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A population-based study of race-specific risk for placental abruption

BMC Pregnancy and Childbirth volume 8, Article number: 43 (2008) Cite this article

Abstract

Background

Efforts to elucidate risk factors for placental abruption are imperative due to the severity of complications it produces for both mother and fetus, and its contribution to preterm birth. Ethnicity-based differences in risk of placental abruption and preterm birth have been reported. We tested the hypotheses that race, after adjusting for other factors, is associated with the risk of placental abruption at specific gestational ages, and that there is a greater contribution of placental abruption to the increased risk of preterm birth in Black mothers, compared to White mothers.

Methods

We conducted a population-based cohort study using the Missouri Department of Health's maternally-linked database of all births in Missouri (1989–1997) to assess racial effects on placental abruption and the contribution of placental abruption to preterm birth, at different gestational age categories (n = 664,303).

Results

Among 108,806 births to Black mothers and 555,497 births to White mothers, 1.02% (95% CI 0.96–1.08) of Black births were complicated by placental abruption, compared to 0.71% (95% CI 0.69–0.73) of White births (aOR 1.32, 95% CI 1.22–1.43). The magnitude of risk of placental abruption for Black mothers, compared to White mothers, increased with younger gestational age categories. The risk of placental abruption resulting in term and extreme preterm births (< 28 weeks) was higher for Black mothers (aOR 1.15, 95% CI 1.02–1.29 and aOR 1.98, 95% CI 1.58–2.48, respectively). Compared to White women delivering in the same gestational age category, there were a significantly higher proportion of placental abruption in Black mothers who delivered at term, and a significantly lower proportion of placental abruption in Black mothers who delivered in all preterm categories (p < 0.05).

Conclusion

Black women have an increased risk of placental abruption compared to White women, even when controlling for known coexisting risk factors. This risk increase is greatest at the earliest preterm gestational ages when outcomes are the poorest. The relative contribution of placental abruption to term births was greater in Black women, whereas the relative contribution of placental abruption to preterm birth was greater in White women.

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Background

Placental abruption, defined as premature separation of a normally implanted placenta prior to delivery, results from the culmination of underlying pathophysiologic processes that may either be initiated by a single precipitating event (e.g. premature rupture of membranes), or, more commonly, associated with chronic uteroplacental vascular insufficiency (e.g. chronic hypertension) [1]. Placental abruption complicates 0.8 to 1.0% of pregnancies [2], and the incidence appears to be increasing [3]. Furthermore, histologic evidence of decidual hemorrhage has been noted in 2 to 4% of deliveries, even though most cases are not associated with clinical diagnoses of abruption [4].

Placental abruption, especially marginal or peripheral placental abruption, has also been associated with preterm labor [5]. The incidence of abruption peaks at 24 to 26 weeks of gestation [6]. Furthermore, histologic evidence of old hemorrhage was demonstrated in the placentas of over 50% of women with preterm birth (PTB) in one analysis [7]. Interestingly, there appears to be evidence for heterogeneity in the clinical pathways of placental abruption in term and preterm gestations, with acute inflammation more prevalent at preterm than term gestations, and chronic processes present throughout gestation [8]. Risk factors associated with placental abruption comprise previous abruption (strongest risk factor), mechanical factors (i.e. trauma), chronic hypertension, gestational hypertension, cigarette smoking, cocaine use, preterm premature rupture of fetal membranes (PPROM), multiparity, multiple gestations, advanced maternal age, inherited thrombophilias, and polyhydramnios [3, 9–20].

Differences in risk of placental abruption based on ethnicity have also been reported. Placental abruption is more common among African-American women (1 in 595) than among White (1 in 876) or Latin-American (1 in 1423) women [21]. Furthermore, the rate of abruption has increased 92% among Black women between 1979–1981 (0.76%) and 1999–2001 (1.43%), whereas the rate increased by 15% among White women over the same period (0.82% in 1979–1981 to 0.94% in 1999–2001) [3].

The influence of maternal race on the risk for PTB has been demonstrated in many studies [22–24]. Black women who have had a PTB are disproportionately at higher risk for subsequent PTB than White women, and this difference in risk based on ethnicity is not adequately explained by socioeconomic status (SES) or access to health care [22–24]. Since Black maternal race is a risk factor for placental abruption as well as PTB, and placental abruption is associated with PTB, we would expect a greater contribution of placental abruption to the increased risk of PTB in Black mothers. However, epidemiological studies to date that have examined racial disparity in placental abruption at different gestational age categories are lacking.

