Reduced fetal growth velocity precedes antepartum fetal death.

OBJECTIVES: To determine whether decreased fetal growth velocity precedes antepartum fetal death and to evaluate whether fetal growth velocity is a better predictor of antepartum fetal death compared to a single fetal biometric measurement at the last available ultrasound scan prior to diagnosis of demise. METHODS: This was a retrospective, longitudinal study of 4285 singleton pregnancies in African-American women who underwent at least two fetal ultrasound examinations between 14 and 32 weeks of gestation and delivered a liveborn neonate (controls; n = 4262) or experienced antepartum fetal death (cases; n = 23). Fetal death was defined as death diagnosed at ≥ 20 weeks of gestation and confirmed by ultrasound examination. Exclusion criteria included congenital anomaly, birth at < 20 weeks of gestation, multiple gestation and intrapartum fetal death. The ultrasound examination performed at the time of fetal demise was not included in the analysis. Percentiles for estimated fetal weight (EFW) and individual biometric parameters were determined according to the Hadlock and Perinatology Research Branch/Eunice Kennedy Shriver National Institute of Child Health and Human Development (PRB/NICHD) fetal growth standards. Fetal growth velocity was defined as the slope of the regression line of the measurement percentiles as a function of gestational age based on two or more measurements in each pregnancy. RESULTS: Cases had significantly lower growth velocities of EFW (P < 0.001) and of fetal head circumference, biparietal diameter, abdominal circumference and femur length (all P < 0.05) compared to controls, according to the PRB/NICHD and Hadlock growth standards. Fetuses with EFW growth velocity < 10th percentile of the controls had a 9.4-fold and an 11.2-fold increased risk of antepartum death, based on the Hadlock and customized PRB/NICHD standards, respectively. At a 10% false-positive rate, the sensitivity of EFW growth velocity for predicting antepartum fetal death was 56.5%, compared to 26.1% for a single EFW percentile evaluation at the last available ultrasound examination, according to the customized PRB/NICHD standard. CONCLUSIONS: Given that 74% of antepartum fetal death cases were not diagnosed as small-for-gestational age (EFW < 10th percentile) at the last ultrasound examination when the fetuses were alive, alternative approaches are needed to improve detection of fetuses at risk of fetal death. Longitudinal sonographic evaluation to determine growth velocity doubles the sensitivity for prediction of antepartum fetal death compared to a single EFW measurement at the last available ultrasound examination, yet the performance is still suboptimal. © 2020 International Society of Ultrasound in Obstetrics and Gynecology.

Erysipelothrix Septicaemia and Hepatitis in a Colony of Humboldt Penguins (Spheniscus humboldti).

This report describes an outbreak of erysipelas in a colony of captive Humboldt penguins (Spheniscus humboldti). The only previously reported case in a related species was of an individual little blue penguin (Eudyptula minor). Five Humboldt penguins in a mixed colony displayed non-specific signs of illness, including lethargy, inappetence and regurgitation after movement for exhibit upgrading. There was no improvement after 5 days of treatment with oral enrofloxacin (10 mg/kg q24h). Four Humboldt penguins, including two that were not part of the original five displaying signs of illness, died during this outbreak and Erysipelothrix rhusiopathiae was cultured from organ samples collected post mortem. Oral clavulanic acid/amoxycillin (125 mg/kg q12h) was added to the treatment of the sick Humboldt penguins, as well as itraconazole (8.5 mg/kg q12h) and silymarin (10 mg/kg q24h) for 10 days (both per os), which resolved their clinical signs. The likely source of E. rhusiopathiae was the fish they were fed, but this could not be confirmed. Another contributing factor to the growth of E. rhusiopathiae in the exhibit pool was the increase in water temperature due to a fault in the water circulating system. The temperature of the pool water had increased to 29°C, which was rectified, and the water temperature decreased to 13°C. However, there was one further Humboldt penguin death after the decrease in water temperature. This episode suggests that E. rhusiopathiae infection should be high on the differential list of piscivorous avian species with non-specific clinical signs. A liver biopsy for bacterial culture and sensitivity may be required for definitive diagnosis.

