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Chorioamnionitis with or without funisitis increases the risk of hypotension in very low birthweight infants on the first postnatal day but not later.

OBJECTIVE: To evaluate the relation between chorioamnionitis and hypotension in very low birthweight infants. METHODS: Retrospective cohort study in infants with a birth weight of <1500 g born between January 2002 and September 2004. The placentas were examined for evidence of chorioamnionitis and funisitis. Hypotension was defined by the use of vasopressors. RESULTS: Of 105 infants, 37 (35%) were chorioamnionitis positive. The onset of hypotension had a skewed distribution: day 1 for 30 episodes and scattered from day 2 to day 19 for the remaining 22. Of the 30 infants who developed hypotension on day 1, 17 (57%) were chorioamnionitis positive. The mean maturity of the chorioamnionitis positive group was 27.91 weeks, marginally less than the mean maturity of 29.05 weeks of the chorioamnionitis negative group (p = 0.05). After adjustment of the effects for confounding variables (birth weight, gestation, surfactant therapy, mechanical ventilation on day 1, high frequency oscillatory ventilation, patent ductus arteriosus), chorioamnionitis was the significant factor in line with hypotension developing on day 1 (adjusted odds ratio 5.14, 95% confidence interval 1.51 to 17.50). There was no evidence that hypotension developing after day 1 was associated with chorioamnionitis. CONCLUSIONS: There is a strong association between chorioamnionitis and hypotension developing on day 1 in very low birthweight infants.

Age Factors↗

Effect of chorioamnionitis on neurodevelopmental outcome in preterm infants.

OBJECTIVE: To assess the association of neurodevelopmental outcome with the placental diagnosis of chorioamnionitis in very low-birth-weight infants. METHODS: One hundred seventy-seven surviving very low-birth-weight infants, 22 to 29 weeks' gestational age, born after varying severity of chorioamnionitis, were evaluated at a mean +/- SD age of 19 +/- 6 months' corrected age with Bayley Scales of Infant Development II and neurologic examination. Select maternal and infant variables were abstracted from the medical records. Neonatal morbidities, Mental Developmental Index (MDI) score, Psychomotor Developmental Index (PDI) score, probability of normal MDI and PDI scores (>84), and cerebral palsy between the chorioamnionitis and the control groups were assessed, controlling for gestational age, sex, and the maternal use of steroids and antibiotics. RESULTS: The chorioamnionitis group of 102 infants was compared with 75 control infants (mean +/- SD birth weight, 947 +/- 236 g and 966 +/- 219 g, respectively; mean +/- SD gestational age, 26.1 +/- 2.8 weeks and 27.1 +/- 1.5 weeks, respectively). Infants with chorioamnionitis, compared with controls, had a significantly higher incidence of intraventricular hemorrhage (30% vs 13%) and retinopathy of prematurity (68% vs 42%). Cerebral palsy was diagnosed in 8.6% of the infants with chorioamnionitis and 6.6% of the controls. The MDI and PDI scores were similar between the chorioamnionitis and control groups (mean +/- SD MDI score, 96 +/- 16 vs 97 +/- 18 and mean +/- SD PDI score, 94 +/- 19 vs 92 +/- 19, respectively). CONCLUSIONS: In very low-birth-weight infants we found a higher incidence of intraventricular hemorrhage and retinopathy of prematurity but similar MDI and PDI scores and risk of cerebral palsy associated with chorioamnionitis.

Chorioamnionitis↗

Chorioamnionitis and cerebral palsy in term and near-term infants.

