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PubMed1993

The inhibition of fibroblast-populated collagen lattice contraction by human amniotic fluid: a chronologic examination.

The effect of human amniotic fluid on fetal wound healing remains to be fully elucidated and may lead to the isolation of factors that could modulate adult wound healing. This study uses an in vitro model of wound contraction, the fibroblast-populated collagen lattice, to examine the effects of chronologically sampled human amniotic fluid on contraction of lattices composed of either human adult or fetal fibroblasts. This chronology has not been reported previously. Human amniotic fluid was obtained in a sterile fashion via amniocentesis from 120 different women at different time points in gestation, ranging from 13 to 24 weeks. At each time point of gestation, three to five samples were individually examined in duplicate sets. Only fluid from pregnancies deemed normal by amniocentesis was included. Contaminated specimens were discarded. Using Bell's protocol, lattices were constructed of acid-soluble rat tail collagen, growth medium, and either human adult fibroblasts or human fetal fibroblasts. Lattices contained 20% v/v human amniotic fluid. In the control lattices, phosphate-buffered saline replaced amniotic fluid in equal volumes. Area was measured at 24-hour intervals, and all tests were run in duplicate for each specimen. The mean area at each interval was computed for each gestational week examined. Data were analyzed for significance with ANOVA and Dunnett's t test against control.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1983

Stimulation of myometrial and decidual prostaglandin production by amniotic fluid from term, but not midtrimester pregnancies.

The effect of amniotic fluid obtained from second trimester (16-20 wks) and term pregnancies (38-41 wks) on the production of PGE and F by human amnion, decidua and myometrium at term was determined using tissue slices incubated in vitro. Midpregnancy amniotic fluid neither inhibited nor stimulated the prostanoid production by any of the tissues. In contrast, term amniotic fluid obtained before as well as after the onset of labor markedly increased the production of both PGE and PGF in decidua and myometrium from levels in Krebs solution. The prostanoid production (PGE + PGF) in amnion was not significantly increased but the proportion of PGF was raised during incubations in term amniotic fluid. In decidua and myometrium the increase in PGE and PGF production in term amniotic fluid was approximately 200 and 400 percent respectively, from control values in Krebs solution. We propose that the stimulatory activity in term amniotic fluid is responsible for the accelerated synthesis of prostaglandins after rupture of membranes, which is reflected in raised PGF metabolite levels in maternal circulation. It may also be the reason for the rise in amniotic fluid prostaglandin levels around the 35th week of gestation, and perhaps for the onset of labor.

Amnion↗
PubMed1980

The prenatal determination of fetal sex: amniotic fluid testosterone as a preliminary screening test.

Amniotic fluid testosterone levels were measured by radioimmunoassay without chromatography on 101 specimens obtained at amniocenteses between 15 and 19 wk gestation. For the male fetus, the amniotic fluid testosterone level of 553 +/- 23 pmol/l (mean +/- SE) was significantly higher (P less than 0.0005) than the concentration found for the female fetus (206 +/- 9 pmol/l). There was an overlap of the ranges 74-1120 pmol/l for the male and 122-399 pmol/l for the female fetuses. Amniotic fluid testosterone levels above 400 pmol/l were observed in 84% of the male and in none of the female fetuses. The method allowed determination of testosterone levels within 8 h. It is concluded that amniotic fluid testosterone measured by radioimmunoassay without chromatography is a rapid and effective preliminary screening test for the prenatal diagnosis of fetal sex.

Amniocentesis↗
PubMedDate not supplied

Variables influencing growth and morphology of colonies of cells from human amniotic fluid.

Growth of cells from amniotic fluid was studied with respect to cell concentration in the inoculum, blood contamination of the fluid, fluid colour, fluid clarity, gestational age of the pregnancy, and growth factors. Dependent variables measured were colony formation, colony size, and colony morphology after 7, 11, and 14 days of culture. The following conclusions were established from these studies: small sample volumes are the most efficient for producing colonies; cells from very bloody or dark brown fluids have a slower rate of growth; growth of cells from cloudy (noncontaminated) fluids is better than growth of cells from clear fluids; the proportion of colonies that are epithelioid varies with gestational age; the stimulating effect of 100 ng/ml fibroblast growth factor on cells from amniotic fluid was confirmed.

