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PubMed1977

Falling amniotic fluid palmitates in diabetic pregnancies.

Palmitic acid levels were measured in samples of amniotic fluid obtained from 15 patients with diabetes. Seven patients had palmitate values which decreased at some time in pregnancy but only one of the infants developed respiratory distress. Eight of the 15 patients had final amniotic fluid palmitate values which were greater than 0.07 mmol/l and one infant developed respiratory distress. The other seven patients had final amniotic fluid palmitate values of 0.07 mmol/l or less and one of the infants developed respiratory distress. The significance of falling amniotic fluid palmitate values is discussed.

Amniotic Fluid↗
PubMed1980

Amniotic fluid secretor typing: validation for use in prenatal prediction of myotonic dystrophy.

Use of the well-established linkage of the secretor locus (Se) to the myotonic dystrophy locus (Dm) as an indirect means for prenatal prediction of myotonic dystrophy requires that the phenotypic expression of the fetal secretor locus be accurately and reliably assessed in amniotic fluid. Secretor status determinations on 89 amniotic fluids obtained by second trimester amniocentesis were compared with results of postnatal secretor typing of saliva samples collected from the resulting 89 offspring. The secretor types of the paired amniotic fluid-saliva samples were in agreement in all cases. The only unusual typing result was on an amniotic fluid from a blood group O secretor fetus in which the level of soluble H antigen was estimated to be about one-third that observed for other H secretors. Though it is possible that rare secretor fetuses with very low titers of soluble antigen at the time of amniocentesis could be mistyped as non-secretors, our results indicate that such an erroneous typing result would only occur in about 1-2% of all amniotic fluids tested. Constructed mixtures of 10% heparinized blood in non-secretor amniotic fluid or of 10% serum in amniotic fluid derived from secretor fetuses did not introduce sufficient levels of soluble antigen or of antibody to interfere with accurate secretor typing, thus providing reassurance that maternal and/or fetal blood contamination of amniotic fluid does not compromise accuracy of fetal secretor typing. This study documents the accuracy and reliability of amniotic fluid secretor typing for prenatal prediction of fetal risk for later development of myotonic muscular dystrophy.

ABO Blood-Group System↗
PubMed1985

Evaluation of amniotic fluid in preterm labor with intact membranes.

Amniotic fluid was obtained from 35 pregnant women in preterm labor with intact membranes. Their gestational ages ranged from 24 to 34 weeks. Bacteria were detected in only 1 (3%) of the 35 amniotic fluid samples. The anaerobic culture grew Bacteroides corrodens and Fusobacterium nucleatum. The L/S ratio was greater than 4.0 in six patients (17%), 2.5-4.0 in two (6%) and less than 2.5 in 23 (66%); the quantity of fluid was inadequate for L/S analysis in four (11%). None of the 35 newborns developed evidence of infection in the neonatal period. Only two women (6%) were febrile postpartum, and none experienced a prolonged hospital stay. Seven (20%) of the infants developed respiratory distress syndrome. Five (14%) developed hyaline membrane disease, and two (6%) had transient tachypnea of the newborn. Intrauterine infection may play a lesser role in preterm labor with intact membranes than previously postulated. Amniocentesis may provide useful information for directing management by permitting one to assess fetal pulmonary maturity and the presence of meconium.

Adolescent↗
PubMed2006

[Amniotic fluid embolism: two case reports].

We report two cases of amniotic fluid embolism, confirmed by histological examination. Both patients had an immediate post-partum haemorrhage that required an haemostatic hysterectomy. A typical symptomatology of amniotic fluid embolism revelated the first case. The patient survived without any sequelae. In the second case, amniotic fluid embolism occurred immediately after the delivery. The patient developed an acute respiratory distress with a shock syndrome. Despite haemostatic hysterectomy and resuscitative efforts, she died 6 days later.

Adult↗
PubMed1998

Elevated fetal fibronectin in midtrimester amniotic fluid is involved with the onset of preeclampsia.

