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Biomedical subjects

C Y Spong

Publications and source records attributed to C Y Spong.

At least 37 records · Page 2Linked to original sources
PubMed2000

Protective peptides derived from novel glial proteins.

In studying the mediators of VIP neurotrophism in the central nervous system, two glial proteins have been discovered. Both of these proteins contain short peptides that exhibit femtomolar potency in preventing neuronal cell death from a wide variety of neurotoxic substances. Extension of these peptides to models of oxidative stress or neurodegeneration in vivo have indicated significant efficacy in protection. These peptides, both as individual agents and in combination, have promise as possible protective agents in the treatment of human neurodegenerative disease and in pathologies involving oxidative stress.

Animals↗
PubMed1999

VIP and D-ala-peptide T-amide release chemokines which prevent HIV-1 GP120-induced neuronal death.

Vasoactive intestinal peptide (VIP) and DAPTA (D-ala(1)-peptide T-amide, a gp120-derived octapeptide homologous to VIP) prevent neuronal cell death produced by five variants of HIV-1 (human immunodeficiency virus) envelope protein (gp120). VIP or DAPTA treatment of astrocyte cultures resulted in the release of macrophage inflammatory protein-1alpha (MIP-1alpha) and RANTES, beta chemokines known to block gp120 interactions with microglial chemokine receptors. In rat cerebral cortical cultures, gp120-induced neuronal killing was partially or completely prevented by chemokines that stimulate the CXCR4, CCR3 or CCR5 chemokine receptors. Chemokines exhibited marked differences in potency and efficacy in preventing toxicity associated with five gp120 variants (LAV/BRU, CM243, RF, SF2, and MN). RANTES had the broadest and most potent inhibition (IC(50)<3 pM for RF isolate). An octapeptide derived from RANTES also exhibited neuroprotection from gp120 (RF isolate) toxicity (IC(50)=0.3 microM). Treatment with chemokines alone had no detectable effect on neuronal cell number. However, antiserum to MIP-1alpha produced neuronal cell death that was prevented by co-treatment with MIP-1alpha, suggesting that this endogenous chemokine exerts a tonic regulation important to neuronal survival. The neuroprotective action of VIP on gp120 was attenuated by co-treatment with anti-MIP-1alpha. These studies suggest that the neuroprotective action of VIP is linked in part to its release of MIP-1alpha. Furthermore, neuroprotection produced by chemokines is dependent on both the type of chemokine and the variant structure of gp120 and may be relevant to drug strategies for the treatment of AIDS dementia.

Animals↗
PubMed1999

Risk of abnormal triple screen for Down syndrome is significantly higher in patients with female fetuses.

Previous studies have shown that mid-trimester maternal serum alpha-fetoprotein (AFP) levels are significantly higher and human chorionic gonadotrophin (hCG) levels significantly lower in women with male compared with female fetuses. We have evaluated whether triple-screen criteria are more likely to identify women with female fetuses as at risk for Down syndrome. From the Georgetown University genetics database we obtained the absolute values and corresponding multiples of the median (MoM) for AFP, hCG and unconjugated oestriol (uE3) in singleton gestations for the period database November 1992 July 1996. A Down syndrome risk of 1/270 or greater at mid-trimester was considered as high risk. A total of 977 patients with triple screen and outcome information were identified, including 502 female and 475 male fetuses. Patients with female fetuses were significantly more likely to have lower serum AFP (p=0.003) and a positive triple screen for Down syndrome (72 (14 per cent) versus 45 (9 per cent), p<0.02) than those with male fetuses. The gestational age at triple screen, maternal serum hCG and uE3, race and diabetes were not significantly different between the two groups. Since Down syndrome is less common in female than male fetuses, and the rates of female and male Down syndrome fetuses detected by triple screen and subsequent amniocentesis are not significantly different, the excess of positive mid-trimester maternal serum triple screen in women with female fetuses is likely due to false-positive results.

Adult↗
PubMed1999

Glycosylated hemoglobin as a predictor of fetal pulmonic maturity in insulin-dependent diabetes at term.