Probing the validity of average Hamiltonian theory for spin I=1, 3/2 and 5/2 nuclei by analyzing a simple two-pulse sequence.

In this work, we investigate the accuracy of controlling spin I=1, 3/2 and 5/2 spin systems by average Hamiltonian theory. By way of example, we consider a simple two-pulse echo sequence and compare this perturbation scheme to a numerical solution of the Von Neumann equation. For the different values of I, we examine this precision as a function of the quadrupolar coupling as well as various experimental parameters such as the pulse spacing and pulse width. Experiments and simulations on I=3/2 and I=5/2 spin systems are presented that highlight a spectral artifact introduced due to finite pulse widths as predicted by average Hamiltonian theory. The control of these spin systems by this perturbation scheme is considered by investigating a phase cycling scheme that suppresses these artifacts to zeroth-order of the Magnus expansion.

Epigenetic silencing of the dual-role signal mediator, ANGPTL4 in tumor tissues and its overexpression in the urothelial carcinoma microenvironment.

Urothelial carcinoma (UC) carcinogenesis has been hypothesized to occur through epigenetic repression of tumor-suppressor genes (TSGs). By quantitative real-time polymerase chain reaction array, we found that one potential TSG, angiopoietin-like 4 (ANGPTL4), was expressed at very low levels in all bladder cancer cell lines we examined. Previous studies had demonstrated that ANGPTL4 is highly expressed in some cancers, but downregulated, by DNA methylation, in others. Consequently, owing to these seemingly conflicting functions in distinct cancers, the precise role of ANGPTL4 in the etiology of UC remains unclear. In this study, using methylation-specific PCR and bisulfite pyrosequencing, we show that ANGPTL4 is transcriptionally repressed by DNA methylation in UC cell lines and primary tumor samples, as compared with adjacent noncancerous bladder epithelium. Functional studies further demonstrated that ectopic expression of ANGPTL4 potently suppressed UC cell proliferation, monolayer colony formation in vitro, and invasion, migration, and xenograft formation in vivo. Surprisingly, circulating ANGPTL4 was significantly higher in plasma samples from UC patients than normal control, suggesting it might be secreted from other cell types. Interestingly, our data also indicated that exogenous cANGPTL4 could promote cell proliferation and cell migration via activation of signaling through the Erk/focal adhesion kinase axis. We further confirmed that mouse xenograft tumor growth could be promoted by administration of exogenous cANGPTL4. Finally, immunohistochemistry demonstrated that ANGPTL4 was downregulated in tumor cells but overexpressed in tumor adjacent stromal tissues of muscle-invasive UC tissue samples. In conclusion, our data support dual roles for ANGPTL4 in UC progression, either as a tumor suppressor or oncogene, in response to microenvironmental context.

Multi-organ Metastasis of Fibrolamellar Hepatocellular Carcinoma in a Malayan Gharial (Tomistoma schlegelii).

A 38-year-old Malayan gharial (Tomistoma schlegelii) with a 2-week history of anorexia was found dead and presented for post-mortem examination. Numerous white firm nodules of various sizes were found on the surface of the liver, both left and right kidneys, the spleen and the serosa of the intestinal tract. All masses had similar microscopical appearance and were diagnosed as metastasizing fibrolamellar hepatocellular carcinoma. Immunohistochemically, the tumour cells did not react with antibodies specific for pan-cytokeratin, vimentin or HepPar-1. The anti-HepPar-1 and anti-pan-cytokeratin antibodies also did not react with normal hepatocytes or exocrine pancreatic cells. This is the first description of fibrolamellar hepatocellular carcinoma with metastases in a crocodilian.

Thrombomodulin: a new marker for placental abruption.