CONTEXT: Half of all cases of cerebral palsy (CP) occur in term infants, for whom risk factors have not been clearly defined. Recent studies suggest a possible role of chorioamnionitis. OBJECTIVE: To determine whether clinical chorioamnionitis increases the risk of CP in term and near-term infants. DESIGN, SETTING, AND PATIENTS: Case-control study nested within a cohort of 231 582 singleton infants born at 36 or more weeks' gestation between January 1, 1991, and December 31, 1998, in the Kaiser Permanente Medical Care Program, a managed care organization providing care for more than 3 million residents of northern California. Case patients were identified from electronic records and confirmed by chart review by a child neurologist, and comprised all children with moderate to severe spastic or dyskinetic CP not due to postnatal brain injury or developmental abnormalities (n = 109). Controls (n = 218) were randomly selected from the study population. MAIN OUTCOME MEASURE: Association between clinical chorioamnionitis and increased risk of CP in term and near-term infants. RESULTS: Most CP cases had hemiparesis (40%) or quadriparesis (38%); 87% had been diagnosed by a neurologist and 83% had undergone neuroimaging. Chorioamnionitis, considered present if a treating physician made a diagnosis of chorioamnionitis or endometritis clinically, was noted in 14% of cases and 4% of controls (odds ratio [OR], 3.8; 95% confidence interval [CI], 1.5-10.1; P =.001). Independent risk factors identified in multiple logistic regression included chorioamnionitis (OR, 4.1; 95% CI, 1.6-10.1), intrauterine growth restriction (OR, 4.0; 95% CI, 1.3-12.0), maternal black ethnicity (OR, 3.6; 95% CI, 1.4-9.3), maternal age older than 25 years (OR, 2.6; 95% CI, 1.3-5.2), and nulliparity (OR, 1.8; 95% CI, 1.0-3.0). The population-attributable fraction of chorioamnionitis for CP is 11%. CONCLUSION: Our data suggest that chorioamnionitis is an independent risk factor for CP among term and near-term infants.

Asphyxia Neonatorum↗

Chorioamnionitis does not affect fetal urine production in patients with premature rupture of membranes.

The objective of this study was to evaluate fetal urine production rate in patients with premature rupture of membranes in the presence or absence of chorioamnionitis and to determine its clinical usefulness. Fetal urine production was evaluated in 30 women between 24 and 39 weeks' gestational age with ruptured membranes. Fetal bladder measurements were determined every 3-5 min for 30-90 min. Chorioamnionitis was defined by both clinical criteria and histological examination of the placenta. The last determination of fetal urine production rate prior to delivery was compared in patients with and without histologic and/or clinical chorioamnionitis. Fetal urine production rate was corrected for gestational age using birth weight prior to analysis. A total of 96 assessments of fetal urine production were performed (range 1-16 per patient). Twelve subjects (40%) had no evidence of chorioamnionitis (group 1), 10 (33%) had histologic chorioamnionitis alone (group 2), and eight (27%) had both clinical and histologic chorioamnionitis (group 3). The mean (+/- SD) urine production rates in these groups were 9.43 +/- 3.15 ml/kg/hr, 10.65 +/- 3.43 ml/kg/hr, and 9.97 +/- 2.81 ml/kg/hr, respectively. The difference in fetal urine production rate between the three groups was not statistically significant. A power analysis revealed that individual group sizes were adequate to document a 50% increase in fetal urine production rate with a type II error of < 10%. There were no documented cases of fetal infection based on neonatal cultures. The presence of histologic or clinical chorioamnionitis does not significantly affect fetal urine production in patients with premature rupture of membranes. The prospective assessment of fetal urine production rate does not appear to be clinically useful as an early indicator of chorioamnionitis.

Chorioamnionitis↗

Maternal and umbilical serum concentrations of granulocyte colony-stimulating factor and its messenger RNA during clinical chorioamnionitis.