In insulin dependent diabetic (IDDM) gestations, fetal pulmonary maturity is delayed in the presence of suboptimal glycemic control. Serum glycosylated hemoglobin (HbA1c) provides a means of assessing glycemic control. We evaluated maternal HbA1c in IDDM pregnancies at term undergoing amniocentesis for lung maturity to establish if euglycemia is associated with improved fetal lung maturity. Between July 1995 and June 1996, IDDM patients undergoing amniocentesis at term for lung maturity studies had a maternal serum sample analyzed for HbA1c. Fetal lung maturity was established by the presence of phosphatidylglycerol (PG) in amniotic fluid. HbA1c was considered elevated if >6.2%. Mean HbA1c level was 6.8% (range 4.4 to 9.9%). PG was present in 54% of patients with elevated HbA1c (7/13) versus 80% of those with normal HbA1c (8/10) (p = 0.4). Although birth weight was higher in the elevated than in the normal HbA1c group (3770 +/- 514 vs. 3215 +/- 610 g), no association was present between birth weight and HbA1c level (r = 0.22, p = 0.4). The rate of a mature pulmonic profile at term is not significantly different between IDDM women with good or poor glycemic control. HbA1c values should not be used to predict the presence or absence of amniotic fluid PG.

Adult↗
PubMed1999

Regulation of postimplantation mouse embryonic growth by maternal vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP) is an identified regulator of growth in the embryonic day (E) 9-11 mouse. Mouse embryonic and extra-embryonic tissues were studied to identify the source of VIP at this critical time. VIP and mRNA was detected in the decidua/trophoblast at E8 and declined until E10, after which it was not detectable. VIP mRNA was not apparent in the embryo until E11-E12. At E9, cells in decidua had VIP as well as lymphocyte marker (delta and CD3) immunoreactivity. VIP binding sites were dense in the decidua/trophoblast at E6, which gradually decreased until E10. VIP binding sites were detected in embryonic neuroepithelium by E9. The transient presence of VIP binding sites and mRNA in the decidua/trophoblast correlate with the identified period of VIP growth regulation, when VIP mRNA is absent in the embryo. Therefore, these findings suggest that maternal decidual lymphocytes are the source of VIP that regulate early postimplantation embryonic growth.

Animals↗
PubMed1999

Maternal regulation of embryonic growth: the role of vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP) is an important growth regulator of the embryonic day (E)9-E11 mouse. In comparably aged rat embryos, VIP messenger RNA (mRNA) is not detectable; however, peak concentrations of VIP in maternal rat serum indicate a nonembryonic source. In the current study, mouse maternal and embryonic tissues were examined from E6-E12. Although RT-PCR revealed VIP mRNA in E6-E7 conceptuses, by E8 (when extraembryonic tissues could be separated from the embryo), VIP mRNA was detected only in the decidua/trophoblast. Decidual/trophoblastic VIP mRNA decreased until E10, after which it was not detectable. VIP mRNA was not apparent in the embryo until E11-E12. At E9, VIP immunoreactivity was localized to abundant, diffuse cells in the decidua basalis, which were also immunoreactive for T cell markers. VIP binding sites were dense in the decidua/trophoblast at E6, but gradually decreased until E10, after which they were not apparent. VIP binding sites were detected in embryonic neuroepithelium by E9. The transient presence of VIP binding sites and mRNA in the decidua/trophoblast correlate with the critical period of VIP growth regulation, when VIP mRNA is absent in the embryo. These findings suggest that maternal lymphocytes are the source of VIP's regulating early postimplantation embryonic growth.

Animals↗
PubMed1998

Is maternal serum triple screening a better predictor of Down syndrome in female than in male fetuses?

Among euploid gestations, female fetuses have been reported to have significantly lower maternal serum alpha-fetoprotein (MSAFP) and higher human chorionic gonadotropin (hCG) levels than male fetuses. Since in maternal serum triple screening, low MSAFP and high hCG MOM independently confer greater risk of a Down syndrome fetus, we investigated the hypothesis that maternal serum triple screening is more efficacious at detecting female than male Down syndrome fetuses. A database containing all karyotypes from amniocentesis performed between August 1994 and August 1996 was accessed. All trisomy 21 cases were identified. The male-to-female ratio among trisomy 21 fetuses detected at amniocentesis after abnormal maternal serum triple screening was compared with that among trisomy 21 fetuses detected at amniocentesis for advanced maternal age (AMA), which served as the control group. Statistical analysis utilized chi-square, Fisher's exact test, and Student's t-test. A P value of less than 0.05 was considered statistically significant. Forty-nine trisomy 21 fetuses were detected in the women who underwent amniocentesis because of abnormal triple screening and 311 were detected in the control group. The proportion of male fetuses among the triple screening group was not significantly different from that of the AMA group (55 per cent vs. 57 per cent; P=0.9). Our study had a power of 80 per cent to detect a difference of 25 per cent in the male-to-female ratio (alpha=0.05, beta=0.20). The reported differences in MSAFP and hCG levels between male and female euploid fetuses do not appear to affect the sex ratio among Down syndrome fetuses detected because of an abnormal maternal serum triple screening.

