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PubMed1982

Neutralization of herpes simplex virus by antibody in amniotic fluid.

The ability of amniotic fluid to neutralize herpes simplex virus type 2 (HSV-2) was quantitated and compared with the serum neutralization titer in 158 pregnant women. Neutralizing activity was expressed as the ability of 0.1 ml of amniotic fluid to reduce the expected number of plaque-forming units (pfu) in the inoculum by 99%. All amniotic fluid samples from 32 women with serum titers of 1:40 or greater neutralized 5 pfu or more; at term, 96% of these fluid samples neutralized 50 pfu or more, 83% neutralized 500 pfu or more, and 61% neutralized 5000 pfu or more. Only 76% of the amniotic fluid samples obtained at term from women with serum titers of 1:5 to 1:39 contained detectable neutralizing activity and only 8% neutralized 5000 pfu or more. None of the amniotic fluid samples from 30 women with serum titers less than 1:5 neutralized 5 pfu or more. All neutralizing activity was removed when immunoglobulin G was removed from the amniotic fluid samples. Sera were obtained from 51 pregnant women 4 to 8 weeks prior to delivery. All women with serum titers of 1:40 or higher gave birth to infants who also had serum titers of 1:40 or higher. Therefore, it is possible to predict the neutralization titer in amniotic fluid and in the infant's serum by measuring the mother's titer in the third trimester.

Amniotic Fluid↗
PubMed1996

Rheumatoid factor-associated high-molecular-weight complexes in the menstrual and amniotic fluids.

We have previously described the identification of the human decidua-associated protein hDP200 as a rheumatoid factor [1]. Assuming that rheumatoid factor binds to Fc of immunoglobulins, the existence of high-molecular-weight complexes was studied in decidual extract, pooled uterine fluid from proliferative and early secretory phase, menstrual fluid and amniotic fluid. High-molecular-weight complexes containing hDP200 and other immunoglobulins were found only in menstrual and amniotic fluids and not in decidual extract or uterine fluid. It is possible that complexing of the immunoglobulins by hDP200 serves as one of the mechanisms that ensure suppression of the immune response to fetal antigens.

Adult↗
PubMed1982

The association between the absence of amniotic fluid bacterial inhibitory activity and intra-amniotic infection.

We studied the relationship of amniotic fluid bacterial inhibition in 50 patients with intra-amniotic infection to that in 50 matched control patients. Amniotic fluid was collected through a transcervical intrauterine catheter. All infected patients had clinical signs of intra-amniotic infection and greater than or equal to 10 2 colony-forming units per milliliter of a high-virulence organism. None of the control patients became infected. The matching characteristics for the intra-amniotic infection group versus the control group were: interval from rupture of the membranes to delivery (14.30 +/- 7.96 versus 15.00 +/- 7.19 hours, NS), interval from rupture of the membranes to collection of amniotic fluid (12.41 +/- 6.37 versus 12.16 +/- 6.46 hours NS), and gestational age (40.3 +/- 1.6 versus 40.0 +/- 1.6 weeks, NS). All patients were in labor. We tested each sample of amniotic fluid for inhibitory activity to Escherichia coli by a plate-count technique. Thirty-five samples (70%) of intra-amniotic infection fluid were noninhibitory, whereas 16 samples (32%) of control fluid were noninhibitory. The conclusion was that amniotic fluid from patients with intra-amniotic infection was significantly less likely to be inhibitory to E. coli (p less than 0.001).

Adolescent↗
PubMed1983

Inhibition of group B streptococci by amniotic fluid from patients with intra-amniotic infection and from control subjects.

This study describes the inhibition of group B streptococci by amniotic fluid from 50 patients with intra-amniotic infection and 50 matched, noninfected control subjects. Patients were matched for gestational age, time from rupture of membranes to delivery, and time from rupture of membranes to collection of the sample of fluid. Study patients had the clinical diagnosis of intra-amniotic infection and greater than or equal to 10(2) colony-forming units of a high-virulence organism per milliliter. None of the control patients became infected or received antibiotics. We collected the amniotic fluid in the study patients prior to antibiotic therapy. A comparison of bacterial growth in the amniotic fluid versus the amniotic fluid plus phosphate showed that only eight (16%) of the intra-amniotic infection samples of fluid were inhibitory, whereas 18 (36%) of the control samples of fluid were inhibitory (X2 = 5.20, p less than 0.02). However, a comparison of group B streptococci growth in amniotic fluid and Todd-Hewitt broth did not show a statistically significant difference. We conclude that the amniotic fluid bacterial inhibitory assay with group B streptococci is technically more difficult to perform and interpret.