OBJECTIVE: To examine early midtrimester amniotic fluid for its significance in pregnancy outcomes, especially with connection to the pathogenesis of preeclampsia. METHODS: A prospective, nested, case-control study was conducted. Fetal fibronectin in early midtrimester (16-20 weeks gestation) amniotic fluid was measured by EIA method. Results were compared by their pregnancy outcomes. RESULTS: Amniotic fluid levels of fetal fibronectin were significantly higher in the group subsequently developing severe preeclampsia (106.8 +/- 13.2 micrograms/ml, mean +/- SD, n = 12) compared with matched controls (66.7 +/- 7.1 micrograms/ml, n = 12) (p < 0.05). CONCLUSION: High levels of fetal fibronectin were found in the amniotic fluid of women subsequently developing severe preeclampsia before any symptom appear. Involvement of extracellular injury or cellular hyperactivity in the midtrimester placental site with the onset of preeclampsia is suggested.

Adult↗
PubMed1979

Unconjugated and total estriol in human amniotic fluid--changes in the ratios between the two estriol levels with advancing gestational age.

In 172 amniotic fluid samples of the early second and the third trimester from 115 normal pregnancies the concentrations of unconjugated and total estriol were measured by means of radioimmunoassay. The mean concentrations of unconjugated estriol in amniotic fluid rose from 1.22 ng./ml. in the gestational weeks 15-18 to 7.82 ng./ml. in the gestational weeks 37-40, that is 6.4 times the former value. In contrast, the mean concentrations of total estriol in amniotic fluid increased more strongly, namely from 27.51 ng./ml. in the gestational weeks 15-18 to 777.15 ng./ml. in the gestational weeks 37-40, that is 28.3 times the former value. With advancing pregnancy the proportion of unconjugated estriol to total estriol in amniotic fluid fell, obeying a significant correlation, from 4.43% in the gestational weeks 15-18 to 1.01% in the gestational weeks 37-40. The presumable reasons for this are the rising conjugation rate of estriol excreted with fetal urine, concomitant to fetal maturation, and the relative transfer diminution of unconjugated estriol from maternal plasma into amniotic fluid with the advance of gestation.

Amniotic Fluid↗
PubMed1989

Evaluation and quality control of a monoclonal antibody based enzyme antigen immunoassay of acetylcholinesterase in amniotic fluid.

We have evaluated a new monoclonal antibody based enzyme antigen immunoassay (EAIA) for acetylcholinesterase in amniotic fluid, intended for the detection of open fetal abnormalities, especially open neural tube defects. With a sample volume of 50 microliters, the detection limit is 0.7 nkat/l and linearity is found up to an amount 200-times the detection limit. CV's are less than or equal to 6.6% within assays and less than or equal to 10.3% between assays; recoveries averaged 103%. The upper limit of the reference range for amniotic fluids from non-affected pregnancies is 8.5 nkat/l for clear specimens and 25.0 nkat/l for haemolysed specimens. Amniotic fluid specimens from 1473 patients (1388 normal and 85 pathological pregnancies) were examined with both the new EAIA and the original procedure using a polyclonal rabbit antiserum. The two procedures showed identical sensitivities and specificities of about 100%, except for amniotic fluid samples containing haemolysed blood. For the latter the new EAIA showed a specificity of 100% compared to 55.6% for the original procedure. We conclude that the new EAIA is accurate and reproducible and shows, compared with the original procedure, an increased specificity in the analysis of amniotic fluid samples containing haemolysed blood.

Acetylcholinesterase↗
PubMed1994

Maternal cell contamination in amniotic fluid samples as a consequence of the sampling technique.

Maternal cell contamination in amniotic fluid samples is easily detected by in situ hybridization if the karyotype of the fetus differs from the karyotype of the mother. One out of two amniotic fluid samples appears to contain more than 20% maternal cells. Bloody samples often contain even more than 50% maternal cells. Maternal cells can also be identified on the basis of their nuclear morphology. Maternal cell contamination is regularly observed in pregnancies with an anterior placenta, whereas it is rare in posterior placenta pregnancies. The maternal cells are therefore thought to be artificially introduced into the amniotic fluid sample, as a result of placental bleeding during amniocentesis. The implications of maternal cell contamination for prenatal diagnosis using uncultured amniotic fluid samples are discussed.

Amniocentesis↗
PubMed1991

The incidence of meconium-stained amniotic fluid from 1980 through 1986, by year and gestational age.