The Missouri Department of Health's maternally linked birth-death certificate database is a unique and comprehensive resource for assessing birth outcomes across racial, SES and maternal medical risk factors. Using this database to analyze potential racial, SES and medical contributors to the occurrence of placental abruption, we tested the hypothesis that race, while adjusting for other known risk factors, is associated with the risk of placental abruption. Furthermore, we proceeded to estimate the relative contribution of placental abruption to PTB in Black and White mothers, testing the hypothesis that there is a greater contribution of placental abruption to the increased risk of PTB in Black mothers, compared to White mothers.

Methods

Study design

The protocol for this study was approved by the Missouri Department of Health and Senior Services, and was exempt from review by the Human Studies Committee of Washington University in Saint Louis and the Missouri Department of Health and Senior Services Institutional Review Board. We developed a study to analyze the Missouri Department of Health's de-identified maternally linked birth-death certificate database, which includes all 1,577,082 live births or fetal deaths in Missouri from 1978 through 1997. This cohort includes 245,136 (15.6%) births to Black mothers and 1,310,462 (83.3%) births to White mothers. Hispanic mothers were incorporated into the major racial categories. Birth certificate data were entered into the database by hospital agents, and were subjected to quality assurance measures. Methods for constructing and evaluating the database with live birth and fetal death records organized into siblingships using probabilistic linkage methods and calculation of weighted scores for every possible pair of records that reflects the likelihood that they belong to the same person have been described [25].

Because our primary interest is to determine racial, SES and maternal medical risk factors associated with placental abruption leading to live births, we excluded fetal deaths in utero. Congenital anomalies and multiple gestation births were also excluded due to their known association with birth complications. Since the cohort analysis compares Black and White racial contributions (i.e. exposures) to placental abruption, births from mothers of other races were excluded. Restriction to Black and White races was based largely on the fact that the prevalence of other races is very low (0.20% Native American, 0.16% Chinese, 0.05% Japanese, 0.01% Hawaiian, 0.15% Filipino, 0.03% other, 0.57% missing) in Missouri, precluding a meaningful analysis of rare outcomes. The analysis was further restricted to live births at gestational ages ≥ 20 and ≤ 44 weeks. Because the rate of missing data prior to 1989 was unacceptably high, we limited the analysis to the years from 1989 to 1997, in which the missing data rate was < 5%. We conducted a population-based cohort study on the remaining singleton live births for the occurrence of placental abruption, and its relation to racial, SES and maternal medical factors.

Measure

Placental abruption was defined as occurring if coded affirmatively in the database. Maternal race was coded in the database by self-report by patient. PTB as defined by the World Health Organization is delivery at less than 37 weeks gestational age[26]. We focused our analysis for preterm placental abruption to those births occurring at less than 35 weeks in order to avoid borderline gestational ages, which are more prone to misclassification bias, and to identify the population of infants born at the earliest gestations when prognoses are often poor. We defined late PTB as those occurring between 32 and 346/7 weeks, very PTB as those occurring between 28 and 316/7 weeks, and extreme PTB as those births occurring at less than 28 weeks of gestation.

The primary exposure was race, including categories Black race, and White race, with White race being the reference group. The primary binary outcome variable was the occurrence of placental abruption. We then created a categorical outcome variable that was the occurrence of placental abruption resulting in birth at various gestational age categories, (1) term or post-term, (2) late PTB, (3) very PTB, and (4) extreme PTB. The reference category was no occurrence of placental abruption across all gestational ages. We also performed stratified analyses examining the risk of placental abruption with race for various high and low risk groups. High risk groups include mothers with low SES, mothers with no prenatal care, mothers who smoked cigarettes during pregnancy, mothers with chronic hypertension, and mothers with gestational hypertension. The low risk group includes mothers with more than 12 years of education, no indicators of low SES (Medicaid, food stamps, or WIC), married status, some level of prenatal care, maternal age between 20 and 35, no gestational hypertension, chronic hypertension, diabetes or renal problems, and no alcohol or cigarette use during pregnancy. Furthermore, we analyzed the occurrence of placental abruption stratified by gestational age. For each gestational age stratum, the binary outcome variable was the occurrence of placental abruption, and the reference category was no occurrence of placental abruption in that gestational age category.