Amniocentesis↗
PubMed1998

Are the cytokines interleukin-6 and angiogenin stable in frozen amniotic fluid?

OBJECTIVE: To determine the stability of cytokines in frozen stored amniotic fluid samples, we measured angiogenin, a potent inducer of neovascularization and interleukin-6, an inflammatory cytokine, in the same sample of midtrimester amniotic fluid 1 year apart. STUDY DESIGN: In this study paired aliquots of amniotic fluid kept at -70 degrees C were immunoassayed for angiogenin and interleukin-6 at two different time periods 1 year apart. Inclusion criteria were (1) samples with clearly identifiable numbers, (2) no evidence of breaks in sealing of samples, and (3) singleton gestation. Amniotic fluid was immunoassayed for angiogenin and interleukin-6 in July 1995 and 1996. Angiogenin sensitivities were 0.078 and 0.026 ng/ml, interassay coefficients of variation were 3.8% and 4.6%, and intraassay coefficients of variation were 2.7% and 2.9%, respectively, in 1995 and 1996. Interleukin-6 sensitivities were 1.74 and 2.37 pg/ml, interassay coefficients of variation were 8.9% and 2.6%, and intraassay coefficients of variation were 3.5% and 1.9%, respectively, in 1995 and 1996. Statistical analysis included paired t test, Wilcoxon signed-rank test, and regression with p < 0.05 significant. Angiogenin and interleukin-6 values were normalized with natural log transformation for statistical analysis. RESULTS: Paired amniotic fluid samples from 30 patients were immunoassayed from 1993 to 1995. The values of angiogenin were significantly lower in the 1996 assay compared with the 1995 assay (median 12.4 [range 5.6 to 61.3] vs 26.7 [range 13.6 to 159.2] ng/ml, p < 0.001). A significant correlation was found between the change in angiogenin levels and the year of the sample, with older samples having the greatest change in values (r=0.5, p=0.008). The values of interleukin-6 were significantly lower in the 1996 assay compared with the 1995 assay (median 230.8 [range 40.9 to 3711.3] vs 289.2 [range 53.7 to 19100.0] pg/ml, p < 0.001). CONCLUSIONS: Angiogenin and interleukin-6 values in amniotic fluid appear to decrease with time despite optimal freezing conditions. The year of sampling and length of storage should be taken into consideration when evaluating amniotic fluid cytokine levels from stored samples.

Adult↗
PubMed1998

Elevated second-trimester maternal serum hCG: a marker of inadequate angiogenesis.

OBJECTIVE: To measure angiogenin, a potent inducer of neovascularization and interleukin-6, as an indicator of acute inflammation, in second-trimester amniotic fluid of patients with elevated maternal serum hCG. METHODS: In this case-control study, 20 patients with elevated maternal serum hCG (at least 2.0 multiples of median) at triple screen were matched 2:1 with controls on the basis of year of amniocentesis, parity, and race. Inclusion criteria were 1) singleton gestation, 2) no evidence of anomalies, and 3) genetic amniocentesis. Amniotic fluid was immunoassayed for angiogenin and interleukin-6. The immunoassay sensitivity for angiogenin was 0.026 ng/mL, interassay coefficient of variation 4.6%, and intra-assay coefficient of variation 2.9%. For interleukin-6, the immunoassay sensitivity was 2.37 pg/mL, interassay coefficient of variation 2.7%, and intra-assay coefficient of variation 1.9%. Angiogenin and interleukin-6 values were normalized by using natural log transformation for statistical analysis. Statistical analysis included analysis of variance and stepwise regression, with P < .05 significant. RESULTS: After correcting (by multivariate regression) for gestational age at sampling and nulliparity, amniotic fluid angiogenin levels were significantly lower in the study subjects than in controls (26%+/-11% lower, P=.004), whereas the interleukin-6 levels did not change significantly (34%+/-40% lower, P=.3). CONCLUSION: Amniotic fluid angiogenin levels are significantly lower in patients with elevated maternal serum hCG at triple screen, suggesting inadequate angiogenesis, but interleukin-6 values do not differ significantly.