Amniocentesis↗
PubMed1997

Lipid peroxidation in cord blood: the effect of amniotic fluid volume.

OBJECTIVE: To assess the effect of amniotic fluid volume on umbilical cord arterial lipid peroxide levels in relation to intrapartum events. DESIGN: Prospective observational study. SETTING: Delivery suite of a teaching hospital, the Chinese University of Hong Kong. POPULATION: Women with singleton, term, cephalic presentation, and an initially normal fetal heart rate tracing. METHODS: All pregnancies had amniotic fluid index assessments before and after amniotomy and cord arterial lipid peroxide determination at delivery. Multiple regression analysis. MAIN OUTCOME MEASURES: Cord arterial malondialdehyde and organic hydroperoxide levels. RESULTS: In 247 cases following amniotomy levels were inversely correlated with intrapartum amniotic fluid index. Amniotic fluid index during labour was an independent determinant of cord arterial lipid peroxide concentration, along with duration of second stage, absence of epidural, presence of tight nuchal cord entanglement and evidence of fetal distress. CONCLUSIONS: Oligohydramnios during labour is associated with high levels of lipid peroxidation in the fetus, reflecting an increase in hypoxic cellular damage by free radicals.

Amnion↗
PubMed1997

Effect of fetal movement on the amniotic fluid index in diamniotic twin gestations.

Fetal movement changes the size and location of amniotic fluid pockets during measurement of the amniotic fluid index. In singleton gestations, the effect of redistributing the fixed intrauterine fluid volume on the amniotic fluid index is clinically insignificant. In this study, we tested the hypothesis that the index in twin pregnancies is unaffected by fetal movement. A single examiner prospectively determined the amniotic fluid index before and after three discrete episodes of movement by both fetuses of 82 diamniotic twin pregnancies referred for obstetric sonograms between 20 and 38 weeks' menstrual age. A reliable blinded examiner provided a second post-movement measurement as a control. Data were analyzed by the paired t-test. The mean change in the amniotic fluid index after fetal movement was 2.1 +/- 0.2 cm and 3.7 +/- 0.3 cm for post-movement determinations by the same and blinded examiners, respectively (p < .001). Interobserver variation was 3.5 cm. Intraobserver variation was 1.8 cm for the first examiner and 2.2 cm for the second examiner. Therefore, interobserver and intraobserver variation can account for the observed change in the amniotic fluid index following movement of both diamniotic twins.

Amniotic Fluid↗
PubMed1989

[Forensic medicine and morphologic aspects of fatal amniotic fluid aspiration].

The massive aspiration of amniotic fluid as one cause of a fatal postpartal asphyxia will be demonstrated under the aspect of preliminary criminal law proceedings against physicians because of medical negligence. The pathomorphologically established diagnosis of a fatal aspiration of amniotic fluid supposes extensive and systematic quantitative histological examination of both lungs. The technique of histological cross sections through the entire lung combined with morphometry is a suitable method to exactly record the alterations of bronchi and lung parenchyma by aspiration of amniotic fluid and their complications, such as interstitial emphysema.

Amniotic Fluid↗
PubMed1980

Amniotic fluid lipids in sickle cell disease.

Amniotic fluid of sickle cell disease patients past the thirty-seventh week of pregnancy contained 63.4%, 71.7%, and 48.6% less total lipids, total nonpolar lipids, and total phospholipids, respectively, as compared with amniotic fluid of normal patients. No remarkable variation in the composition of nonpolar lipids was noticed between the two groups. However, the phospholipid composition was significantly varied. For example, the percentage amounts of choline glycerophospholipids (lecithin) was low and the percentage amounts of other phospholipids was high in sickle cell pregnancy as compared with normal pregnancy. Furthermore, increased levels of polyunsaturated fatty acids and fluorescent lipid pigments were found in amniotic fluids of sickle cell patients.

Amniotic Fluid↗
PubMed1990

Recognition of insulin-like-growth-factor-binding proteins in serum and amniotic fluid by an antiserum against a low-molecular-mass insulin-like-growth-factor-inhibitor/binding protein.