Thrombomodulin (TM), a marker of endothelial cell damage, has been localized to the placental syncytiotrophoblast. A prospective cohort study of twenty-five pregnant women who were admitted with a clinical diagnosis of placental abruption was undertaken. Abruption was confirmed after delivery in eight cases (Group 1). Group 2 consisted of seventeen patients with no clinical or pathologic evidence of placental abruption after delivery. TM was significantly elevated in Group 1 (71.59+/-5.35 vs. 48.29+/-3.53 ng/ml, p = 0.001). The sensitivity and specificity of TM > or =60 ng/ml as a marker for abruption was 87.5 and 76.5%, respectively. In comparison, the sensitivity of an abnormal coagulation profile, maternal Kleihauer-Betke and ultrasound in patients with abruption was 0, 16.7 and 28.6%, respectively. TM is a highly sensitive and specific marker for acute placental abruption.

Elevated amniotic fluid nucleosome levels in women with intra-amniotic infection.

OBJECTIVE: To compare amniotic fluid (AF) soluble nucleosome levels in pregnant women with and without intra-amniotic infection. METHODS: Amniocentesis was performed in 74 pregnant women with preterm contractions, labor, or premature rupture of membranes. Intra-amniotic infection was defined as a positive AF culture. Amniotic fluid tests for Gram stain, glucose, neutrophils, creatinine, pH, and specific gravity were performed. Amniotic fluid soluble nucleosome levels were determined by enzyme-linked immunosorbent assay and were normalized by AF creatinine levels. RESULTS: Twenty-eight patients had intra-amniotic infection and 46 did not. Amniotic fluid soluble nucleosome levels were significantly higher in pregnant women with intra-amniotic infection than in those without infection (48.1+/-21.3 compared with 0.0+/-0.0 U/mg creatinine; P = .005). The AF nucleosome levels were positively correlated with AF neutrophil counts and negatively correlated with AF glucose concentrations. CONCLUSION: Our data indicate that elevated AF nucleosome levels are associated with intra-amniotic infection and may have potential as a clinical marker to detect intra-amniotic infection.

Serum soluble Fas in the syndrome of hemolysis, elevated liver enzymes, and low platelets.

OBJECTIVE: To assess whether serum levels of soluble Fas and soluble Fas ligand are altered in the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP). METHODS: Serum samples from 22 pregnant women diagnosed with HELLP syndrome were compared with sera from 37 healthy women with noncomplicated singleton pregnancies. Serum levels of soluble Fas and soluble Fas ligands were determined by enzyme immunoassay. Student t, chi(2), Pearson's correlation coefficient, and multiple regression tests were used for statistical analyses. RESULTS: Both soluble Fas and soluble Fas ligand were detected in the sera of normal pregnancies as well as in those with HELLP syndrome. The mean serum level of soluble Fas was significantly higher in women with HELLP syndrome than in healthy gravidas (10.75 +/- 0.93 versus 5.81 +/- 0.37 U/mL, P <.001). However, there was no significant difference in mean serum soluble Fas ligand levels of the two groups (0.60 +/- 0.06 compared with 0.50 +/- 0.22 ng/mL, P =.23). In women with HELLP syndrome, there were no significant correlations between serum levels of soluble Fas or soluble Fas ligand with liver transaminases (aspartate and alanine aminotransferase) and platelet count. CONCLUSION: Serum levels of soluble Fas, but not soluble Fas ligand, are significantly higher in women with HELLP syndrome than healthy gravidas. The source of elevated serum levels of soluble Fas in HELLP syndrome remains to be determined.

Serum soluble Fas levels in preeclampsia.

OBJECTIVE: To determine if serum soluble Fas levels are altered in women with preeclampsia. METHODS: Thirty-four pregnant women with preeclampsia and 34 normotensive pregnant women were studied. Subjects were matched as much as possible for demographics. Preeclampsia was defined as proteinuric hypertension. Serum soluble Fas levels were measured by enzyme-linked immunoassay. Two-tailed Student t test, chi(2) test, Pearson correlation coefficients, and analysis of variance with post hoc test were used for statistical analyses. RESULTS: Mean serum soluble Fas levels were significantly higher in preeclamptic than normotensive women (10.59 +/- 0.68 U/mL versus 5.65 +/- 0.35 U/mL, P <.001). CONCLUSION: Elevated serum soluble Fas is associated with preeclampsia. Such elevation might indicate protection of maternal T-lymphocyte apoptosis and consequently lead to the maternal immune intolerance noted in preeclampsia.