Adult↗
PubMed1998

Recurrence of gestational diabetes mellitus: identification of risk factors.

The objective of this paper is to evaluate the influence of maternal and neonatal factors on the recurrence of gestational diabetes mellitus (GDM). A study was conducted on 164 predominantly Hispanic patients whose index pregnancy was complicated by GDM and whose subsequent consecutive pregnancy was managed at our institution between January 1988 and December 1992. The diagnosis of GDM was based on the criteria recommended by the National Diabetes Data Group using a 100-g oral glucose tolerance test. One-hundred and eleven (68%) of the 164 women had recurrence of GDM. Fifty-three (32%) did not demonstrate recurrence in their subsequent pregnancy. Patients with recurrence had GDM diagnosed earlier (30.3 vs 32.5 weeks, p = 0.03), frequently required insulin (25 vs. 8%, p <0.05) and had more hospital admissions (32 vs. 10% p <0.05) in their index pregnancy compared to women who did not have recurrence of GDM. Women who had recurrence had elevated mean third-trimester plasma glucose values: fasting 87.6 vs. 83 mg/dL, (p = 0.009) and 2-hr postprandial 109.7 vs. 102.2 mg/dL, (p = 0.008). Neonates of patients with recurrence were heavier (3656 vs. 3373 g, p = 0.004) and had an increased incidence of macrosomia (26 vs. 10%, p <0.05). No significant differences were observed in maternal age, prepregnancy body mass index, HbgA1C values, second-trimester blood glucose levels, method of delivery, incidence of shoulder dystocia and Apgar scores between the two groups of women. Hispanic patients with history of GDM have significant risk of recurrence in their subsequent pregnancy. The risk for recurrence in women is increased if GDM is diagnosed earlier, they require insulin, have elevated third-trimester plasma glucose level, and deliver macrosomic infants in their index pregnancy. It appears that obesity does not increase the risk of recurrence of gestational diabetes in Hispanics.

Adult↗
PubMed1998

Characterization and prognostic significance of variable decelerations in the second stage of labor.

The characteristics of variable decelerations (VD) in the second stage of labor and the relationship between the number, frequency, or severity and neonatal outcome have not been studied. We have analyzed the characteristics of VD in the second stage of labor and their prognostic significance in the prediction of Apgar scores. In this descriptive study, fetal heart tracings containing VD from 250 singleton, vaginal deliveries between June 1994 and July 1996 were reviewed blinded to outcome information. Excluded were: (1) deliveries at <36 weeks, (2) uninterpretable tracing, (3) absence of VD in second stage of labor, and (4) absence of exam establishing beginning of second stage of labor. VD characteristics evaluated: shape (U, V, W); anterior and posterior "shoulders"; slow return to baseline (< or = 30-degree curve); cumulative depth of VD per 10 min, second stage oxytocin dose. Outcome information collected: method of delivery, birth weight and Apgar scores. Statistical analysis included regression and analysis of variance (ANOVA). The mean maternal age was 32+/-5 years and gestational age 39+/-1.3 week. In the second stage of labor, the mean oxytocin dose was 3+/-5 mu/min, length of the second stage 65+/-57 min, total number of VD averaged 21+/-17 and uterine contractions 26+/-22 per patient. The percentage of VD <100 bpm was 50+/-27%, VD <70 bpm 13+/-20%, anterior shoulders 76+/-30%, posterior shoulders 75+/-30% and slow return to baseline 12+/-17%. The number of VD significantly increased with the length of the second stage of labor (r=0.85, p <0.001). The total number and percentage of VD <70 bpm were inversely correlated with 5-min Apgar score (p=0.038, 0.015 respectively). The sum of the depth of VD/length of second stage as well as the percentage of VD with anterior and/or posterior shoulders and slow return to baseline were not significantly related to Apgar scores (p=0.08, 0.72, 0.73, 0.99, respectively). Patients with a higher percentage of decelerations with slow return to baseline had a higher rate of operative vaginal deliveries (20 vs. 11 %, p=0.002); but no significant differences in Apgar scores compared with those with spontaneous delivery (p=0.9). Second stage VD <70 bpm were significantly associated with lower 5-min Apgar scores. Although the presence of VD with a slow return to baseline was significantly associated with operative delivery, there was no difference in 5-min Apgar scores.