An antiserum (R8) raised against a purified specific low-Mr (16,000-18,000) insulin-like-growth-factor (IGF)-inhibitor/binding protein, which is immunologically related to the native growth hormone (GH)-dependent Mr-150,000 IGF-binding protein in serum, has been used to probe a possible additional relationship to the predominant non-GH-dependent IGF-binding protein (Mr approximately 30,000) of human amniotic fluid. Amniotic-fluid fractions and an IGF-inhibitory fraction of serum were analysed by covalent cross-linking, ligand-blotting and immunoblotting techniques. Western blotting of the serum fraction using the R8 antiserum gave five immunoreactive (ir) bands, of which at least three (Mr 38,000, 34,000 and 23,000) possessed IGF-binding activity, as indicated by ligand (125I-IGF-I) blotting. Western blotting of two differently prepared amniotic-fluid fractions, which both showed potent IGF-inhibitory bioactivity, gave several (Mr range 14,500-73,000) ir bands, of which two (Mr 28,000 and 17,000) were most prominent. Ligand-blotting analysis gave a single intensely labelled band at Mr 28,000, consistent with the major presence of the Mr-28,000-30,000 amniotic-fluid IGF-binding protein. Covalent cross-linking of the amniotic-fluid fractions to 125I-IGF-I gave three specifically cross-linked complexes (Mr 36,000, 32,000 and 23,000), which, assuming a 1:1 binding stoichiometry with IGF (Mr 7500), represent binding proteins of Mr 28,500, 24,500 and 15,500 respectively. The Mr-15,500 binding protein, very similar to the Mr-17,000 ir band, in all likelihood represents the IGF-inhibitor protein. Our results indicate that inhibitor-sized binding proteins and IGF-inhibitor bioactivity are present in human amniotic fluid, and that the IGF-inhibitor protein (Mr 16,000) and amniotic-fluid IGF-binding protein (Mr 28,000) are immunologically related. Since the IGF-inhibitor protein is also immunologically and structurally related to the native, GH-dependent, Mr-150,000 binding protein in serum, our data suggest a heretofore-unrecognized immunological similarity between the Mr-150,000 binding protein and the amniotic-fluid binding protein and its serum analogue, the Mr approximately 30,000, non-GH-dependent, binding protein.

Ammonium Sulfate↗
PubMed1976

The Determination of Peroxidase in Amniotic Fluid.

Analyzing total peroxidase activity in amniotic fluid is extremely simple, requiring only 1 1/2 minutes of incubation at room temperature and a spectrophotometer. Peroxidase, clearly detectable at as early as 17 weeks' gestation in the amniotic fluid, increases 100-fold by term. The increase follows a predictable rising curve and can be used to estimate the fetal age. Maturation of the fetal salivary gland is most probably the source of rising amniotic fluid peroxidase levels. Samples from complicated pregnancies are lower than normal, do not increase as rapidly, and probably can be bracketed into their own ranges for gestational age evaluation.

Amniotic Fluid↗
PubMed1983

HLA-D and -DR antigens on human amniotic fluid cells. I. Lack of expression of HLA-D.

Human amniotic fluid cells, known to express HLA-A, -B, and -C antigens, were tested for the presence of lymphocyte-stimulating antigens (LD or HLA-D) using modifications of the mixed lymphocyte culture (MLC) and primed lymphocyte typing (PLT) tests. Peripheral blood lymphocytes were co-cultured with various concentrations of allogeneic amniotic fluid cells, either growing as a monolayer culture in microtiter plates or suspended in medium following treatment with trypsin. The kinetics of such mixed lymphocyte amniotic fluid cell culture (MLAC) reactions were followed during days 3 to 8. Under none of these conditions did amniotic fluid cells significantly stimulate allogeneic lymphocytes, even after lymphocytes were specifically primed in the PLT assay to the HLA-D antigens segregating in the family of the amniotic fluid cell donor. Furthermore, in three-cell experiments, amniotic fluid cells failed to inhibit an ongoing MLC reaction, indicating that the absence of proliferative response to amniotic fluid cells is not due to active suppression. Taken together, these data strongly suggest that amniotic fluid cells either do not express HLA-D antigens or do not express them in a form that is detectable in either primary or secondary MLC.

Amniotic Fluid↗
PubMedDate not supplied

Identification of vasopressor constituents of amniotic fluid in pregnancy toxaemia.