The annual incidence of meconium-stained amniotic fluid was analyzed for changes in a total obstetric sample of 45,115 singleton, vertex, liveborn infants over a 7-year study period. The incidence of meconium-stained amniotic fluid for the total obstetric population was calculated for each year of the study period. The sample was then stratified by estimated gestational age, and the incidence of meconium-stained amniotic fluid was calculated for each gestational age group. The incidence of meconium-stained amniotic fluid increased 40.9% over the study period, from 18.8% in 1980 to 26.5% in 1986 (P less than .001). This increase was found to be in a consistent linear trend (P less than .05). The incidence of meconium-stained amniotic fluid was also found to increase significantly in a linear trend as gestational age of the fetus increased. These findings lend support to both the maturational theory and the stress theory of meconium passage in utero.

Amniotic Fluid↗
PubMed2002

Identification of matrix metalloproteinase-9 in amniotic fluid and amniochorion in spontaneous labor and after experimental intrauterine infection or interleukin-1 beta infusion in pregnant rhesus monkeys.

OBJECTIVE: The purpose of this study was to examine the roles of intrauterine infection, inflammation, and spontaneous labor on the expression of matrix metalloproteinase-9 in fetal membranes and amniotic fluid of late pregnant rhesus monkeys. STUDY DESIGN: Pregnant rhesus monkeys with timed gestations were chronically catheterized to allow serial sampling of amniotic fluid before and during experimentally induced intrauterine inflammation. Six animals received group B streptococci into the chorionic-decidual space, and 4 animals received intra-amniotic interleukin-1 beta infusions (10 microg). Three additional animals were serially sampled by amniocentesis through late pregnancy until spontaneous term labor. Amniotic fluid samples were examined by zymography for matrix metalloproteinase-9 and -2 and Western immunoblot for matrix metalloproteinase-9 and -2 and tissue inhibitors of metalloproteinase-1 and -2. Fetal membranes were obtained at cesarean delivery during labor (before rupture), formalin fixed, and embedded in paraffin for immunocytochemistry of matrix metalloproteinase-9 and in situ hybridization of matrix metalloproteinase-9 messenger RNA. Tissues from 2 additional animals were collected as age-matched non-labor controls. RESULTS: In amniotic fluid, the 92-kd latent matrix metalloproteinase-9 was detectable in late pregnancy and increased dramatically, followed by the appearance of the 83-kd active form before spontaneous term delivery. Amniotic fluid matrix metalloproteinase-2 levels (both latent and active forms) remained relatively constant throughout pregnancy and in labor. Both bacteria and interleukin-1 beta rapidly increased the signal of latent matrix metalloproteinase-9 without a consistent increase in the active form before the onset of labor. Chorionic-decidual inoculation of group B streptococci was followed by the expression of latent matrix metalloproteinase-9 before the appearance of group B streptococci in amniotic fluid or the onset of labor. Matrix metalloproteinase-2 increased to a new steady-state level or remained unchanged after group B streptococci inoculation or interleukin-1 beta infusion, respectively. Amniotic fluid tissue inhibitors of metalloproteinase-1 declined and tissue inhibitors of metalloproteinase-2 remained unchanged during early group B streptococci infection, after interleukin-1 beta infusion and on the day of spontaneous term labor. However, both tissue inhibitors of metalloproteinase-1 and -2 levels increased after preterm labor that was induced by group B streptococci. Immunocytochemistry localized matrix metalloproteinase-9 protein to amnion and chorion epithelial and mesenchymal cells and decidual stromal cells. Granular matrix metalloproteinase-9 staining was observed in the connective tissue layer of inflamed fetal membranes. In situ hybridization for messenger RNA confirmed the production of matrix metalloproteinase-9 by amnion and chorion. CONCLUSION: Bacterial- and interleukin-1 beta-induced preterm labor and spontaneous term labor are preceded and accompanied by progressive increases in amniotic fluid matrix metalloproteinase-9 (92 kd) in rhesus monkeys. Amniotic fluid matrix metalloproteinase-9 may serve as a clinical marker for the onset of both preterm and term labor.

Amnion↗
PubMed1992

Increased inorganic sulfate concentrations in amniotic fluid.