The following factors were used to identify mothers with low SES at the time of delivery: mother was a recipient of state-funded Medicaid assistance, food stamps or the Special Supplemental Nutrition Program for Women, Infants and Children (WIC Program). A binary composite SES variable was created, using the individual dichotomous indicators of low SES, and was defined as low SES if any indicator was present (recipient of Medicaid, food stamps or WIC). A binary variable of low maternal education was created indicating education < 12 years. Maternal age was analyzed as a categorical variable with the following categories: teenage pregnancy (reference), maternal age ≥ 20 years and < 35 years, and advanced maternal age (≥ 35 years). A binary variable was created for lack of prenatal care (derived from a continuous variable that indicated the month of pregnancy at which prenatal care was initiated). We created a continuous variable of maternal pre-pregnancy body mass index (BMI) from maternal height and pre-pregnancy weight, and from this created a categorical variable with low BMI (< 20 kg/m2), intermediate BMI (≥ 20 kg/m2 and ≤ 30 kg/m2), and high BMI (> 30 kg/m2). We created a dichotomous variable for primigravida from the gravidity variable. Other maternal risk factors considered included cigarette smoking, alcohol use, pre-gestational diabetes, chronic hypertension, gestational hypertension, and chronic renal disease.

Statistical analysis

Data were analyzed using Stata SE 9.2 for Windows (College Station, Texas). For binary outcome variables, unadjusted relative risks were calculated using chi-square tests, and adjusted odds ratios were calculated using binary logistic regression models. For higher-order categorical outcome variables, unadjusted and adjusted odds ratios (aOR) were approximated with the relative risk ratio (RRR) using multinomial logistic regression models. The chi-square test was used to test significance for trend by gestational age (unadjusted). Significant covariates and interaction variables (between race and covariates such as SES) were selected for inclusion in the final multivariable models if there was a 10% or greater difference between the adjusted and unadjusted estimate of the effect, and if the confounding relationship was clinically and biologically important and plausible. All occurrence analyses were adjusted for clustering in siblingships as identified by a unique siblingship number, by which births to the same mothers were identified.

Results

Population demographics

The cohort analyzed included 664,303 singleton live births with 108,806 (16.4%) births to Black mothers, and 555,497 (83.6%) births to White mothers. Black mothers, compared to White mothers, delivered at a lower mean gestational age, had a younger mean maternal age, and had a greater proportion of teenage pregnancies. Black mothers were also characterized by a greater proportion having maternal education < 12 years, indicators of low SES, unmarried status, no prenatal care, and obesity (BMI > 30 kg/m2). A greater proportion of White mothers, compared to that of Black mothers, was primigravida, had pre-pregnancy BMI < 20 kg/m2, and smoked cigarettes during pregnancy, compared to Black mothers. Furthermore, Black mothers were characterized by a greater proportion with chronic hypertension, gestational hypertension, renal disease, and alcohol use during pregnancy. There was no significant difference in proportion of pre-gestational diabetes between Black and White mothers (see Table 1).

Table 1 Baseline characteristics by race for individual births (n = 664,303)
Full size table

The cases of placental abruption included 5,065 births (0.76% of the total, 95%CI 0.74–0.78), including 1,108 (1.02%, 95% CI 0.96–1.08) births to Black mothers, and 3,957 (0.71%, 95% CI 0.69–0.73) births to White mothers. Among cases of placental abruption, Black mothers, compared to White mothers, were more likely to deliver at a younger gestational age, be at a younger age (teenage pregnancy), have < 12 years of education, have indicators of low SES, be unmarried, be multiparous, have no prenatal care, be obese (BMI > 30 kg/m2), have chronic hypertension and have used alcohol during pregnancy. A lower proportion of Black mothers reported cigarette use during pregnancy (see Table 2).

Table 2 Baseline characteristics by race in cases of placental abruption (n = 5,065)
Full size table

Risk of placental abruption associated with race

Black mothers, compared to White mothers, were overall 1.32 times more likely to have placental abruption (95% CI 1.22–1.43). The magnitude of relative risk increase of placental abruption for Black mothers, compared to White mothers, increased as the severity of prematurity worsened (p < 0.001). Black mothers were only slightly more likely to have placental abruption term or post-term (aOR 1.15, 95% CI 1.02–1.29), compared to White mothers, but Black mothers were almost twice as likely to have placental abruption with extreme preterm birth (aOR 1.98, 95% CI 1.58–2.48) (see Table 3).

Table 3 Risk of placental abruption in Black compared to White women by gestational age category (categorical analysis)
Full size table

Significant covariates included in the regression model for race and placental abruption were unmarried status (aOR 1.07, 95% CI 1.01–1.14), cigarette use (aOR 1.75, 95% CI 1.65–1.86, no prenatal care (aOR 2.51, 95% CI 2.19–2.87), chronic hypertension (aOR 1.76, 95%CI 1.44–2.15), and gestational hypertension (aOR 2.24, 95% CI 2.06–2.44). Other variables that had a significant effect on placental abruption (but were not part of the final explanatory regression model because they did not alter the estimate of the effect of race) were age 20–30 relative to teenage pregnancy (aOR 1.16, 95% CI 1.06–1.26), advanced maternal age relative to teenage pregnancy (aOR 1.56, 95% CI 1.38–1.76), primigravida (aOR 0.77, 95% CI 0.73–0.81), pre-pregnancy BMI < 20 (aOR 1.33, 95% CI 1.24–1.42), pre-pregnancy BMI > 30 (aOR 0.82, 95% CI 0.75–0.90), renal disease (aOR 1.84, 95% CI 1.30–2.60), and alcohol use (aOR 1.30, 95% CI 1.13–1.49).