Adult↗
PubMed2005

Proteomic biomarker analysis of amniotic fluid for identification of intra-amniotic inflammation.

BACKGROUND: Intra-amniotic inflammation is associated with poor neonatal outcome independent of prematurity. We applied proteomic technology (SELDI: surface-enhanced laser desorption ionisation) to identify the proteomic profile of intra-amniotic inflammation. DESIGN: One hundred and four samples of amniotic fluid were analysed. In stage 1, samples from patients with symptoms of preterm labour and known outcomes were tested to identify the characteristic profile for inflammation. We extracted the profile using a novel, stepwise logical approach comparing SELDI tracings from patients who delivered preterm and had intra-amniotic inflammation in response to infection to the tracings of patients who had symptoms of preterm labour but delivered at term. In stage 2, we applied the algorithm to samples from pregnancies whose outcomes were unknown to the investigators. SETTING: North-American university in collaboration with Ciphergen field demonstration laboratory. SAMPLE: One hundred and four samples of human amniotic fluid from transabdominal amniocentesis. METHODS: SELDI (surface-enhanced laser desorption ionisation) and Mass Restricted analysis, a novel algorithm for extraction of clinical and biological relevant biomarkers from proteomic SELDI tracings. MAIN OUTCOME MEASURE: Presence of intra-amniotic inflammation and/or infection leading to preterm birth. RESULTS: Patients with intra-amniotic inflammation that deliver preterm have a distinctive amniotic fluid proteomic profile of three or four of the following proteins: neutrophil defensins-1 and -2, and calgranulins A and C. Based on the presence or absence of these biomarkers, we devised the mass restricted (MR) score ranging from 0 (all biomarker peaks absent) to 4 (all biomarker peaks present). In stage 1, MR score > 2 had 92.9% sensitivity (95% CI 76.5-98.9) and 91.8% specificity (95% CI 80.4-97.7) for detection of intra-amniotic inflammation. In blind testing (stage 2), MR score > 2 provided 100% specificity and sensitivity (95% CI 100-100). A MR score > 2 was associated with imminent preterm delivery. CONCLUSION: Proteomic analysis of amniotic fluid reveals the presence of biomarkers characteristic of intrauterine inflammation. This methodology may identify the subgroup of patients that might benefit most from interventions to prevent fetal damage in utero.

Adult↗
PubMed1982

Fetal neural tube defects detected by rocket-on-line immunoelectrophoresis of amniotic fluids.

Immunization of rabbits with human fetal brain membranes evoked antisera with reactivity against D-2 protein from brain and cerebrospinal fluid. In amniotic fluids from pregnancies with fetal neural tube defects the presence of D2-protein could be demonstrated by rocket-on-line immunoelectrophoresis. In a prospective study on 72 amniotic fluids with increased alphafetoprotein concentration neural tube defects were correctly predicted in 26 pregnancies. One false-negative and four false-positive pregnancies were encountered. D2-protein determination may thus have a role in antenatal diagnosis of neural tube malformations as a supplement to alphafetoprotein analysis.

Amniocentesis↗
PubMed1981

Studies on serum apolipoproteins and lipids in amniotic fluid and neonatal urine.

Amniotic fluid and neonatal urine were examined for the presence of lipids and serum apolipoproteins. Human apolipoproteins A-I, A-II, and ApoD found principally in serum high density lipoproteins were identified in both neonatal urine and amniotic fluid. A lecithin/sphingomyelin ratio of greater than 5 associated with fetal lung maturity was accompanied by the disappearance of A-II from amniotic fluid. Dissimilarities of total fatty acid composition of amniotic fluid when compared to cord serum or neonatal urine indicate other tissue sources for fatty acids found in amniotic fluid. In addition, the presence of serum apolipoproteins and lipids in both amniotic fluid and neonatal urine suggests that a least a portion of these constituents could be derived from fetal urine.

Amniotic Fluid↗
PubMed1985

Particulate fraction in amniotic fluid at second trimester.

Amniotic fluid at 15-20 weeks contains high concentrations of microvillar enzymes which serve as markers for the prenatal diagnosis of cystic fibrosis. We found that these enzymes were mostly bound to amniotic fluid particulate fraction which eluted in the void volume on Sepharose 6B chromatography and precipitated in ultracentrifugation at 100,000g. Electron microscopy showed that the particulate fraction comprised membrane fragments and small vesicles. It represented less than 1% of the total protein in cell free amniotic fluid. Sorbitol gradient centrifugation showed heterogeneity in the particulate fraction. The enzyme patterns of amniotic fluid and meconium particulate fractions resembled each other. Antiserum against particulate fraction in amniotic fluid strongly reacted with early meconium and fetal small intestine in immunodiffusion, enzyme immunoassay, and staining with immunoperoxidase. The results suggest that most of the enzyme rich particulate fraction in early amniotic fluid originates in the fetal intestine.