We assayed inorganic sulfate by ion chromatography in 49 amniotic fluid samples from pregnancies of 14 to 38 weeks gestation. In second trimester samples (14 to 26 weeks gestation), amniotic fluid sulfate concentrations (317 +/- 22 mumol/L, mean +/- SE; n = 32) were not different from previously reported maternal serum values but were significantly lower (p < 0.001) than in the third trimester (693 +/- 42 mumol/L; n = 16). In third trimester samples, sulfate concentrations were significantly correlated with creatinine and uric acid but not chloride, suggesting that renal excretion may be the major source of the amniotic fluid sulfate in the late stages of gestation.

Adolescent↗
PubMed1987

Microproteins in amniotic fluid as an index of changes in fetal renal function during development.

Protein content and protein composition were studied in amniotic fluid obtained from 171 healthy pregnant women between the 16th and 38th week of gestation, using microgradient gel electrophoresis to separate proteins according to their molecular size into albumin (68 KD), proteins of low molecular weight (LMW proteins, less than 68 KD), and proteins of high molecular weight (HMW proteins, greater than 68 KD). Additionally alpha-1-microglobulin (alpha-1-MG, 33 KD) and beta-2-microglobulin (beta-2-MG, 11,8 KD) were analysed as micromolecular marker proteins. Concentrations of LMW proteins were 0.15-0.22 g/l, of alpha-1-MG 28.4-34.5 mg/l, and of beta-2-MG 7.2-11.6 mg/l during the second trimester of gestation, and thereafter decreased progressively to 0.03 g/l, 14.1 mg/l and 2.4 mg/l respectively near term. The same developmental trends were confirmed by calculating the protein/creatinine ratios in amniotic fluid. The concentrations of LMW proteins found in the first postnatal urine of 73 healthy infants born prematurely or at term were similar to those in amniotic fluid of corresponding fetal age. Concentrations of albumin and HMW proteins in postnatal urine were about 5% and 15% respectively when compared with amniotic fluid concentrations. No strong correlation existed between gestational age and either of the analysed proteins which would allow accurate assessment of fetal maturation by protein analysis in amniotic fluid. It is concluded that fetal urinary excretion is the major determinant of the microprotein content of amniotic fluid. Microproteins seem to reflect an increasing tubular reabsorption capacity, which accelerates rapidly after the second trimester of gestation.

Adult↗
PubMed1975

Heterogeneity for adenosine deaminase deficiency: Expression of the enzyme in cultured skin fibroblasts and amniotic fluid cells.

Adenosine deaminase (ADA) could be quantitated and the isozyme pattern characterized in cultured amniotic fluid cells. In 20 amniotic fluid cell cultures the mean specific activity was 14.3 U/g protein +/- 6.7 (SD) and compared favorably with values of 14.6 U/g protein +/- 6.8 (SD) observed in 26 cultures of skin fibroblasts. In cultures of skin fibroblasts established from two obligate heterozygotes for ADA deficiency, the specific activity of ADA was 7.0 and 7.7 U/g protein. The ADA isozyme pattern that existed in cultures of amniotic fluid cells was the same as that observed in cultured skin fibroblasts. This identification of the same apparent enzyme may permit the prenatal diagnosis of that form of combined immunodeficiency disease caused by ADA deficiency. Residual enzyme activity of less than 1% and 10% of the mean of normal fibroblasts could be measured in cultured fibroblasts from two unrelated children with ADA deficiency and combined immunodeficiency disease. The tissue-specific enzyme from cultured skin fibroblasts from the child with 10% residual activity had a faster electrophoretic mobility and greater heat stability than normal ADA. This enzymatic evidence indicates that at least two mutant alleles exist at the locus for ADA which predispose to combined immunodeficiency disease when present in the homozygous state.

Adenosine↗
PubMed1986

The successful use of human amniotic fluid for mouse embryo culture and human in vitro fertilization, embryo culture, and transfer.