When we examined the risk of placental abruption associated with race in subgroups of women selected for various high or low risk characteristics, overall we found that these subsets of Black women had an increased risk of placental abruption, compared to the same subsets of White women. In the subgroup of women positive for indicators of low SES (n = 293,386), Black women had a 30% increase in risk of placental abruption, compared to White women (RR 1.27, 95% CI 1.17–1.38). Black women who had no prenatal care also had a 60% increase in risk of placental abruption, compared to White women who also had no prenatal care (n = 9,042, RR 1.63, 95% CI 1.23–2.17). Black smokers also had an increased risk of placental abruption compared to White smokers (n = 146,198, RR 1.48, 95% CI 1.31–1.67). In the subgroup of women with chronic hypertension, Black women did not have a statistically significant increase in risk of placental abruption, compared to White women (n = 5,340, RR 1.56, 95% CI 0.99–2.44). Black women who had gestational hypertension had a higher risk of PPROM, compared to White women with gestational hypertension (n = 27,075, RR 1.31, 95% CI 1.05–1.63). In the low-risk subgroup of women with no major SES or medical risk factors (n = 223,780), low-risk Black women also had an increased risk of placental abruption, compared to low-risk White mothers (RR 1.45, 95% CI 1.13–1.87).

Relative contribution of placental abruption to preterm birth

For the subset of women delivering at term or post-term gestational ages, there was a significantly greater proportion of placental abruption in Black mothers (0.61%), compared to White mothers (0.50%) (p < 0.001). In contrast, the proportion of Black mothers with placental abruption delivering at late preterm, very preterm, or extreme preterm birth gestation ages was lower than White mothers (see Table 4). The frequency of placental abruption in these preterm birth categories increased as gestational age at birth decreased for both Black mothers and White mothers (see Table 4).

Table 4 Relative contribution of placental abruption to preterm birth in Black compared to White women (stratified analysis)
Full size table

Discussion

In this study, we examined the association among placental abruption, preterm birth and maternal race. We found that self-reported Black maternal race, compared to White race, was significantly associated with an increased risk of placental abruption, even after adjusting for SES and maternal medical risk factors. These findings confirmed previous epidemiological studies showing increased risk of placental abruption in Black mothers, compared to White mothers [3, 9, 21]. We also observed that the relative risk increase for placental abruption for Black mothers was greater at earlier gestational age categories, compared to White mothers.

Since we confirmed Black race to be a risk factor for placental abruption, and both Black race and placental abruption have been identified as risk factors for PTB, we expected a greater contribution of placental abruption to the increased risk of PTB in Black mothers. However, we did not find that to be the case. We found that for the subset of women delivering preterm, there was a significantly lower proportion of placental abruption in Black mothers, compared to White mothers. Conversely, for the subset of women delivering at term, there was a significantly higher proportion of placental abruption in Black mothers, compared to White mothers.

While this result may seem initially contradictory to the finding that Black women, compared to White mothers, were at an increased risk of placental abruption, and that there was a trend with severity of prematurity, this perspective highlights preterm birth frequency issues. Firstly, numerous studies have shown that Black mothers, compared to White mothers, are at significantly higher risk of PTB (and recurrence), even after adjustment for important SES and maternal medical risk factors [22–24]. This study shows that specific mechanisms of PTB other than placental abruption, such as spontaneous preterm labor (SPTL) and PPROM, may have much greater contributions to the increased risk of PTB in Black women, compared to the mechanism of placental abruption.

Secondly, the fact that Black women have a greater proportion of placental abruption in term pregnancies, but have a lesser proportion placental abruption in preterm pregnancies, may hint at different causative pathways at preterm and at term gestations that culminate in placental abruption. Evidence from previous studies suggests that placental abruption is the manifestation of at least two distinct clinical pathways: 1) acute inflammation-associated pathways (such as premature rupture of membranes, etc.), and 2) chronic clinical processes (such as chronic hypertension, gestational hypertension, diabetes, smoking, etc.) [7, 8, 16, 27]. At preterm gestations, placental abruption seems to be more frequently associated with acute inflammation, notably PPROM, whereas chronic clinical processes seem to be associated with an increased risk, both at term and preterm births[8].