OBJECTIVE: To determine whether women with chorioamnionitis developed elevated serum granulocyte colony-stimulating factor (G-CSF) concentrations and, if so, whether the G-CSF crossed to the fetus. METHODS: We quantified G-CSF before, during, and after delivery and in the cord blood of 12 women with clinical chorioamnionitis and 12 matched controls. We also measured G-CSF messenger RNA (mRNA) transcripts in mononuclear cells isolated from maternal and cord blood at delivery. RESULTS: At study entry, G-CSF concentrations were much higher in women with chorioamnionitis (1397 +/- 950 pg/mL, mean +/- standard error of mean) than in controls (17 +/- 5 pg/mL, P < .05). At delivery, concentrations had increased in both groups (2752 +/- 1100 pg/mL in the chorioamnionitis group, 165 +/- 61 pg/mL in controls; P < .05). After delivery, G-CSF concentrations had diminished to 839 +/- 594 pg/mL in women with chorioamnionitis and to 83 +/- 16 pg/mL in controls (P < .05). Concentrations in the cord blood were 2729 +/- 974 pg/mL for the chorioamnionitis group and 51 +/- 17 pg/mL for controls (P < .05). Granulocyte colony-stimulating factor mRNA transcripts were more abundant in women with chorioamnionitis than in controls but were scarce in all matched cord blood samples tested. CONCLUSION: Serum G-CSF concentrations were elevated during clinical chorioamnionitis, and similar levels were found in maternal and cord serum. Because G-CSF mRNA levels were very low in cord mononuclear cells, the G-CSF in cord serum might be maternal in origin.

Adult↗

A fetal response to chorioamnionitis is associated with early survival after preterm birth.

OBJECTIVE: The purpose of this study was to determine, in a large preterm cohort (20-34 completed weeks of gestation), the incidence of histologic chorioamnionitis and the incidence of a histologic fetal response to chorioamnionitis (umbilical vasculitis with or without funisitis) in neonatal survivors (to 28 days) and perinatal deaths. STUDY DESIGN: Placental histopathology was reviewed (n=3928 reports). In a subset of this cohort (n=2076 reports), evidence of a histologic fetal response was compared in neonatal survivors and perinatal deaths. RESULTS: The incidence of histologic chorioamnionitis ranged from 66% at 20 to 24 weeks of gestation (n=261 neonates) to 16% at 34 weeks (n=770 neonates). The overall incidence was 31% (n=3928 neonates). At 25 to 29 weeks of gestation, neonatal survivors had a higher incidence of histologic chorioamnionitis (P=.02; 95% CI, 1.02-1.21). In addition, neonatal survivors had a higher incidence of a histologic fetal response to chorioamnionitis at 25 to 29 weeks of gestation (P=.01; 95%CI, 0.33-0.86) and 30 to 34 weeks of gestation (P=.02; 95%CI, 0.18-0.85). CONCLUSION: Histologic chorioamnionitis is inversely related to gestational age. Both histologic chorioamnionitis and a histologic fetal response to chorioamnionitis were observed to be more common in preterm survivors of the neonatal period.

Australia↗

Interleukin-8 level in maternal serum as a marker for screening of histological chorioamnionitis at term.

OBJECTIVE: To establish a clinical method for immediate diagnosis of histological chorioamnionitis, by maternal blood sampling at term. METHOD: The sera of 22 mothers with chorioamnionitis and 81 mothers without chorioamnionitis at term delivery were collected. The serum levels of cytokines including interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8) were titered and other conventional markers such as white blood cell and CRP were measured simultaneously. Chorioamnionitis was histopathologically confirmed after delivery. RESULT: The sera of mothers with histological chorioamnionitis showed a significant increase in IL-8 titer, but not in those of other cytokines or conventional markers, compared with those without chorioamnionitis. A positive correlation was observed between maternal and cord serum IL-8 levels. Maternal IL-8 showed the highest predictive value for diagnosis of histological chorioamnionitis. CONCLUSION: Measurement of maternal IL-8 is useful for rapid prenatal screening of histological chorioamnionitis at term.

Adult↗

Chorioamnionitis and the prognosis for term infants.