Thrombomodulin levels in preeclampsia, gestational hypertension, and chronic hypertension.

OBJECTIVE: To measure the circulating levels of thrombomodulin in women with preeclampsia, gestational hypertension, and chronic hypertension. METHODS: Serum levels of thrombomodulin were measured in 34 women with preeclampsia, 15 with gestational hypertension, 11 with chronic hypertension, and 34 normotensive pregnant women in the third trimester. Preeclampsia, gestational hypertension, and chronic hypertension were defined by ACOG criteria. Soluble thrombomodulin antigen was measured by a two-site enzyme-linked immunosorbent assay. RESULTS: Mean (+/- standard error) serum thrombomodulin levels were significantly higher in patients with preeclampsia (69.7 +/- 6.3 ng/mL) than in those with gestational hypertension (46.0 +/- 3.2 ng/mL) or chronic hypertension (46.2 +/- 3.3 ng/mL), and normotensive controls (50.1 +/- 3.1 ng/mL). There were no significant differences among the gestational hypertension, chronic hypertension, and normotensive control groups. CONCLUSION: Thrombomodulin may serve as a clinically meaningful marker to differentiate preeclampsia from other forms of hypertensive disorders in pregnancy.

Amniotic fluid soluble fas levels in intra-amniotic infection.

OBJECTIVE: Membrane Fas can induce apoptosis in sensitive cells. It has been reported that soluble Fas (sFas) is elevated in septicemia. We examined amniotic fluid (AF) sFas levels in patients with and without intra-amniotic infection. METHODS: Forty-two AF specimens were studied. Intra-amniotic infection was defined as the presence of a positive AF culture. Twenty-one specimens were from patients with intra-amniotic infection and 21 were from patients without intra-ammotic infection. Amniotic fluid sFas was determined by an enzyme immunoassay and normalized by AF creatinine levels. The Mann-Whitney U test, contingency table method, and Spearman's rank correlation test were used for statistical analyses. Data were expressed as median with ranges. RESULTS: There were no significant differences in maternal age, gestational age, parity, and race between the groups. The median AF sFas was significantly higher with intra-amniotic infection than without it (5.07 U/mL, range 0.32-13. 25 compared with 1.95 U/mL, range 0.01-5.35; P =.004). After normalizing to AF creatinine, infected fluids also had significantly higher median sFas/creatinine than uninfected amniotic fluids (289.1 U/mg creatinine, range 16.6-920.5 compared with 126.8 U/mg creatinine, range 0.5-546.2; P =.01). Amniotic fluid sFas and sFas/creatinine were positively correlated with AF leukocytes and negatively correlated with AF glucose. CONCLUSION: Elevated AF sFas is associated with intra-amniotic infection. High production of AF sFas in intra-amniotic infection may play a role in the inhibition of apoptosis of AF leukocytes, leading to the persistence of inflammation.

Uterine rupture associated with recent antepartum cocaine abuse.

BACKGROUND: The diagnosis of uterine rupture is aided by the identification of risk factors, such as oxytocin administration. In several experiments, cocaine has been shown to stimulate uterine contractility. Complications from cocaine abuse during pregnancy have increased dramatically in the United States, and cocaine may increase the risk for uterine rupture. CASES: Two cases of uterine rupture were associated with recent cocaine abuse. CONCLUSION: These cases and recent experiments on the effect of cocaine on the pregnant uterus suggest that antepartum cocaine abuse may increase the risk of uterine rupture.

Elevated serum nicked and urinary beta-core fragment hCG in preeclamptic pregnancies.