Finally, the association between placental abruption and maternal race, especially abruption-associated PTB, prominent even after controlling for SES and maternal medical risk factors, may suggest the possibility of a genetic contribution along with environmental components to the pathogenesis of placental abruption. Self-reported race in general accurately reflects ancestry, but the heterogeneity of nativity in Black mothers have also been shown to influence birth outcomes [28, 29]. Thus, self-reported race is a reasonable, but not perfect, correlate for ancestry and genetics. However, we also acknowledge that unmeasured confounding environmental risk factors must be considered, and may contribute much of the disparity we observed.

Placental abruption is a distinct and dependent mechanism of PTB. Placental abruption, PPROM, and SPTL have overlapping causes, and probably similar biochemical pathways. Although evidence for environmental contribution for PTB is compelling, there has been increasing evidence for genetic contributions to PTB. Family-based, twin, and ethnic-comparison studies have all suggested that genetics may play a role in PTB, in addition to environmental factors [22, 24, 30–33]. Several recent candidate gene studies for PTB have also supported the case for genetic contributions [34–38]. Unfortunately, most of the genetic studies in placental abruption have concentrated on polymorphisms in various coagulation genes only, and little or no information is available in African populations or those of African descent [39].

The limitations of our study are typical to those of large, population-based studies. Possible sources of bias concerning measurement error in the database comprise recall, underreporting, miscoding, misclassification and information bias. Recall bias, such as the underreporting of social habit variables (i.e. cigarette smoking, alcohol use, and illicit drug use) and inaccurate reporting and underreporting of prenatal care, weight, past medical history and obstetrics complication variables, likely results in bias towards the null since bias is most likely nondifferential across race. Preterm birth was defined at less than 35 weeks of gestation, in order to decrease the effects of miscoding error and misclassification bias of borderline gestational ages. Information bias may include lack of data on certain maternal medical co-morbidities. Cocaine use is an important contributor to placental abruption, but is not a coded variable in the database. However, it is not likely to influence race-specific effects on placental abruption, as the reported frequency of cocaine use in complicated deliveries is extremely low [40]. We chose to exclude fetal deaths in utero, because it likely represents a group of complicated births having different pathological mechanisms unrelated to placental abruption. Even though the most severe cases of placental abruption (causing death) may be excluded, the effect of that on the relationship between maternal race and placental abruption should be limited. Furthermore, placental abruption may be underestimated in term and post-term gestations, shifting cases of placental abruption toward a lower median gestational age at delivery, but we do not anticipate this shift to be biased by maternal race. Finally, because the racial distribution of Missouri consisted of mainly Black and White races, it precluded analysis of adverse birth outcomes in other races. The population-based nature of the study offers generalizability to a broad spectrum of clinical populations. The large sample size also permits sufficient statistical power for subgroup analysis of a relatively rare outcome in various gestational age categories. More importantly, the results have broad research and clinical implications.

Conclusion

We find that Black women are at increased risk for placental abruption, especially at early gestational ages, but placental abruption makes up a smaller proportion of causes of PTB for Black women. In addition, the difference in relative contribution of placental abruption between term and preterm gestations suggests heterogeneity in clinical pathways between these two importantly different birth outcomes.

References

  1. Karegard M, Gennser G: Incidence and recurrence rate of abruptio placentae in Sweden. Obstet Gynecol. 1986, 67 (4): 523-528.

    CAS  PubMed  Google Scholar 

  2. Sher G: A rational basis for the management of abruptio placentae. J Reprod Med. 1978, 21 (3): 123-129.

    CAS  PubMed  Google Scholar 

  3. Ananth CV, Oyelese Y, Yeo L, Pradhan A, Vintzileos AM: Placental abruption in the United States, 1979 through 2001: temporal trends and potential determinants. Am J Obstet Gynecol. 2005, 192 (1): 191-198. 10.1016/j.ajog.2004.05.087.

    Article  PubMed  Google Scholar 

  4. Brame RG, Harbert GM, McGaughey HS, Thornton WN: Maternal risk in abruption. Obstet Gynecol. 1968, 31 (2): 224-227.

    Article  CAS  PubMed  Google Scholar 

  5. Harris BA, Gore H, Flowers CE: Peripheral placental separation: a possible relationship to premature labor. Obstet Gynecol. 1985, 66 (6): 774-778.

    PubMed  Google Scholar 

  6. Rasmussen S, Irgens LM, Bergsjo P, Dalaker K: The occurrence of placental abruption in Norway 1967–1991. Acta Obstet Gynecol Scand. 1996, 75 (3): 222-228. 10.3109/00016349609047091.