OBJECTIVE: To assess the effects of clinical chorioamnionitis and labor complications on short-term neonatal morbidity, including seizures. METHODS: This was a retrospective cohort study of all live-born term infants who weighed more than 2500 g delivered between 1988 and 1997 at Parkland Memorial Hospital, Dallas, Texas. Infant outcomes were compared between women with and without clinical diagnoses of chorioamnionitis. Chorioamnionitis was based on maternal fever of 38C or greater with supporting clinical evidence including fetal tachycardia, uterine tenderness, and malodorous infant. RESULTS: A total of 101,170 term infants were analyzed, 5144 (5%) of whom were born to women with chorioamnionitis. Apgar scores of 3 or less at 5 minutes, umbilical artery pH of 7.0 or less, delivery-room intubation, sepsis, pneumonia, seizures in the first 24 hours, and meconium aspiration syndrome were all increased in infants exposed to chorioamnionitis. After adjustment for confounding factors, including route of delivery and length of labor, chorioamnionitis remained significantly associated with intubation in the delivery room (odds ratio [OR] 2.0; 95% confidence interval [CI] 1.5, 2.6), pneumonia (OR 2.2; 95% CI 1.7, 2.8), and sepsis (OR 2.9; 95% CI 2.1, 4.1). Short-term neurologic morbidity, manifest as seizures, was not related to maternal infection during labor, but was significantly related to other labor complications. CONCLUSION: The main short-term neonatal consequence of chorioamnionitis is infection. Short-term neurologic morbidity in infants is related to labor complications and not chorioamnionitis per se.

Adult↗

Evidence for fetal involvement in the pathologic process of clinical chorioamnionitis.

OBJECTIVE: Clinical and histologic chorioamnionitis have recently been identified as risk factors for cerebral palsy. Proinflammatory cytokines have been implicated in the mechanisms that are responsible for brain injury in cases of intrauterine infection. The purpose of this study was to determine whether clinical chorioamnionitis, which is a maternal syndrome, is associated with an elevation in the fetal plasma interleukin-6 (IL-6) that is indicative of fetal inflammation. STUDY DESIGN: A cross-sectional study was designed to determine plasma concentrations of IL-6 in umbilical venous blood from patients with clinical chorioamnionitis (n = 26) and a control group (n = 111). Umbilical cord blood was obtained at the time of delivery. Plasma concentrations of IL-6 were measured with a sensitive and specific immunoassay. Nonparametric statistics were used for analysis. RESULTS: Plasma concentrations of IL-6 were detectable in all samples of umbilical venous plasma. The median concentration of plasma IL-6 was higher in neonates born to mothers with clinical chorioamnionitis than in neonates born to mothers in the control group (clinical chorioamnionitis: median, 27.46 pg/mL; range, 1.3-5550.0 pg/mL; vs control: median, 2.13 pg/mL; range, 0.6-812.3 pg/mL; P <.001). Sixty-two percent of neonates (16/26) who were born to women with clinical chorioamnionitis had fetal plasma concentrations of IL-6 >11 pg/mL and 54% (14/26) had fetal plasma concentrations of IL-6 >18 pg/mL (these cutoff points have been used previously to define the fetal inflammatory response syndrome). CONCLUSION: Umbilical vein plasma concentrations of interleukin-6 are elevated in the neonates who were born to mothers with clinical chorioamnionitis, which suggests that the inflammatory process that is responsible for the maternal syndrome of clinical chorioamnionitis frequently involves the human fetus.

Adolescent↗

Recurrence of clinical chorioamnionitis in subsequent pregnancies.

OBJECTIVE: To establish the role of clinical chorioamnionitis as an independent risk factor for recurrence in a subsequent pregnancy. METHOD: This was a historical cohort study of pregnant women who had their first and second deliveries at our institution between January 1988 and May 2005. The index pregnancy was restricted to those who delivered vaginally. Data were collected from a continuously updated obstetric database and included demographic and labor characteristics and neonatal outcomes. Chorioamnionitis was diagnosed clinically. RESULTS: The study population consisted of 23,397 women. During the index pregnancy, 10% of women developed chorioamnionitis. This group was significantly different from the rest of the cohort in terms of age, ethnicity, length of labor, epidural analgesia, use of internal monitors, and incidence of prolonged rupture of membranes. In the second pregnancy, 6% of those women again developed chorioamnionitis compared with 2% of women who did not have chorioamnionitis in the first pregnancy (odds ratio 2.93, 95% confidence interval 2.40-3.57). After adjusting for the above confounders, the increased risk of recurrence persisted (odds ratio 1.85, 95% confidence interval 1.49-2.30). CONCLUSION: Women delivering vaginally who were diagnosed with chorioamnionitis during their first pregnancy are at increased risk for chorioamnionitis in a subsequent pregnancy. This supports the concept that there may be a predisposition to chorioamnionitis that should be further investigated. LEVEL OF EVIDENCE: II-2.