OBJECTIVE: To determine whether different molecular forms of hCG in serum and urine are elevated in preeclamptic pregnancies. METHODS: Forty-three pregnant women were studied: 25 preeclamptic women and 18 normotensive women. Immediately after blood and urine samples were collected, the protease inhibitors leupeptin (0.35 mM) and phenanthroline (22 mM) were added. Various molecular forms of hCG in serum (complete hCG, nonnicked hCG, complete free beta hCG) and in urine (complete hCG, beta-core fragment hCG) were measured by matched immunoassays with a common enzyme-labeled tracer antibody. The nicked hCG assay used a coating of beta-subunit monoclonal antibody with the addition of scavenger antibody to remove nonnicked hCG. Mann-Whitney U test and chi 2 test were used for statistical analyses. RESULTS: Preeclamptic women had significantly higher median (range) levels of serum complete and nicked hCG than did normotensive women (3620 [850-12,000] versus 2420 [310-4840] ng/mL, P = .024; and 102 [45-275] versus 71 [11-143] ng/mL, P = .010, respectively). Both median (range) urinary complete hCG-creatinine and beta-core fragment-creatinine ratios were significantly higher in preeclamptic women than in normotensive women (37.6 [0.5-185] versus 11.3 [1.9-54], P = .013; and 11.8 [2-67] versus 5.3 [0.3-29], P = .009, respectively). CONCLUSIONS: Various molecular forms of hCG in serum and urine were significantly higher in preeclamptic than in normotensive pregnancies.

Antepartum and postpartum thrombomodulin levels in preeclamptic and normotensive pregnancies.

OBJECTIVE: To determine whether changes in plasma levels of thrombomodulin from antepartum to postpartum reflect the postpartum regression of preeclampsia. METHODS: Twenty-four preeclamptic women and 34 healthy, normotensive women with singleton pregnancies were studied in the third trimester. Plasma levels of thrombomodulin in the antepartum and postpartum periods were measured by a two-site immunoenzymatic assay. Two-tailed Student t test and paired-comparison t test were used for statistical analyses. The results were expressed as mean +/- standard error. RESULTS: Antepartum plasma thrombomodulin levels in preeclampsia were significantly higher than postpartum levels (71.3 +/- 8.5 versus 55.5 +/- 5.4 ng/mL; P = .006), which was not seen in the normotensive controls (49.9 +/- 3.1 versus 44.2 +/- 3.8 ng/mL; P > .05). Antepartum plasma levels of thrombomodulin in preeclamptic women were significantly higher than those in the normotensive controls (P = .01). However, postpartum plasma levels of thrombomodulin in preeclamptic women were not significantly higher than those in the normotensive controls (P > .05). CONCLUSION: Significantly decreased postpartum plasma thrombomodulin levels in preeclamptic pregnancies strongly correspond to clinical postpartum regression of preeclampsia.

Elevated amniotic fluid nitric oxide metabolites and interleukin-6 in intra-amniotic infection.

OBJECTIVE: To compare amniotic fluid nitric oxide metabolites and interleukin-6 (IL-6) concentrations in patients with and without intra-amniotic infection. METHODS: Amniotic fluid nitric oxide metabolites, IL-6, Gram stains, glucose, leukocyte counts, leukocyte esterase activity, creatinine, pH, and specific gravity were determined in 14 patients with intra-amniotic infection and 26 patients without intra-amniotic infection. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture. The nitric oxide metabolites, nitrate and nitrite (NOx), were measured using Greiss reagent after reduction of nitrate to nitrite with aspergillus nitrate reductase. Interleukin-6 was measured by a two-site, enzyme-linked immunosorbent assay. Amniotic fluid nitric oxide metabolites and IL-6 concentrations were normalized by amniotic fluid creatinine levels. The Mann-Whitney U test, contingency table method, and Spearman's rank correlation test were used for statistical analyses. RESULTS: Amniotic fluid NOx and IL-6 levels were significantly higher in patients with intra-amniotic infection than in those without intra-amniotic infection (NOx: median = 2.06 mumol/mg creatinine, range = 0.74-6.81 versus 1.35 mumol/mg creatinine, range = 0.99-1.60, P = .01, IL-6: median = 2.00 micrograms/mg creatinine, range = 0.026-4.07 versus median = 0.04 micrograms/mg creatinine, range = 0.004-3.210, P = .0009, respectively). Patients with intra-amniotic infection had significantly elevated leukocyte counts, leukocyte esterase activity, Gram positive stains, and significantly lower amniotic fluid glucose levels compared with those without intra-amniotic infection. There were no differences in gestational age, maternal age, parity, race, pH, or specific gravity between the two groups. Amniotic fluid NOx was significantly correlated with IL-6 (r = .4, P = .02). Both amniotic fluid NOx and IL-6 were also positively correlated with amniotic fluid leukocyte counts, leukocyte esterase activity and Gram stains, and negatively correlated with glucose levels. CONCLUSIONS: Amniotic fluid NOx and IL-6 are significantly elevated and positively correlated during intra-amniotic infection. Both increased amniotic fluid IL-6 and nitric oxide may exert cytotoxic and cytostatic effects on the target cells. We suggest that measurements of amniotic fluid NOx and IL-6 may serve as useful clinical markers in patients with intra-amniotic infection.