    Article  CAS  PubMed  Google Scholar 

  7. Salafia CM, Lopez-Zeno JA, Sherer DM, Whittington SS, Minior VK, Vintzileos AM: Histologic evidence of old intrauterine bleeding is more frequent in prematurity. Am J Obstet Gynecol. 1995, 173 (4): 1065-1070. 10.1016/0002-9378(95)91327-0.

    Article  CAS  PubMed  Google Scholar 

  8. Ananth CV, Getahun D, Peltier MR, Smulian JC: Placental abruption in term and preterm gestations: evidence for heterogeneity in clinical pathways. Obstet Gynecol. 2006, 107 (4): 785-792.

    Article  PubMed  Google Scholar 

  9. Misra DP, Ananth CV: Risk factor profiles of placental abruption in first and second pregnancies: heterogeneous etiologies. J Clin Epidemiol. 1999, 52 (5): 453-461. 10.1016/S0895-4356(99)00017-7.

    Article  CAS  PubMed  Google Scholar 

  10. Lindqvist PG, Happach C: Risk and risk estimation of placental abruption. Eur J Obstet Gynecol Reprod Biol. 2006, 126 (2): 160-164. 10.1016/j.ejogrb.2005.08.003.

    Article  PubMed  Google Scholar 

  11. Kramer MS, Usher RH, Pollack R, Boyd M, Usher S: Etiologic determinants of abruptio placentae. Obstet Gynecol. 1997, 89 (2): 221-226. 10.1016/S0029-7844(96)00478-4.

    Article  CAS  PubMed  Google Scholar 

  12. Ananth CV, Savitz DA, Bowes WA, Luther ER: Influence of hypertensive disorders and cigarette smoking on placental abruption and uterine bleeding during pregnancy. Br J Obstet Gynaecol. 1997, 104 (5): 572-578.

    Article  CAS  PubMed  Google Scholar 

  13. Kaminsky LM, Ananth CV, Prasad V, Nath C, Vintzileos AM: The influence of maternal cigarette smoking on placental pathology in pregnancies complicated by abruption. Am J Obstet Gynecol. 2007, 197 (3): e271-275. 10.1016/j.ajog.2007.06.026.

    Article  Google Scholar 

  14. Ananth CV, Wilcox AJ, Savitz DA, Bowes WA, Luther ER: Effect of maternal age and parity on the risk of uteroplacental bleeding disorders in pregnancy. Obstet Gynecol. 1996, 88 (4 Pt 1): 511-516. 10.1016/0029-7844(96)00236-0.

    Article  CAS  PubMed  Google Scholar 

  15. Hoskins IA, Friedman DM, Frieden FJ, Ordorica SA, Young BK: Relationship between antepartum cocaine abuse, abnormal umbilical artery Doppler velocimetry, and placental abruption. Obstet Gynecol. 1991, 78 (2): 279-282.

    CAS  PubMed  Google Scholar 

  16. Ananth CV, Oyelese Y, Srinivas N, Yeo L, Vintzileos AM: Preterm premature rupture of membranes, intrauterine infection, and oligohydramnios: risk factors for placental abruption. Obstet Gynecol. 2004, 104 (1): 71-77.

    Article  PubMed  Google Scholar 

  17. Mackenzie AP, Schatz F, Krikun G, Funai EF, Kadner S, Lockwood CJ: Mechanisms of abruption-induced premature rupture of the fetal membranes: Thrombin enhanced decidual matrix metalloproteinase-3 (stromelysin-1) expression. Am J Obstet Gynecol. 2004, 191 (6): 1996-2001. 10.1016/j.ajog.2004.08.003.

    Article  CAS  PubMed  Google Scholar 

  18. Vollset SE, Refsum H, Irgens LM, Emblem BM, Tverdal A, Gjessing HK, Monsen AL, Ueland PM: Plasma total homocysteine, pregnancy complications, and adverse pregnancy outcomes: the Hordaland Homocysteine study. Am J Clin Nutr. 2000, 71 (4): 962-968.

    CAS  PubMed  Google Scholar 

  19. Prochazka M, Happach C, Marsal K, Dahlback B, Lindqvist PG: Factor V Leiden in pregnancies complicated by placental abruption. Bjog. 2003, 110 (5): 462-466.

    Article  CAS  PubMed  Google Scholar 

  20. Nurk E, Tell GS, Refsum H, Ueland PM, Vollset SE: Associations between maternal methylenetetrahydrofolate reductase polymorphisms and adverse outcomes of pregnancy: the Hordaland Homocysteine Study. Am J Med. 2004, 117 (1): 26-31. 10.1016/j.amjmed.2004.01.019.

    Article  CAS  PubMed  Google Scholar 

  21. Pritchard JA, Cunningham FG, Pritchard SA, Mason RA: On reducing the frequency of severe abruptio placentae. Am J Obstet Gynecol. 1991, 165 (5 Pt 1): 1345-1351.

