +/- 6.6 fmol/ml. Plasma levels of ACTH were characterized in the first two trimesters by values twice those recorded for nonpregnant women, and decreased at term to 8.9 +/- 1.4 fmol/ml. In the pregnant patients with fetuses affected by Cooley's disease (second trimester) and in those with edema-proteinuria-hypertension (EPH) gestosis (third trimester), amniotic fluid levels of beta-endorphin, beta-lipotropin, and ACTH were in the same range as those in healthy pregnant women.
Circadian rhythms and hormonal interactions among the maternal, fetal, and amniotic fluid compartments were studied in long-term catheterized rhesus macaque monkeys between days 127 and 138 of gestation (term = 167 days). Blood samples were collected at 3-hour intervals for 48 hours and analyzed by radioimmunoassay for estrone, estradiol, cortisol, progesterone, dehydroepiandrosterone sulfate, and prolactin. Distinct circadian rhythms were present for cortisol and progesterone in the maternal circulation and for progesterone and dehydroepiandrosterone sulfate in the fetal circulation (p less than 0.05). Although maternal and fetal estrogen levels were higher in AM samples than in PM samples, a statistically significant circadian rhythm was not present (p greater than 0.10). Fetal levels of progesterone and dehydroepiandrosterone sulfate and maternal levels of progesterone were highest between 9:00 PM and 3:00 AM and lowest between 9:00 AM and 3:00 PM. Maternal levels of cortisol were highest between 6:00 AM and 9:00 AM and lowest between 6:00 PM and 12 midnight. The circadian patterns of maternal cortisol and progesterone were inversely related to each other (r = -0.68; p less than 0.01). Amniotic fluid cortisol levels were highest between 9:00 AM and 12 noon and lowest between 6:00 PM and 3:00 AM (p less than 0.10). With the possible exception of cortisol, amniotic fluid steroid hormones did not demonstrate distinct diurnal fluctuations, nor did they correlate with steroid changes in maternal or fetal blood. Because the rhesus placenta is permeable to glucocorticoids it is likely that transplacental passage of maternal cortisol influences the activity of the fetal pituitary and adrenal so that the circadian rhythm in the fetal axis is 180 degrees out of phase with that of the maternal axis. The circadian rhythms in fetal dehydroepiandrosterone sulfate and progesterone in late gestation parallel the biorhythm in uterine contraction frequency and amplitude, with peaks during periods of darkness between 9:00 PM and 3:00 AM.
Concentrated term amniotic fluid samples from 44 women smokers and 44 controls were investigated with respect to mutagenic effect in the Salmonella/mammalian-microsome mutagenicity test, using tester strains TA98 and TA100. Tests with freeze-dried specimens of term amniotic fluid showed increases in the number of revertant colonies over background values, regardless of smoking status. However, samples from heavy smokers produced a higher number of revertants than did samples from nonsmokers in several experiments with tester strain TA98. The increase was statistically significant, using either total tar content or number of cigarettes smoked to identify heavy smokers. Experimental series with tester strain TA100 also resulted in higher group means for heavy smokers than for nonsmokers, but the difference was not statistically significant with the concentrations used in this assay. We conclude that heavy smokers may expose their unborn children to mutagenic substances.
We have developed a high-performance liquid chromatographic (HPLC) method for the analyses of surface-active amniotic fluid phospholipids, lecithin (L), sphingomyelin (S), phosphatidyl glycerol (PG), phosphatidyl inositol (PI), phosphatidyl ethanolamine (PE), and phosphatidyl serine (PS), which are important in the prediction of fetal lung maturity. The method incorporates an internal standard in the amniotic fluid extract, and utilizes a 10-microliter aliquot of a 2:1 chloroform-methanol extract of amniotic fluid injected onto a 5-micron DIOL or CN HPLC column, and a variable-wavelength detector set at 203 nm. Amniotic fluid phospholipid estimations were determined on 40 amniotic fluid samples by the HPLC method and by the routine thin-layer chromatographic (TLC) method. Good agreement was observed between the two methods for the L/S ratio, PG, and PI (rPG 0.94, rPI 0.95, rL/S 0.97). The advantages of the HPLC procedure include: Selective separation for PG, PI, PS, and PE, as well as L and S at the same time. The internal standard allows individual concentration of phospholipids to be estimated. The procedure is rapid: 16 min for a single assay compared with 50 min for the standard TLC procedure.