Relation of the estrogen receptor alpha gene microsatellite polymorphism to bone mineral density and the susceptibility to osteoporosis in postmenopausal Chinese women in Taiwan.

OBJECTIVE: Osteoporosis is a common disorder with a strong genetic component. Our aim was to investigate the correlation of the estrogen receptor alpha gene microsatellite polymorphism (TA dinucleotide repeat polymorphism 5' upstream of exon 1) with bone mineral density and their relationship to osteoporosis. METHODS: We determined the estrogen receptor alpha gene microsatellite polymorphism using polymerase chain reaction-based microsatellite analysis in postmenopausal Chinese women in Taiwan. Bone mineral density of the lumbar spine and proximal femur were measured using dual-energy X-ray absorptiometry. RESULTS: The ERalpha genotype was classified into '12' through '27' according to the number of TA dinucleotide repeats they contained, as a 'signpost'. After adjustment for potential confounding factors including age, height, and weight, subjects with genotype 18+ (n=4) had lower bone mineral density values and a 54.5 times greater risk for osteoporosis when compared with subjects with genotype 18- (n=170) at the lumbar spine. This should be interpreted with caution because of the small number of subjects with the unfavorable genotype 18+. According to mean number of TA dinucleotide repeats, women with a high number of repeats (TA > or =20) (n=38) had the lowest bone mineral density and a 6.1 times greater risk for osteoporosis than women with a low number of repeats (TA < or =15) (n=61) at the femoral neck, after adjustment for potential confounding factors such as age, height, and weight. CONCLUSION: The present study suggests that the estrogen receptor alpha gene microsatellite polymorphism may be a candidate genetic marker for risk of osteoporosis in postmenopausal Chinese women in Taiwan.

Urogenital infection in preeclampsia.

OBJECTIVE: The purpose of this study was to determine whether the incidence of urinary tract infections and postpartum endometritis were increased in preeclamptic pregnancies. METHOD: We conducted a retrospective study of 13852 pregnant women, using a perinatal database at The Johns Hopkins Hospital, over the past 5 years. The incidence of urinary tract infections and postpartum endometritis was analyzed using the chi-squared test and logistic regression analysis. Statistical significance was set at P < 0.05. RESULTS: There were 345 (2.5%) mild preeclamptics and 440 (3.2%) severe preeclamptics. The incidence of urinary tract infections and postpartum endometritis in preeclamptic patients was significantly higher than that in non-hypertensive pregnant patients. After controlling for confounding variables, severe preeclampsia was still found to be an independent significant risk factor for both urinary tract infections and postpartum endometritis. CONCLUSION: Our data show a significant increase in urogenital infection in preeclamptic pregnancy. This may reflect higher rates of underlying renal disease and placental bed abnormalities occurring in preeclampsia.

Placental pathologies are not associated with hyperuricemia in preeclamptic pregnancies.