The vasopressor activity of human amniotic fluid was assessed in 46 primigravidas during the third trimester of pregnancy. The subjects included 20 normal and 26 cases of pregnancy toxaemia. For identification of the vasopressor activity of the amniotic fluid, blood pressure measurements were made in the intact rat, and the smooth muscle contraction of the rat ascending colon preparation was determined in vitro. The samples of amniotic fluid showing vasopressor activity were lyophilized and subjected to gel filtration using Sephadex G-100. The various fractions thus obtained were monitored at 280 nm and the pressor activity was re-estimated. It was observed that most of the pressor activity of the amniotic fluid of the toxaemic patients was capable of causing contraction of the rat colon as well as a significant rise in the systolic blood pressure of the intact rat. Furthermore, this activity was found to be heat-labile and was completely blocked by cinnarizine. Fractionation of the amniotic fluid showing vasopressor activity by gel filtration further substantiated the findings reported above. On the basis of these results it was concluded that the pressor activity of the amniotic fluid was due to the presence of an angiotensin II-like substance. Its concentration was found to be higher in the toxaemic group than in normotensive subjects.

Amniotic Fluid↗
PubMed2006

Sources of amniotic fluid erythropoietin during normoxia and hypoxia in fetal sheep.

OBJECTIVE: Erythropoietin is present in human amniotic fluid and has been suggested as a marker of fetal hypoxia. The objectives of the present study were to determine whether erythropoietin is present in ovine amniotic fluid, fetal urine, and/or lung liquid and whether concentrations in these compartments change in parallel with endogenous fetal plasma erythropoietin concentration when the latter is increased experimentally. STUDY DESIGN: In late gestation chronically catheterized fetal sheep, samples of amniotic fluid and plasma, urine and plasma, lung liquid, amniotic fluid, and plasma were collected before and up to 7 days after induction of 4 types of fetal hypoxia: (1) acute anemic hypoxia that was induced by a single fetal hemorrhage, (2) progressive anemic hypoxia that was induced by daily exchange transfusion, (3) acute hypoxic hypoxia that was induced by the reduction of maternal inspired oxygen content, or (4) chronic placental insufficiency that was induced by daily umbilicoplacental embolization for 4 days. Erythropoietin concentrations were determined by radioimmunoassay. Statistical testing included analysis of variance and least squares regression. RESULTS: Under basal, nonhypoxic conditions, amniotic fluid erythropoietin concentration averaged 33.2% +/- 1.6% (SE) of fetal plasma erythropoietin concentration, and basal fetal urine and lung liquid erythropoietin concentrations ranged from low (<10% of plasma concentration) to nondetectable. Unlike the strong correlation in humans, basal amniotic fluid and plasma erythropoietin concentrations were correlated only weakly (r = 0.259; r2 = 6.7%; P = .0027; n = 132). Amniotic fluid erythropoietin concentration approximately doubled after 12 hours of severe hypoxic hypoxia or after 24 hours of embolization-induced severe hypoxia but was unchanged after 12 hours of mild-moderate hypoxic hypoxia or 24 hours of anemic hypoxia. Concomitant fetal plasma erythropoietin concentrations increased to 28.1 +/- 5.3, 12.5 +/- 2.7, 10.8 +/- 4.6, and 10.0 +/- 1.3 times basal values, respectively. During progressive fetal anemia, urinary erythropoietin concentration increased almost 10-fold (P = .0023) but remained a small fraction (3.7% +/- 0.4%) of plasma concentration; at 12 hours of hypoxic hypoxia, lung liquid erythropoietin concentration did not vary with the severity of the hypoxia and remained low relative to plasma concentration (4.2% +/- 2.1%). CONCLUSION: Erythropoietin is present in ovine amniotic fluid, urine, and lung liquid. With only 3 potential sources, the fetal membranes appear to be the primary source of amniotic fluid erythropoietin in the nonhypoxic ovine fetus because basal urine and lung liquid erythropoietin concentrations are much lower than amniotic fluid concentrations. Although unchanged during mild-to-moderate fetal hypoxia, amniotic fluid erythropoietin concentration increases modestly during severe fetal hypoxia. In sheep, fetal urinary erythropoietin may contribute to this rise in amniotic fluid erythropoietin concentration during severe hypoxia, because fetal urinary and plasma concentrations increase in parallel during anemia.

Amniotic Fluid↗
PubMed1982

[Contents and distribution of Fe, Cu, Zn, Ni, and Mn in fetuses, amniotic fluid, placenta, and uterus of rats].