Adult↗

Chorioamnionitis: a comparative histologic, bacteriologic, and clinical study.

Using morphologic and bacteriologic techniques, we examined placentas from 224 deliveries considered potentially complicated by infection. The severity of the chorioamnionitis was graded histologically according to the intensity of the inflammatory infiltrate. Chorioamnionitis or funisitis occurred in 111 placentas. Neonatal morbidity in this group was 48 (43%) as compared with 14 (12%) in those without chorioamnionitis. Pathogens were cultured from 49 of the 111 placentas with chorioamnionitis. Neonatal morbidity or mortality occurred in 28 (58%) of the group with positive cultures but occurred also in 20 (32%) of the 63 with chorioamnionitis from which no pathogens were cultured. Perinatal mortality was especially high (64%) among premature infants (less than 30 weeks) with infection. A comparison of culture techniques (surface swab versus swab of subchorionic fibrin after searing amnionic surface) showed similar rates of recovery but less contamination using the deep culture technique. Neonatal morbidity and mortality with severe chorioamnionitis (grades II and III; 62% and 82%) were significantly greater than with little or no chorioamnionitis (grades I and 0; 43% and 36%). Higher grades of histologically demonstrable chorioamnionitis are associated significantly with the highest rates of neonatal morbidity or mortality. In many instances, pathogens are not recovered by conventional aerobic and anaerobic bacteriologic study. A search for other infectious agents (viruses, mycoplasmas, chlamydiae) deserves attention.

Acute Disease↗

The association of chorioamnionitis with preterm delivery.

To ascertain what proportion of preterm deliveries are attributable to the association with chorioamnionitis, the authors examined prospectively the placentas from all 2774 women who delivered at the Johns Hopkins Hospital during 1980. The incidence of preterm delivery was 5.4% (110 of 2027) when neither chorioamnionitis nor premature rupture of membranes (PROM) was present, 11.9% (29 of 243) when chorioamnionitis was present without PROM, and 56.7% (51 of 90) when both chorioamnionitis and PROM were present (P less than .05). Only 27 of 333 cases of histopathologic chorioamnionitis or 8.1% had maternal antepartum fever, and only 11 of 333 or 3.3% had neonatal sepsis. Using logistic regression analysis to control for confounding variables, approximately 25% of the preterm deliveries were statistically attributable to histopathologic chorioamnionitis, occurring either alone or in association with PROM. In light of the infrequency with which histopathologic chorioamnionitis is clinically evident, the strong relationship between histopathologic chorioamnionitis and preterm delivery suggests that occult antepartum infection of the genital tract is an important cause of preterm delivery.

Chorioamnionitis↗

Histologic chorioamnionitis & its association with prematurity in a hospital-based study.

This prospective study was undertaken to study the occurrence of histologic chorioamnionitis and determine its association with prematurity; and to assess whether colonization of the genital tract of pregnant women by genital mycoplasmas or Chlamydia trachomatis is a risk factor for histologic chorioamnionitis. A total of 268 women with singleton pregnancies of over 26 weeks gestation were subjected to high vaginal cultures of genital mycoplasmas and endocervical specimens for chlamydia antigen. Placental histopathology was performed on multiple sections. Histologic chorioamnionitis was documented in 22.4 per cent (60/208) placentae. Genital tract colonization with Ureaplasma urealyticum or C. trachomatis was not a risk factor for histologic chorioamnionitis. Neonates born in association with histologic chorioamnionitis had a mean birth weight 111 g lower than those born without this lesion (2626.9 +/- 702 g vs 2737.8 +/- 500 g, NS). The relative risk (95% confidence interval) of prematurity in the presence of histologic chorioamnionitis was 1.49 (0.87-2.53). Analysis of linear trend in proportions for prevalence of histologic chorioamnionitis with decreasing gestation showed a significant association (P = 0.047, 1-tail). These results taken together suggest that histologic chorioamnionitis may be a risk factor of prematurity, but of only a modest magnitude.