The development of mouse and human embryos was assessed in human amniotic fluid to determine its suitability as a culture medium for human in vitro fertilization (IVF). Two-cell mouse embryos developed to blastocysts after 72 hours at rates similar to that in Whittingham's T6 + 10% fetal calf serum. Significantly more mouse embryos hatched in amniotic fluid. No difference was found between individual patient's amniotic fluids obtained at 16 to 21 weeks' gestation. A preliminary trial comparing amniotic fluid with T6 + maternal serum in human IVF showed no significant difference in fertilization rate and embryo development during 42 to 48 hours in vitro. Expanded blastocysts were obtained in amniotic fluid after 5 days in vitro. Four pregnancies were obtained in 9 patients' transferred embryos grown in amniotic fluid and with 2 or 12 patients' transferred embryos grown in T6 + maternal serum.

Amniotic Fluid↗
PubMed1988

Fetal outcome in gestational diabetes with elevated amniotic fluid insulin levels. Dietary versus insulin treatment.

Of 228 women with gestational diabetes between 28 and 32 gestational weeks, 195 had a normal amniotic fluid insulin level (4.8 +/- 3.6 microU/ml) while 33 (14.5%) had an elevated level (23.1 +/- 10 microU/ml). Women with a normal amniotic fluid insulin level were treated by diet alone. Fourteen of the women with an elevated level were treated by diet alone; 19 received insulin treatment additionally. The fetal outcome of patients with a normal amniotic fluid insulin level and dietary therapy and of those with an elevated level and insulin treatment was similar to that of metabolically healthy women. The newborns of gestational diabetics with elevated amniotic fluid insulin treated by diet alone showed a significantly higher incidence of neonatal hyperinsulinism, hypoglycemia, hyperbilirubinemia, high birth weight, respiratory distress syndrome and hypocalcemia. While 2/14 (14%) of the neonates in the dietary group had fatal respiratory distress syndrome, there were no deaths in the group with elevated amniotic fluid insulin and insulin treatment. The data demonstrate that in gestational diabetics with normal amniotic fluid insulin (low-risk group), dietary therapy is sufficient while insulin therapy is required to ensure healthy offspring in patients with elevated amniotic insulin (high-risk group).

Amniotic Fluid↗
PubMed1980

Bacteriology of amniotic fluid.

The incidence of aerobic and anaerobic bacteria in the amniotic fluid and the cervix of 101 healthy parturients, with intact membranes, was studied. Pharynx, urine and umbilical cord of the newborns were also examined for the same pathogens. Although positive cultures from the cervix were found in 41.58% of the cases, the contamination of the amniotic fluid was only 1.98%. Our results support the view of the antibacterial activity of amniotic fluid.

Amniotic Fluid↗
PubMed1978

Amniotic fluid infection at term.

The incidence of amniotic fluid infection, determined by histological examination of the placenta and cord and cytological examination of gastric aspirate, was found to be high (52%) in term deliveries. A detailed histological system of grading the inflammatory response was used. No relationship was found between maternal nutritional factors or the baby's weight and inflammatory response, as judged by histological examination. The presence of pus cells in the gastric aspirate was of only limited diagnostic value. The absence of clinically obvious infection in the infants suggested amniotic fluid colonization without spread to the fetus.

Amniotic Fluid↗
PubMed1975

Creatinine exchange between mother, fetus, and amniotic fluid.

Creatinine exchange between mother, fetus, and amniotic fluid was investigated in rhesus monkeys in late pregnancy in which a different radioactive-labeled form of creatinine was injected simultaneously into either of two of the three possible compartments. Creatinine specific activity was then determined for each isotope in each compartment over the ensuing 4-6 h. A rapid and extensive bidirectional exchange occurred between all three compartments. Maternal-fetal flux, while bidirectional, seemed to be predominately from mother to fetus. Approximately 35% of labeled creatinine originally injected into the fetus and 25% of labeled creatinine originally injected into the mother were present in the amniotic sac within 2 h. Creatinine pool size was calculated to be approximately 6 mg/kg in both mother and fetus. Comparison of experiments involving living had dead fetuses indicated that the route of creatinine transfer from mother to amniotic fluid was through the living fetus and directly across the chorioamnion in the dead fetus. In addition, the time required for 'mixing' of creatinine injected into the amniotic sac was longer with a dead than with a living fetus but its half-life averaged 4.5 h regardless of fetal status.

Amnion↗