Fetuses, amniotic fluid, placenta, and uterus were taken from five gravid rats shortly prior to delivery, and the contents of Fe, Cu, Zn, Ni, and Mn were analyzed. Fe, Cu, Zn, and Mn exhibited a similar concentration in dry matter (DM) in all tested reproductive organs, whereby Fe-contents were five to ten times higher than Zn-contents and those five to ten times higher than Cu-contents, which amounted to 10-20 ppm. The Mn-contents range about a factor of ten below. Ni-concentration in DM of fetuses, placenta and uterus is below 1 ppm, whereas in contrast to this, Ni-concentration of 14 ppm in DM of amniotic fluid is 34 times higher than in fetuses and placenta. Uterus contained twice as much Ni as fetuses. Concerning the total content of the individual trace elements, Ni reacts also different as compared to Fe, Cu, Zn, and Mn. Its amniotic content exceeds the fetal content by 40%. Total excretion of Fe, Cu, Zn, Mn, and also DM is distributed differently as compared to Ni. Fetuses contain 60%-70% of these trace elements, placenta 15%-25%, uterus 6%-16%, and amniotic fluid only 1%-2%. Ni, however, is excreted mostly via amniotic fluid by about 35% of total excretion and only by about 25% via fetuses. These findings, concerning Ni, are discussed in detail.

Amniotic Fluid↗
PubMed2003

Amniotic fluid levels of immunoreactive monocyte chemotactic protein-1 increase during term parturition.

OBJECTIVE: Parturition is characterized by an influx of inflammatory cells into gestational tissues, a phenomenon conducive to increased myometrial contractility, cervical ripening and decidual/membrane activation. Monocyte chemotactic protein-1 (MCP-1), a potent chemoattractant and activator of monocytes/macrophages, is expressed in gestational tissues and, thus, may participate in the final common pathway of labor. This study was undertaken to determine whether the amniotic fluid concentrations of immunoreactive MCP-1 are altered with gestational age or spontaneous labor at term with and without prelabor rupture of the gestational membranes. We also sought to identify intrapartum differences in the concentrations of immunoreactive MCP-1 between the upper and lower amniotic fluid compartments. METHODS: A cross-sectional study was conducted to assess the concentrations of immunoreactive MCP-1 in amniotic fluid. Amniotic fluid samples were obtained from 225 women as follows: (1) women undergoing mid-trimester (14-18 weeks of gestation) amniocentesis for genetic indications, whose pregnancy outcome was normal (n = 84); (2) women in labor (n = 52) and not in labor (n = 31) at term, with intact gestational membranes; (3) women with rupture of the gestational membranes in labor (n = 18) and not in labor (n = 26), at term; and (4) women in labor at term for whom paired amniotic fluid samples were obtained through transvaginal and transabdominal amniocenteses (n = 14). Immunoreactive MCP-1 was assessed with a specific and sensitive immunoassay that had been validated for amniotic fluid. Non-parametric statistics were used for analysis. RESULTS: Immunoreactive MCP-1 was detected in all amniotic fluid samples. Spontaneous human parturition was associated with a significant increase in the amniotic fluid concentrations of immunoreactive MCP-1 (not in labor: median 595 pg/ml, range 183-3579 pg/ml vs. in labor: median 862 pg/ml, range 183-9609 pg/ml; p = 0.01). The median amniotic fluid concentrations of immunoreactive MCP-1 were significantly higher in the lower amniotic fluid compartment than in the upper amniotic fluid compartment (lower compartment: median 2913 pg/ml, range 1360-17080 pg/ml vs. upper compartment: median 1603 pg/ml, range 1070-8062 pg/ml; p = 0.004.). Spontaneous rupture of the gestational membranes at term was not associated with a significant change in the amniotic fluid concentrations of immunoreactive MCP-1. CONCLUSIONS: Immunoreactive MCP-1 is a physiological constituent of the amniotic fluid. The amniotic fluid levels of immunoreactive MCP-1 increase during spontaneous labor at term. A topographic difference in the concentration of immunoreactive MCP-1 was observed in the amniotic cavity, with higher concentrations being noted in the lower amniotic fluid compartment, as compared with the upper amniotic fluid compartment. These findings support the hypothesis that MCP-1 may play a role in the final common pathway of spontaneous labor.

Adolescent↗
PubMedDate not supplied

Fluorescence polarization changes with gestational age in amniotic fluid of rabbit and guinea pig.