Alkaline Phosphatase↗
PubMed2005

Monocyte chemotactic protein-2 and -3 in amniotic fluid: relationship to microbial invasion of the amniotic cavity, intra-amniotic inflammation and preterm delivery.

OBJECTIVE: To evaluate the presence of monocyte chemotactic protein (MCP)-2 and MCP-3 in cervical and amniotic fluid in women in preterm labor. STUDY DESIGN: Cervical and amniotic fluid was sampled from women with singleton pregnancies (< or =34 weeks) in preterm labor (n = 58). RESULTS: Monocyte chemotactic protein-2 (range: 80-583 pg/ml) and MCP-3 (range: 36-649 pg/ml) were detectable in 7/58 women in preterm labor. Monocyte chemotactic protein-3 was found significantly more often in amniotic fluid of women delivered within 7 days (P < 0.001), <34 weeks (P = 0.002), or with intra-amniotic inflammation (P < 0.001) and microbial invasion of the amniotic fluid (P = 0.003). Women in preterm labor had detectable levels of MCP-2 significantly more often if they gave birth before 34 weeks of gestation (P = 0.038) or had intra-amniotic inflammation (P = 0.042). CONCLUSIONS: The presence of MCPs in amniotic fluid of women in preterm labor was associated with preterm birth before 34 weeks of gestation (MCP-2 and MCP-3), microbial invasion (MCP-3), and inflammation (MCP-2 and MCP-3) of the amniotic cavity.

Adult↗
PubMed2000

Concentrative relationship between polymorphonuclear elastase and urinary trypsin inhibitor in amniotic fluid.

In the amniotic fluid, urinary trypsin inhibitor (UTI) seems to inhibit polymorphonuclear elastase (PMNE) activity. The PMNE and UTI concentrations in normal amniotic fluid at 16-20 and 38-40 gestational weeks were measured. The PMNE concentration increased significantly at 38-40 weeks, whereas UTI concentration decreased significantly. According to concentrative relationships between both substances, PMNE may be activated more at the full term pregnancy. Since PMNE-induced tissue injury potentially causes degradation of amniotic collagen, the present result suggests that the quotient of PMNE and UTI concentrations is a reliable index to estimate the occurrence of rupture of the membranes.

Abortion, Induced↗
PubMed1975

Effect of centrifugation on amniotic fluid phospolipid recovery.

Amniotic fluid lecithin and sphingomyelin were determined quantitatively in 33 samples obtained throughout the last trimester. Each sample was divided into three parts and each part was centrifuged at different relative forces prior to extraction. It is shown that centrifugation always removes considerable amounts of both lecithin and sphingomyelin from the supernatant towards the end of pregnancy, but very little at the beginning of the last trimester. The fatty acid composition of amniotic fluid lecithin, studied by gas liquid chromatography, indicate that surface active lecithin is lost by centrifugation of the fluid prior to extraction.

Amniotic Fluid↗
PubMed1978

Effect of intraamniotic fluid thyroxine injection on fetal serum and amniotic fluid iodothyronine concentrations.

Seven hundred micrograms of T4 were injected into the amniotic cavity 24 h before delivery of five pregnant women scheduled for elective cesarean section at term. T4, T3, and rT3 concentrations were measured by RIA in amniotic fluid obtained at the time of the injection and in amniotic fluid and cord serum samples collected at delivery. Iodothyronine concentrations also were determined on cord samples from 24 full term control infants. The geometric mean serum T4 concentration in the experimental infants was 27.2 micrograms/dl, almost 3 times that of the control population (10.3 micrograms/dl); serum rT3 concentrations were markedly elevated to a mean of 657 ng/dl, compared to 254 ng/dl in control infants. The mean serum T3 concentration was slightly but significantly increased to 61.3 ng/dl (control, 48.3 ng/dl; P less than 0.02). Amniotic fluid T4, T3, and rT3 concentrations all increased significantly. T4 injection into the amniotic fluid is an effective method of increasing fetal serum T4 concentrations. The preferential pathway of monodeiodination of the injected T4 in the human fetus is to rT3 rather than T3.

Amnion↗