Adult↗
PubMed1997

Elevated maternal serum midtrimester alpha-fetoprotein levels are associated with fetoplacental ischemia.

OBJECTIVE: Elevation of maternal serum alpha-fetoprotein in the second trimester is associated with poor pregnancy outcome, including fetal death, preterm delivery, and fetal growth restriction. We hypothesized that placental ischemia may be the common underlying pathogenesis of these outcomes. Thus we tested angiogenin, a potent inducer of neovascularization, in midtrimester amniotic fluid of patients with elevated maternal serum alpha-fetoprotein values to determine whether alpha-fetoprotein elevation is due to ischemia with subsequent stimulation of angiogenesis. STUDY DESIGN: In this case-control study, patients with elevated maternal serum alpha-fetoprotein levels (> or = 2.0 multiples of the median, n = 9) at triple screen were matched with two controls (n = 18) on the basis of year of amniocentesis and maternal age, race, and parity. The median elevation of maternal serum alpha-fetoprotein in the study population was 4.01 multiples of the median (range 2.65 to 7.24 multiples of the median). Inclusion criteria were (1) singleton gestation, (2) no evidence of fetal structural or chromosomal anomalies, and (3) genetic amniocentesis. Amniotic fluid was immunoassayed for angiogenin (Quantikine, R&D Systems; sensitivity 0.026 ng/ml, interassay and intraassay coefficients of variation 4.6% and 2.9%, respectively). Statistical analysis included one-way analysis of variance and regression with p < 0.05 significant. Angiogenin and maternal serum alpha-fetoprotein values were normalized with use of natural log transformation for statistical analysis. RESULTS: Angiogenin values were significantly elevated in patients with high maternal serum alpha-fetoprotein levels (median 31.1 [range 9.2 to 54.6] vs 17.1 [range 9.0 to 29.2] ng/ml, p = 0.02). Mean gestational age at sampling, maternal age, and year of amniocentesis were not significantly different between the study and control groups (each p > 0.05). As anticipated, there was a significant increase in preterm deliveries and small-for-gestational-age neonates in the patients with elevated maternal serum alpha-fetoprotein levels (each p < 0.01). CONCLUSIONS: Midtrimester amniotic fluid angiogenin levels are significantly elevated in patients with elevated midtrimester maternal serum alpha-fetoprotein levels. Because angiogenin is a known marker of tissue ischemia, resulting in neovascularization, we hypothesize that elevation of maternal serum alpha-fetoprotein levels at triple screen is due to placental ischemia.

Adult↗
PubMed1997

Angiogenin: a marker for preterm delivery in midtrimester amniotic fluid.

OBJECTIVE: Neovascularization is a response of tissue to ischemic damage. Placental ischemia is thought to underlie a significant portion of preterm deliveries. Our objective was to evaluate whether angiogenin, a potent inducer of neovascularization, is increased in midtrimester amniotic fluid of patients destined to be delivered preterm. STUDY DESIGN: We designed a case-control study of singleton gestations undergoing midtrimester amniocentesis for standard genetic indications. Inclusion criteria were (1) pregnancy outcome information available, (2) gestational age at amniocentesis 15 to 20 weeks, (3) no evidence of fetal structural or chromosomal anomalies, and (4) absence of conditions associated with preterm delivery. Amniotic fluid angiogenin levels were measured by immunoassay and normalized by natural log transformation for statistical analysis. RESULTS: Eleven patients with preterm deliveries were matched with 33 controls. Amniotic fluid angiogenin levels were significantly higher in patients with preterm deliveries compared with controls (median 30.1 ng/ml [range 13.6 to 71.0 ng/ml] vs 17.8 ng/ml [7.8 to 43.3 ng/ml], p = 0.002). Demographic data were not significantly different. The association between angiogenin levels and preterm delivery persisted after small-for-gestational-age neonates were excluded (p = 0.02). Receiver-operator characteristic curve analysis showed that an angiogenin level of 31.0 ng/ml was the optimal cutoff point for prediction of preterm delivery (sensitivity 45.5%, specificity 91.0%, p = 0.03, odds ratio 6.0). CONCLUSIONS: Midtrimester amniotic fluid angiogenin levels are elevated in patients with preterm delivery. This supports the theory that preexisting intrauterine ischemia and inflammation are important risk factors for preterm delivery and may be already present in the early midtrimester.