    Article  CAS  PubMed  Google Scholar 

  22. Adams MM, Elam-Evans LD, Wilson HG, Gilbertz DA: Rates of and factors associated with recurrence of preterm delivery. Jama. 2000, 283 (12): 1591-1596. 10.1001/jama.283.12.1591.

    Article  CAS  PubMed  Google Scholar 

  23. Kramer MS, Goulet L, Lydon J, Seguin L, McNamara H, Dassa C, Platt RW, Chen MF, Gauthier H, Genest J, Kahn S, Libman M, Rozen R, Masse A, Miner L, Asselin G, Benjamin A, Klein J, Koren G: Socioeconomic disparities in preterm birth: causal pathways and mechanisms. Paediatr Perinat Epidemiol. 2001, 15 (Suppl 2): 104-123. 10.1046/j.1365-3016.2001.00012.x.

    Article  PubMed  Google Scholar 

  24. Goldenberg RL, Cliver SP, Mulvihill FX, Hickey CA, Hoffman HJ, Klerman LV, Johnson MJ: Medical, psychosocial, and behavioral risk factors do not explain the increased risk for low birth weight among black women. Am J Obstet Gynecol. 1996, 175 (5): 1317-1324. 10.1016/S0002-9378(96)70048-0.

    Article  CAS  PubMed  Google Scholar 

  25. Herman AA, McCarthy BJ, Bakewell JM, Ward RH, Mueller BA, Maconochie NE, Read AW, Zadka P, Skjaerven R: Data linkage methods used in maternally-linked birth and infant death surveillance data sets from the United States (Georgia, Missouri, Utah and Washington State), Israel, Norway, Scotland and Western Australia. Paediatr Perinat Epidemiol. 1997, 11 (Suppl 1): 5-22. 10.1046/j.1365-3016.11.s1.11.x.

    Article  PubMed  Google Scholar 

  26. Mattison DR, Damus K, Fiore E, Petrini J, Alter C: Preterm delivery: a public health perspective. Paediatr Perinat Epidemiol. 2001, 15 (Suppl 2): 7-16. 10.1046/j.1365-3016.2001.00004.x.

    Article  PubMed  Google Scholar 

  27. Rasmussen S, Irgens LM, Dalaker K: A history of placental dysfunction and risk of placental abruption. Paediatr Perinat Epidemiol. 1999, 13 (1): 9-21. 10.1046/j.1365-3016.1999.00159.x.

    Article  CAS  PubMed  Google Scholar 

  28. Risch N, Burchard E, Ziv E, Tang H: Categorization of humans in biomedical research: genes, race and disease. Genome Biol. 2002, 3 (7): comment2007.

    Google Scholar 

  29. Howard DL, Marshall SS, Kaufman JS, Savitz DA: Variations in low birth weight and preterm delivery among blacks in relation to ancestry and nativity: New York City, 1998–2002. Pediatrics. 2006, 118 (5): e1399-1405. 10.1542/peds.2006-0665.

    Article  PubMed  Google Scholar 

  30. Bloom SL, Yost NP, McIntire DD, Leveno KJ: Recurrence of preterm birth in singleton and twin pregnancies. Obstet Gynecol. 2001, 98 (3): 379-385. 10.1016/S0029-7844(01)01466-1.

    CAS  PubMed  Google Scholar 

  31. Melve KK, Skjaerven R, Gjessing HK, Oyen N: Recurrence of gestational age in sibships: implications for perinatal mortality. Am J Epidemiol. 1999, 150 (7): 756-762.

    Article  CAS  PubMed  Google Scholar 

  32. Porter TF, Fraser AM, Hunter CY, Ward RH, Varner MW: The risk of preterm birth across generations. Obstet Gynecol. 1997, 90 (1): 63-67. 10.1016/S0029-7844(97)00215-9.

    Article  CAS  PubMed  Google Scholar 

  33. Winkvist A, Mogren I, Hogberg U: Familial patterns in birth characteristics: impact on individual and population risks. Int J Epidemiol. 1998, 27 (2): 248-254. 10.1093/ije/27.2.248.

    Article  CAS  PubMed  Google Scholar 

  34. Roberts AK, Monzon-Bordonaba F, Van Deerlin PG, Holder J, Macones GA, Morgan MA, Strauss JF, Parry S: Association of polymorphism within the promoter of the tumor necrosis factor alpha gene with increased risk of preterm premature rupture of the fetal membranes. Am J Obstet Gynecol. 1999, 180 (5): 1297-1302. 10.1016/S0002-9378(99)70632-0.