Chorioamnionitis↗

Chorioamnionitis: its association with pregnancy outcome and microbial infection.

In a study of 33 cases of perinatal death, chorioamnionitis was observed in 57.6% compared with 5% of 20 control cases (p less than 0.001) and in 70.8% of cases with no morphologic cause compared with 22.2% of cases with a defined cause of death (p less than 0.01). Chorioamnionitis was significantly associated with previous gestations (p less than 0.01), prolonged rupture of the membranes (p less than 0.001), prematurity (20 to 27 weeks' gestation) (p less than 0.001), and low birth weight (less than or equal to 1000 gm) (p less than 0.001) but not with elevated maternal white blood cell count or pyrexia. Overall, in patients with chorioamnionitis, the perinatal death rate was higher (p less than 0.01); more stillbirths occurred compared with early neonatal deaths (p less than 0.05), and there was a higher incidence of deaths with no defined cause (p less than 0.01) compared with cases without chorioamnionitis. Ureaplasma urealyticum or pathogenic bacteria were isolated more frequently from villous tissue of placentas from cases with chorioamnionitis (p less than 0.01) but not Mycoplasma hominis, Chlamydia trachomatis, or viruses. Furthermore, there was a higher prevalence of both elevated fetal antibody titer to U. urealyticum (p less than 0.025) and fetal titer fourfold above maternal titers (p less than 0.05) in cases with chorioamnionitis. The antibody responses and presence of microorganisms suggest that chorioamnionitis is associated with intrauterine infection and an associated increase in perinatal morbidity and mortality.

Bacterial Infections↗

The effect of clinical chorioamnionitis on cord blood gas at term.

OBJECTIVE: We sought to determine the effect of clinical chorioamnionitis on cord blood gas values in term pregnancies not complicated by any other disease. STUDY DESIGN: 2200 consecutive deliveries were studied. Following exclusion of twins, non-viable malformations and stillbirths, as well as mothers with high-risk pregnancy diseases--i.e. hypertension, diabetes, preterm labor, third-trimester bleeding, IUGR, postdates, oligohydramnios, i.v. drug abused, decreased fetal movement, maternal viral infection, UTI or pneumonia (n = 897)--two groups of patients remained: term pregnancies complicated only by clinical chorioamnionitis (n = 81) and uncomplicated term pregnancies (n = 1246). RESULTS: Evaluation of mean cord blood gas values revealed a significant difference in pH, PO2, PCO2 and BE values, with the infants of mothers with clinical chorioamnionitis having lower pH values (7.23 +/- 0.07 vs. 7.28 +/- 0.07). However, evaluating the independent effect of chorioamnionitis on arterial cord blood pH (using a logistic regression model) showed that clinical chorioamnionitis, by itself, did not contribute to this change in arterial cord blood pH. CONCLUSION: Chorioamnionitis was neither the explanation nor the cause for differences in arterial cord blood pH found between the two groups in our study. In cases of chorioamnionitis, these differences were attributed to other factors, such as length of labor, mode of delivery, method of delivery and presence of meconium.

Adult↗

Chorioamnionitis increases neonatal morbidity in pregnancies complicated by preterm premature rupture of membranes.

OBJECTIVE: To compare morbidities of neonates born to women who developed chorioamnionitis after premature preterm rupture of membranes versus those who did not. STUDY DESIGN: We reviewed outcomes in singleton pregnancies with confirmed premature preterm rupture of membranes at 24 weeks or beyond that resulted in delivery less than 37 weeks. Management of premature preterm rupture of membranes included the use of antibiotics, betamethasone if less than 32 weeks, and expectant management with induction at 34 weeks or greater. Composite neonatal major and minor morbidity rates were compared between pregnancies complicated by chorioamnionitis and those that were not. RESULTS: From August 1998 to August 2000, 430 cases of premature preterm rupture of membranes were identified among 6003 deliveries (7.2%). Thirteen percent of women (56/430) with premature preterm rupture of membranes developed chorioamnionitis. The incidence of chorioamnionitis increased significantly with decreasing gestational age. The composite neonatal major morbidity rate was significantly higher in neonates whose mothers developed chorioamnionitis (55%) versus those who did not (18%, P < .0001). In a multiple logistic regression model, chorioamnionitis ( P < .0001), infant gender ( P = .007), latency ( P = .03), and gestational age at delivery ( P < .0001) were significantly associated with composite neonatal morbidity. CONCLUSION: Neonatal morbidities are significantly higher among pregnancies with premature preterm rupture of membranes complicated by chorioamnionitis when compared with pregnancies that were not.