The first step in the determination of phospholipid in amniotic fluid is generally the removal of cells and debris from the fluid by centrifugation. Low-speed centrifugation of the supernatant is reported to have the same phospholipidic profile and L/S, PG/S and PI/S ratios similar to those of the uncentrifuged amniotic fluid sample. With high-speed centrifugation almost all the pulmonary surfactant seems to be recovered in pellet with the same characteristics as the uncentrifuged amniotic fluid.
Apolipoproteins were determined in 50 human amniotic fluids obtained by amniocentesis during weeks 16 and 22 (n = 26) or 33 and 41 (n = 24) of gestation. Whereas apo A-I, A-II, A-IV, and E were identified at levels of 1, 0.7, 0.8 and 1% of normal human adult plasma, respectively, apo B levels were only 0.04% of plasma concentration and apo C-III levels were below the detection limits of the assay. Amniotic fluid levels of apo A-II, A-IV and E did not differ between early and late stages of pregnancy, but levels of apo B decreased and apo A-I increased significantly in late pregnancy. Isofocusing showed apo A-I, A-II and A-IV in identical positions as compared to human adult plasma. Furthermore the known genetic polymorphism of apo A-IV was detectable. Individuals heterozygous, for the variant form apo A-IV-2, showing the phenotype apo A-IV (2-1), had significantly higher levels of apo A-I and A-II as compared to the common phenotype apo A-IV (1-1). We conclude that human amniotic fluid contains the major plasma apolipoproteins at about 1% of plasma levels with the exception of apo B which shows a level at an order of magnitude less than high-density lipoprotein apoproteins in comparison to their plasma counterparts.
OBJECTIVE: Strong evidence implicates chronic intra-amniotic inflammation in the etiology of mid-trimester abortion and spontaneous preterm delivery. The purpose of this study was to determine if concentrations of amniotic fluid matrix metalloproteinase-8, and cytokines such as interleukin-6 and angiogenin can identify patients at risk for spontaneous preterm delivery in patients undergoing mid-trimester amniocentesis. STUDY DESIGN: A case-control study was conducted to compare mid-trimester concentrations of amniotic fluid matrix metalloproteinase-8, interleukin-6, and angiogenin in patients who delivered at term and in those who delivered before term. The study included 19 cases with spontaneous preterm delivery and 95 matched controls with normal outcomes. Patients with abnormal fetal karyotypes or major anomalies were excluded. Matrix metalloproteinase-8, interleukin-6, and angiogenin were measured by using specific immunoassays. Mann-Whitney U tests, Fisher exact tests, and receiver-operating characteristic curves were used for statistical analysis. RESULTS: The median amniotic fluid matrix metalloproteinase-8, interleukin-6, and angiogenin concentrations of patients with spontaneous preterm delivery were significantly higher than those of control cases (matrix metalloproteinase-8: median, 3.1 ng/mL [range, 0.3-1954.9 ng/mL] vs median, 1.3 ng/mL [range, <0.3-45.2 ng/mL], P <.01; interleukin-6: median, 0.32 ng/mL [range, 0.04-2.52 ng/mL] vs median, 0.18 ng/mL [range, 0.01-1.81 ng/mL], P <.01; angiogenin: median, 11.1 ng/mL [range, 4.5-30.7 ng/mL] vs median, 6.7 ng/mL [range, 1.3-21.9 ng/mL], P <.001). Amniotic fluid matrix metalloproteinase-8 concentrations higher than 23 ng/mL had the highest specificity and odds ratio (sensitivity, 42% [8/19]; specificity, 99% [94/95]; OR, 68.4 [95% CI, 7.8-599.1]) in the identification of the patients with preterm delivery after genetic amniocentesis. CONCLUSIONS: Elevated mid-trimester concentrations of amniotic fluid matrix metalloproteinase-8, interleukin-6, and angiogenin are a risk factor for early spontaneous preterm delivery (<32 weeks). An elevated matrix metalloproteinase-8 level of >23 ng/mL is a powerful predictor of spontaneous preterm delivery (<32 weeks) with an odds ratio of 68.4. Amniotic fluid studies can be used to improve the risk assessment for preterm delivery in women who undergo mid-trimester amniocentesis for genetic indications.