    Article  CAS  PubMed  Google Scholar 

  35. Menon R, Velez DR, Simhan H, Ryckman K, Jiang L, Thorsen P, Vogel I, Jacobsson B, Merialdi M, Williams SM, Fortunato SJ: Multilocus interactions at maternal tumor necrosis factor-alpha, tumor necrosis factor receptors, interleukin-6 and interleukin-6 receptor genes predict spontaneous preterm labor in European-American women. Am J Obstet Gynecol. 2006, 194 (6): 1616-1624. 10.1016/j.ajog.2006.03.059.

    Article  CAS  PubMed  Google Scholar 

  36. Fujimoto T, Parry S, Urbanek M, Sammel M, Macones G, Kuivaniemi H, Romero R, Strauss JF: A single nucleotide polymorphism in the matrix metalloproteinase-1 (MMP-1) promoter influences amnion cell MMP-1 expression and risk for preterm premature rupture of the fetal membranes. J Biol Chem. 2002, 277 (8): 6296-6302. 10.1074/jbc.M107865200.

    Article  CAS  PubMed  Google Scholar 

  37. Ferrand PE, Parry S, Sammel M, Macones GA, Kuivaniemi H, Romero R, Strauss JF: A polymorphism in the matrix metalloproteinase-9 promoter is associated with increased risk of preterm premature rupture of membranes in African Americans. Mol Hum Reprod. 2002, 8 (5): 494-501. 10.1093/molehr/8.5.494.

    Article  CAS  PubMed  Google Scholar 

  38. Wang H, Parry S, Macones G, Sammel MD, Kuivaniemi H, Tromp G, Argyropoulos G, Halder I, Shriver MD, Romero R, Strauss JF: A functional SNP in the promoter of the SERPINH1 gene increases risk of preterm premature rupture of membranes in African Americans. Proc Natl Acad Sci USA. 2006, 103 (36): 13463-13467. 10.1073/pnas.0603676103.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  39. Hira B, Pegoraro RJ, Rom L, Govender T, Moodley J: Polymorphisms in various coagulation genes in black South African women with placental abruption. Bjog. 2002, 109 (5): 574-575.

    Article  CAS  PubMed  Google Scholar 

  40. Ebrahim SH, Gfroerer J: Pregnancy-related substance use in the United States during 1996–1998. Obstet Gynecol. 2003, 101 (2): 374-379. 10.1016/S0029-7844(02)02588-7.

    PubMed  Google Scholar 

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Acknowledgements

This work was supported by a grant from Dean's Funds, Washington University in St Louis, and by a grant from March of Dimes.

This work was presented at the 28th Annual Society for Maternal-Fetal Medicine meeting; Jan. 28-Feb. 2, 2008; Dallas, TX.

All of the analyses, interpretations, and conclusions that were derived from the database and included in this article are those of the authors and not the Missouri Department of Health and Senior Services, Bureau of Health Informatics.

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Authors and Affiliations

  1. Department of Pediatrics, Washington University in St. Louis, St. Louis, Missouri, USA

    Tammy T Shen & Louis J Muglia

  2. Center for Preterm Birth Research, Washington University in St. Louis, St. Louis, Missouri, USA

    Tammy T Shen, Emily A DeFranco, David M Stamilio, Jen Jen Chang & Louis J Muglia

  3. Department of Obstetrics and Gynecology, Washington University in St. Louis, St. Louis, Missouri, USA

    Emily A DeFranco, David M Stamilio & Louis J Muglia

  4. Department of Community Health in Epidemiology, School of Public Health, Saint Louis University, St. Louis, Missouri, USA

    Jen Jen Chang

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Correspondence to Louis J Muglia.

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The authors declare that they have no competing interests.

Authors' contributions

TTS has made substantial contributions to conception and design, analysis and interpretation of data, and have been involved in drafting the manuscript and revising it critically for important intellectual content. EAD has made substantial contributions to conception and design, and has been involved in revising the manuscript critically for important intellectual content. JJC and DMS participated in analysis and interpretation of data, as well as in revising the manuscript critically for important intellectual content. LJM has made substantial contributions to conception and design, and has been involved in revising the manuscript critically for important intellectual content. All authors read and approved the final transcript.

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Shen, T.T., DeFranco, E.A., Stamilio, D.M. et al. A population-based study of race-specific risk for placental abruption. BMC Pregnancy Childbirth 8, 43 (2008). https://doi.org/10.1186/1471-2393-8-43

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Keywords

  • Preterm Birth
  • Black Woman
  • Prenatal Care
  • Chronic Hypertension
  • Gestational Hypertension

BMC Pregnancy and Childbirth

ISSN: 1471-2393

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