Adolescent↗

Tumor necrosis factor-alpha promoter gene polymorphism -308 and chorioamnionitis.

OBJECTIVE: A single-base polymorphism within the promoter of the gene for tumor necrosis factor alpha at position -308 relative to the transcriptional start site of the gene is correlated with differences in production of tumor necrosis factor alpha. There are two allelic forms: TNFA1 and TNFA2. The TNFA2 allele is associated with increased production of tumor necrosis factor alpha. The purpose of this study is to assess the relationship between carriage of the TNFA2 allele and clinical chorioamnionitis. METHODS: In this retrospective cohort study, previously banked deoxyribonucleic acid from 149 women who had spontaneous labor from 37 to 42 weeks' gestation was used. Polymerase chain reaction was used for polymorphism assay. Demographic and clinical information was obtained from the medical record. Clinical chorioamnionitis was defined as at least one temperature elevation above 38C combined with at least two of the following signs: maternal or fetal tachycardia, uterine tenderness greater than expected, foul-smelling vaginal discharge, and white blood cell count more than 18,000. RESULTS: Chorioamnionitis was present in 18 women (12.1%). Among women who did not carry TNFA2, the chorioamnionitis rate was 7.4%. Among women who carried TNFA2, the chorioamnionitis rate was 24.4%. The relative risk for chorioamnionitis with carriage of TNFA2 was 3.3 (95% confidence interval 1.3, 7.1). This increased risk was not altered after adjustment for race, type of rupture of membranes, intrauterine pressure catheter use, smoking, and prolonged rupture of membranes. CONCLUSION: Carriage of the TNFA2 allele is associated with a more than three-fold increased risk of clinical chorioamnionitis, even when accounting for important clinical and microbiologic risk factors.

Adolescent↗

Postnatal increase of procalcitonin in premature newborns is enhanced by chorioamnionitis and neonatal sepsis.

BACKGROUND: To determine the influence of chorioamnionitis and neonatal sepsis on procalcitonin (PCT) levels in very-low-birth-weight (VLBW) infants within the first week of life. DESIGN: PCT serum levels were measured in cord blood 1 h after delivery and on day 3 and day 7 of life. Chorioamnionitis and neonatal sepsis within the first week were monitored. RESULTS: Chorioamnionitis was present in eight of 37 patients (21.6%). PCT on day 3 was increased in both the "No chorioamnionitis" (2.54 ng mL(-1), SEM 0.51) and "Chorioamnionitis" (6.96 ng mL(-1), SEM 2.93) groups of VLBW infants compared with the 1st hour values (0.45 and 0.58 ng mL(-1) SEM 0.07 and 0.11, respectively, P < 0.001) of the same patients. The postnatal gain was higher in the "Chorioamnionitis" group (P < 0.01). Neonatal sepsis was diagnosed (after exclusion) in 12 of 32 patients (37.5%). Mean values of maximum PCT in patients with and without sepsis were 8.41 ng mL(-1) (SEM 1.87) and 3.02 ng mL(-1) (SEM 1.38), respectively (P < 0.05). Sensitivity to sepsis of PCT, ratio of immature to total neutrophils (I : T), and C-reactive protein (CRP) were 75%, 50% and 25%, respectively. CONCLUSIONS: In the group of VLBW infants the PCT level within 72 h of delivery was markedly increased in patients with chorioamnionitis. Compared with I : T and CRP, PCT appears to be a more sensitive marker of neonatal sepsis.

C-Reactive Protein↗