Impact of prenatal alcohol consumption on placenta-associated syndromes
Introduction
The placenta is critical for maternal–fetal exchange, and abnormalities (e.g., vascular lesions) are associated with adverse pregnancy outcomes and complications, such as placental abruption, placenta previa, preeclampsia, small for gestational age (SGA), preterm, or stillbirth (Khong, 2004). Because of their associations with vascular abnormalities, these feto-infant morbidities are believed to be placental in origin and are collectively known as placental-associated syndromes (Ray et al., 2005). These disorders are presumed to originate from diseased placental vessels and have previously been examined in aggregate to determine the risk of premature cardiovascular disease in women (Ray et al., 2005). Alcohol may contribute to the development of vascular lesions leading to adverse pregnancy outcomes as it readily crosses the placenta, and exposure causes dose-dependent placental vasoconstrictions and decreases in placental weight (Burd et al., 2007). Although only about 1.6% of pregnant women reported frequent drinking during pregnancy, an even greater percentage, about 12.5%, report consuming at least some alcohol during pregnancy (Floyd and Sidhu, 2004). Less than half of all reproductive aged women abstain from alcohol use (45.4%), an indication that exposure rates may be even higher, especially in early pregnancy before it is recognized (Floyd and Sidhu, 2004).
Previous studies of alcohol consumption during pregnancy and the various components of placenta-associated syndromes (PASs) have had inconsistent results (Aliyu et al., 2008, Henderson et al., 2007a, Yang et al., 2001). Nonetheless, the biology of placental and fetal development suggests that alcohol may play a significant role in increasing the risk of feto-infant morbidity and mortality. The placenta grows throughout pregnancy and this growth is accompanied by an increase in vasculature and trophoblast surface area (Myatt, 2006). Alcohol exposure may cause disruptions in these processes, resulting in impaired development and culminating in any number of feto-infant morbidities or mortality (Burd et al., 2007, Myatt, 2006). It is hypothesized that depending on the timing of the exposure, and the dose received, alcohol exposure can lead to PASs (Burd et al., 2007). However, while previous authors have considered associations between alcohol and adverse pregnancy outcomes, they have not examined PASs as a larger entity. Accordingly, we conducted this population-based study with the following objectives: (1) To examine the impact of prenatal alcohol use on the risk of PASs; and (2) To assess whether there is a dose–response relationship between the amount of alcohol consumed and the level of risk for PAS.
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Materials and methods
We used the Missouri maternally linked cohort data files covering the period of 1989 through 2005. The Missouri vital record system is a reliable one that has been adopted as the “gold standard” to validate U.S. national data sets that involve matching and linking procedures (Martin et al., 2003). For the purpose of this study, we selected singleton births within the gestational age range of 20–44 weeks. On the basis of the previously published reports (McTigue et al., 2006, NHLBI Obesity
Results
A total of 1,312,505 singleton births were available for analysis. We excluded pregnancies before 20 weeks or beyond 44 weeks of gestation (70,803 or 5.4%) and records for which prenatal drinking (7,085), gestational age (7,559), and birth weight (333) values were missing (total = 14,990 or 1.2%). The final data set composed of a total of 1,226,685 singleton records, consisting of drinking (16,003 or 1.3%) and nondrinking gravidas (1,210,682 or 98.7%; the referent group).
Overall, the prevalence
Discussion
In this study, we found that the risk for PASs increases with increasing prenatal alcohol consumption. Women who reported consuming five or more alcoholic drinks per week had more than twofold increased risk of PASs. To our knowledge, previous studies have not examined PASs as a unique entity with the components sharing similar pathophysiologic pathways. Prior studies that have examined the individual components of PASs have found similar associations. For example, a study by Marbury et al.
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2021, American Journal of Obstetrics and GynecologyCitation Excerpt :A single study reported on placenta accreta, finding no effect with the highest level of PAE (Table 2) but a robust increase in the likelihood of this complication when alcohol was considered as a dichotomous predictor (aOR, 3.03; 95% CI, 1.69–5.44; P<.001).51 Similarly, there was a single study of preeclampsia, which reported no difference between the control group and the highest PAE group (Table 2), whereas comparison of the entire alcohol group with the control group resulted in a small but significant decrease in the likelihood of preeclampsia (aOR, 0.84; 95% CI, 0.76–0.92; P<.001).38 There were 7 cohort studies reporting on placental abruption, each with a large sample size (∼1000 to >15 million), and 1 small observational study (Table 2).
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2020, European Journal of Obstetrics and Gynecology and Reproductive BiologyCitation Excerpt :Thereafter it was also demonstrated that the effect of prenatal alcohol consumption on fetal growth restriction is potentiated by concomitant smoking [25]. More recently the same group demonstrated an association between tobacco use in pregnancy and PAS, an informal classification of disease states arising from diseased placental spiral arteries, placental ischemia, and endothelial dysfunction, in a population-based study [9]. The strength of our study is that it was community based in a single population with a prospective collection of data in a structured format, in contrast with large epidemiological studies using retrospective collected data.
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