The variation of amniotic fluid microviscosity with gestational age was measured in rat, rabbit, and guinea pig. In rat, the changes followed the same pattern as known for women, microviscosity being high during early and mid-gestation and markedly lowering 12 h before delivery. Surprisingly, an opposite trend was observed in rabbit and guinea pig amniotic fluid. Moreover, the lecithin to sphingomyelin ratio markedly rose in late gestation in all species considered. Qualitative and quantitative analysis of lipids and phospholipids were performed in woman and rabbit amniotic fluids at early and late gestational ages. Among all the parameters measured, the most important differences that can influence the amniotic fluid microviscosity are the presence of very high levels of lysophosphatidylcholine both in early and late gestation in rabbit (much higher than in woman) and the cholesterol to total phospholipid ratio which decreased with gestational age in woman but remained stable in rabbit. The Arrhenius plot of the logarithm of microviscosity against the reciprocal of absolute temperature of mature and immature amniotic fluids from woman and rabbit was also determined. The temperature profiles confirmed the differences in lipid profile between woman and rabbit in early and late gestation which could be quantified on a physicochemical basis by determining the activation energy (delta E) at 25 degrees and 37 degrees C for each curve. This confirmed the opposite patterns in woman and rabbit and showed that amniotic fluid from the immature rabbit was the most fluid.

Amniotic Fluid↗
PubMed2005

United kingdom amniotic fluid embolism register.

OBJECTIVE: The United Kingdom Amniotic Fluid Embolism Register was established to identify the incidence of the condition and examine any differences or common factors between survivors and fatalities. DESIGN: An anonymous voluntary register. SETTING: The United Kingdom from 1997 to 2004. POPULATION: Any woman with a clinical diagnosis of amniotic fluid embolism. The entry criteria were as follows: acute hypotension or cardiac arrest, acute hypoxia and coagulopathy with onset during labour, caesarean section or within 30 minutes of delivery with no other clinical condition or potential explanation for the symptoms and signs. METHODS: A data collection form was completed after reporting. MAIN OUTCOME MEASURES: Mortality and morbidity rates in women and their babies. RESULTS: Of 66 cases, 44 had sufficient information to be included. Thirteen (29.5%; 95% CI 17-45%) women died. If the five extra deaths in the Confidential Enquiry into Maternal Death were included, the mortality would be 37% (95% CI 23-52%). Of the 31 survivors, 12 women had a cardiac arrest, 7 had a hysterectomy, 2 had further laparotomies, 1 had subglottic stenosis and 2 had persisting neurological impairment. Twenty-four of the 31 survivors were admitted to intensive care units. Of the 13 women who died, 7 of their babies survived. Four were acidotic at birth, of whom two developed hypoxic ischaemic encephalopathy (HIE) and one of these is known to have developed cerebral palsy. In 18 cases, the woman survived and the baby was alive and in utero at the time of the maternal collapse. Four of these died, four had HIE with one known to have developed cerebral palsy and one other was acidotic at birth. CONCLUSION: The mortality of amniotic fluid embolism is high but the majority of women will survive. There is significant maternal and neonatal morbidity even when the woman survives. Continuing assessment of cases of amniotic fluid embolism is important to identify ways of improving outcome.

Adult↗
PubMed1982

Correlation of amylase and lecithin sphingomyelin ratios in amniotic fluid samples.

The use of amniotic fluid amylase (AF amylase) has been proposed as a screening test to determine fetal maturity. We reviewed data from 944 amniotic fluid samples analyzed by our laboratory for amylase and lecithin sphingomyelin (L/S) ratio between 1975 and 1980. AF amylase shows poor overall correlation with L/S ratios (r = 0.256). Retrospective analysis of AF amylase as a screen to determine the need for L/S ratios showed an overall sensitivity of 57%, and an overall specificity of 86% for AF amylase. Three groups were studied: a low amylase group (amylase less than 200 U/L), a middle group (amylase 200-300 U/L), and a high amylase group (amylase greater than 300 U/L). Only 55% of the low amylase group had an immature L/S ratio. The high amylase group had the best correlation between AF amylase and L/S ratio, but 13% of these samples had an immature or borderline L/S ratio. We conclude that AF amylase cannot be used as a screening test to determine the need to perform L/S ratios.

Amniotic Fluid↗