The mechanism of hyperuricemia in preeclampsia remains unknown. As the breakdown of the nuclear rich syncytiotrophoblast might result in the increased formation of uric acid from purine catabolism, the purpose of this study was to investigate whether placental pathologies were associated with hyperuricemia in preeclamptic pregnancies. We retrospectively reviewed medical reports with the availability of maternal serum uric acid levels and placental pathology reports of 83 singleton, preeclamptic pregnant women at Yale-New Haven Hospital. Preeclampsia was defined by the American College of Obstetricians and Gynecologists criteria. Hyperuricemia was defined as, at least greater than or equal to, two standard deviations of normal mean values for gestational age. The placental pathological findings include infarction, syncytial knots, abruption, intravillous thrombosis, and villous pathology (i.e., edema, villitis). The relevance of hyperuricemia to the individual placental pathologic finding and the numbers of placental pathologic findings were investigated. Statistical analyses were performed using contingency table methods. We found that there was no significant correlation between hyperuricemia and individual or multiple placental pathologic findings. We concluded that placental pathologies secondary to ischemic changes may not fully explain hyperuricemia in preeclamptic pregnancies. A prospective study using morphometric measurements is needed to understand the exact role of ischemic placental damage on the maternal serum uric acid level.

Monoamniotic twins in a triplet gestation with favorable outcome.

BACKGROUND: Monoamniotic twins in a triplet gestation is a rare combination. Each condition is separately associated with significant perinatal morbidity and mortality. There are no data about the outcome and management of such gestations. CASE: We report a case of monoamniotic twins in a spontaneous dichorionic triplet gestation with a favorable outcome. Transvaginal ultrasound examination at nine weeks confirmed the diagnosis. Close follow-up was established that included continuous fetal monitoring after 30 weeks. At 35 weeks and after confirming fetal lung maturity, elective cesarean delivery was performed resulting in three liveborn female infants. CONCLUSION: Favorable outcome of such a rare coexistence of monoamniotic twins in a triplet gestation is possible. Vigilant fetal monitoring and timed delivery remain the mainstays of management.

PP079. Evidence of placental and vascular endothelial apotosis and dysfunction by elevated serum human chorionic gonadotropin, soluble selectin and soluble Fas in HELLP syndrome.

INTRODUCTION: The etiology of Hemolysis, Elevated Liver enzyme, and Low Platelets (HELLP) syndrome remains unknown. We hypothesized that placental and vascular endothelial apoptosis and dysfunction might be the pathogenesis of HELLP syndrome. OBJECTIVES: To determine maternal serum levels and association among human chorionic gonadotropin (hCG), soluble Fas (sFas), and E-selectin (sE-selectin) in HELLP syndrome. METHODS: Forty-two singleton pregnant women were studied. Fourteen patients were with HELLP syndrome and 28 patients were healthy gravidas. The serum levels of total beta-hCG, sFas, and sE-selectin were measured by enzyme-linked immunoassays. Mann-Whitney test and Spearman rank correlation were used for statistical analyses. Data were expressed as median and ranges. P value less than 0.05 is considered statistically significant. RESULTS: There were no significant differences in maternal age, gestational age, parity or race in patients with and without HELLP syndrome. The median levels of serum total beta-hCG, sFas, and sE-selectin were significantly higher in women with HELLP syndrome than in healthy gravidas {total beta-hCG: 52,168 (14,936-213,445)mIU/mL vs. 17,942 (966-176,600)mIU/mL, p=0.016; sFas: 8.20 (3.0-22.6)U/ml vs. 5.8 (1.2-18.5)U/ml, p=0.001; sE-selectin: 107.7 (26.2-194.7)ng/mL vs. 23.0 (11.1-107.7)ng/mL, p<0.0001}. Moreover, serum total beta-hCG levels were significantly correlated with serum sFas (r=0.32, p=0.039) and sE-selectin levels (r=0.32, p=0.038). Serum sFas levels were also significantly correlated with serum sE-slectin (r=0.47, p=0.003) CONCLUSION: Our data suggest that placental and vascular endothelial apoptosis in preeclampsia may further lead to placental and endothelial dysfunction as the possible pathogenesis in HELLP syndrome.