Adult↗
PubMed1997

Increased incidence of fetal growth restriction in association with breech presentation in preterm deliveries < 32 weeks.

Breech presentation and fetal growth restriction (FGR) are each related independently with preterm delivery. This study was designed to assess the possible relationship between breech presentation and FGR in deliveries at < 32 weeks' gestation. From an established database of 465 consecutive deliveries at < 32 weeks of nonhypertensive, nondiabetic patients with singleton nonanomalous fetuses, those in whom birth weight, body length, fetal presentation (vertex or breech), and amniotic fluid volume (AFV) had been assessed were studied. Fetal growth restriction (defined as symmetric if both birth weight and body length were < 10th percentile and asymmetric if only the birth weight was < 10th percentile) was studied in relation to maternal age, parity, tobacco use, fetal presentation, AFV, membrane status, and gestational age at delivery. Statistical analyses included contingency tables and analysis of variance, with p < 0.05 considered significant. Two hundred ninety-eight patients met the inclusion criteria. In these patients 85 (28.5%) fetuses were breech and 213 (71.5%) cephalic. A total of 56 (19%) fetuses were growth restricted. Of these, 31 (10.4%) were symmetrically and 25 (8.3%) asymmetrically growth restricted. The incidence of symmetric growth restriction in the breech-presenting fetuses was 16% (n = 14) versus 8% (n = 17) in the cephalic-presenting fetuses, and of asymmetric growth restriction 12% (n = 10) versus 7% (n = 15), (overall p = 0.03). Fetal growth restriction was not associated with significant differences in maternal age, parity, smoking, AFV, membrane status, or gestational age at delivery (each p > 0.10). In preterm deliveries at < 32 weeks' gestation, breech presentation is associated with an increased incidence of intrauterine growth restriction, independent of clinical confounders.

Amniotic Fluid↗
PubMed1997

Residual amniotic fluid volume in preterm rupture of membranes: association with fetal presentation and incidence of clinical and histologic evidence of infection.

The objective of this study was assess whether residual amniotic fluid volume (AFV) following premature rupture of the membranes (PROM) is associated with fetal presentation, or the prevalence of either clinical or histologic infection in patients delivering below 32 weeks' gestation. From an established database of 465 deliveries below 32 weeks' gestation, patients with singleton, nonanomalous fetuses with AFV assessment within 24 hours of delivery were studied (n = 146). Fetal presentation was confirmed by ultrasound identifying 46 breech and 100 vertex-presenting fetuses. Premature rupture of the membranes was diagnosed by sterile speculum examination. Clinical chorioamnionitis was diagnosed by previously published criteria. Histopathology examination of the extraplacental amnion and the umbilical cord were performed by a single pathologist blinded to clinical data. Outcome variables evaluated: rupture-to-delivery interval, gestational age at delivery, neonatal morbidity parameters (1- and 5-min Apgar scores < 5 and 7, respectively; incidence of respiratory distress syndrome; bronchopulmonary dysplasia; retinopathy of prematurity; neonatal sepsis; intraventricular hemorrhage; days of ventilation; and hospitalization), and placental histologic parameters of maternal and/or fetal acute inflammation. Statistical analysis included contingency tables and analysis of variance with p < .05 considered significant, after corrections for multiple comparisons when appropriate. Residual AF volume following PROM was significantly lower in breech compared with vertex presentation (AFV = 0 in 20 vs. 34; AFV = 1 in 19 vs. 27; AFV = 2 in 7 vs. 39, respectively, p = .014). No significant difference was noted in the rupture-to-delivery interval, gestational age at delivery, neonatal morbidity parameters, or histologic evidence of maternal and/or fetal acute inflammation (50% vs. 42%, p > .2) between gestations with breech or vertex presentations. The incidence of clinical chorioamnionitis was significantly lower in breech compared with vertex presentation (40% vs. 60%, p < .05). We conclude that following PROM below 32 weeks' gestation, in breech-presenting fetuses, the residual AFV and incidence of clinical chorioamnionitis are significantly decreased compared with vertex-presenting fetuses.

Acute Disease↗
PubMed1997

Fetal breathing movements within 24 hours of delivery in prematurity are related to histologic and clinical evidence of amnionitis.

Our objective was to determine the association of fetal breathing movements (FBM) within 24 hr of delivery, with the clinical diagnosis of chorioamnionitis and histologic evidence of severe acute amnionitis and umbilical-chorionic vasculitis in women delivering at < 32 weeks' gestation. We performed a cohort study of patients with singleton gestations delivered at < 32 weeks' following preterm labor with intact membranes and sonographically assessed biophysical profile within 24 hr of delivery (n = 111). Patients with FBM were compared with those without FBM, with regard to prevalence of clinical chorioamnionitis (CA) and histologic diagnosis of acute amnionitis and umbilical vasculitis. Maternal and neonatal charts were reviewed and the diagnosis of clinical CA made by previously established criteria. Histologic presence and extent of acute intrauterine inflammation was assessed and scored by a single pathologist blinded to clinical information. Results are presented as chi 2 values and odds ratios with 95% confidence intervals. Of the patients included in the study, FBM were absent in 56 and present in 55. The prevalence of CA was 13% (15 of 111), severe acute amnionitis 34% (38 of 111), and severe umbilical vasculitis 23% (26 of 111). Severe umbilical vasculitis was significantly less frequent in cases with FBM as compared to cases without FBM (15% [8 of 55] vs. 32% [18 of 56], p = 0.049). However, the difference in rate of CA (22% [12 of 55] vs. 34% [19 of 56], p = 0.22) and histologic severe amnionitis (29% [16 of 55] vs. 39% [22 of 56], p = 0.4) between cases with and without FBM was not significant. In the presence of preterm labor with intact membranes, absence of FBM had sensitivities of 73 and 72%, and specificities of 54 and 56% in the prediction of CA and histologic evidence of umbilical vasculitis, respectively. We conclude that absence of FBM is associated with histologic evidence of fetal inflammation in intrauterine infection in patients with preterm labor and intact membranes delivering at < 32 weeks. However, the low positive predictive value of absent FBM in predicting fetal inflammation in intrauterine infection should discourage the guidance of clinical management in patients < 32 weeks' gestation with preterm labor and intact membranes.

Adult↗
PubMed1997

Fetal but not maternal serum cytokine levels correlate with histologic acute placental inflammation.

Our objective was to determine if placental histologic acute inflammation is related to maternal and fetal serum cytokine levels in preterm labor, using a data set previously constructed blinded to histopathologic information. To this goal in 1992, 32 consecutive patients at 20-36 weeks with progressive labor and tocolytic failure were recruited. Maternal serum sampled during the active phase of labor, and fetal (umbilical vein) serum were assayed by ELISA for levels of soluble interleukin-1 beta (IL-1 beta), soluble interleukin-2 receptor (IL-2 R), and interleukin 6 (IL-6) (T-Cell Diagnostics). Acute placental inflammation was scored by two groups blinded to clinical data, and the average scores analyzed for relationships to serum cytokine levels. Weighted kappa values, reflecting interobserver agreement in scoring of acute inflammation, were: amnion 0.84; choriodecidua 0.84; umbilical cord 0.85; and chorionic plate 0.73. Fetal levels of IL-1 beta and IL-2 R were higher with grade 3-4 acute amnionitis than with grades 0-2 (p = 0.022 and p = 0.023). Fetal levels of all three cytokines were higher in grade 3-4 umbilical vasculitis (IL-1 beta p = 0.008, IL-2 R p = 0.01, and IL-6 p = 0.03). In contrast, maternal serum cytokine levels were not associated with presence or severity of histologic evidence of acute placental inflammation. Histologic acute inflammation was not related to duration of labor, interval from membrane rupture to delivery, and presence or duration of antibiotic therapy. We conclude that fetal serum, but not maternal serum cytokine levels, are correlated with histologic evidence of acute placental inflammation, and may reflect a predominant placental origin of the cytokines.

Acute Disease↗