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ORIGINAL RESEARCH |
From the 1Department of Obstetrics and Gynecology, Wayne State University, Detroit, Michigan; 2Department of Allergy at Kaiser Permanente, San Diego, California; 3the 4George Washington University Biostatistics Center, Washington, DC; 5Department of Pulmonary Medicine, Johns Hopkins University, Baltimore, Maryland; 6Department of Obstetrics and Gynecology, Ohio State University, Columbus, Ohio; 7Department of Obstetrics and Gynecology, University of Tennessee, Memphis, Tennessee; 8Department of Obstetrics and Gynecology, Medical University of South Carolina, Charleston, South Carolina; 9the National Heart, Lung, and Blood Institute, Bethesda, Maryland; 10Department of Obstetrics and Gynecology, Alabama, Birmingham, Alabama; 11Department of Obstetrics and Gynecology, University of Chicago, Chicago, Illinois; 12Department of Obstetrics and Gynecology, University of Pittsburgh, Pittsburgh, Pennsylvania; 13National Institute of Child Health and Human Development, Bethesda, Maryland; Department of Obstetrics and Gynecology, University of Texas Southwestern, Dallas, Texas; 14Department of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio; 15Department of Obstetrics and Gynecology, Wake Forest University, Winston-Salem, North Carolina; 16Department of Obstetrics and Gynecology, Thomas Jefferson University, Philadelphia, Pennsylvania; 17Department of Obstetrics and Gynecology, University of Southern California, Los Angeles, California; 18Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah; 19Department of Obstetrics and Gynecology, University of Miami, Miami, Florida; and 20Department of Obstetrics and Gynecology, University of Oklahoma, Norman, Oklahoma; Department of Obstetrics and Gynecology, University of Texas, San Antonio, Texas.
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ABSTRACT |
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 ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXREFERENCES |
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METHODS: This is a secondary analysis of the prospective cohort Asthma During Pregnancy Study. Asthma patients were classified as having either mild or moderate to severe disease at the beginning of the study. Rates of pulmonary complications of asthma in asthmatic women and rates of nonpulmonary complications of pregnancy among asthma patients and controls, were compared between obese (body mass index 
30 kg/m2) and nonobese women.
RESULTS: Maternal body mass index and pregnancy outcome data were available for 1,699 of 1,812 asthmatic women and for 867 of 881 controls. Of the asthma subjects, 30.7% (521) were obese compared with 25.5% of the controls, P = .006. Obese women, regardless of whether they had asthma, were more likely to undergo cesarean delivery (OR 1.6, 95% confidence interval [CI]1.3–2.0) to develop preeclampsia or gestational hypertension (OR 1.7 95% CI 1.3–2.3) and gestational diabetes (OR 4.2, 95% CI 2.8–6.3). There were no differences in the rates of overall asthma improvement (20.6% compared with 23.6%, P = .36) or deterioration (33.3% compared with 28.8%, P = .20) between obese and nonobese asthma patients. After adjustment for confounding variables, obesity, not asthma, was associated with nonpulmonary complications of pregnancy, and obesity was associated with an increase in asthma exacerbations as well (OR 1.3, 95% CI 1.1–1.7).
CONCLUSION: Obesity is associated with an increased risk of asthma exacerbations during pregnancy. The increased rate of nonpulmonary complications of pregnancy in asthma patients is associated with obesity in this population and not with asthma status.
LEVEL OF EVIDENCE: II-1
The prevalence of obesity is rising; in the United States more than 21% of the population is considered to be obese.10 There is growing evidence that associates asthma with obesity for reasons yet to be discovered. Increasing body mass index (BMI, kg/m2) in women has been found to be directly associated with the prevalence of asthma.17,18 Moreover, increased BMI increases the severity of asthma,19 and weight reduction in obese individuals improves their asthmatic condition.20,21 Maternal obesity increases the risk for adverse pregnancy outcomes, including fetal anomalies, miscarriages, preeclampsia, gestational diabetes, cesarean delivery, shoulder dystocia, and intrauterine fetal death.22,23 However, there is limited information regarding the effect of obesity on the adverse nonpulmonary as well as pulmonary pregnancy outcomes previously described in asthmatic women. The objective of this study was to investigate the effect of obesity on pulmonary and nonpulmonary complications of pregnancy in asthmatic women.
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MATERIALS AND METHODS |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXREFERENCES |
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Asthma severity was classified upon enrollment in the study based on predefined criteria as mild or moderate to severe. The control and mild asthma cohorts were prospectively balanced in terms of the proportions of smoking status (any in the past week) with the moderate-severe cohort. Controls were also prospectively balanced for proportion of African-American ethnicity with the moderate-severe cohort. Case finding was by questioning all obstetric patients about ever having physician-diagnosed asthma.
Exclusion criteria at enrollment included known multiple gestation, intrauterine fetal demise, major congenital abnormalities, active pulmonary disease other than asthma, inability to schedule an ultrasound for gestational age confirmation, gestational age 26 weeks or more at intake, or participation in interventional studies. In addition, women who had ever had a physician diagnosis of asthma were excluded from the control group. Demographic, social, and medical information were collected. Spirometry (more than 4 hours after use of bronchodilator) was performed on participants with asthma at enrollment. On each monthly study visit, an FEV1 was obtained, and information regarding symptom frequency, asthma medication use, and the occurrence of asthma exacerbations was recorded. An exacerbation was defined as asthma symptoms (cough, dyspnea, or wheezing) severe enough to result in a medical intervention, including hospitalization, unscheduled visits (physician office or emergency department), or treatment with oral corticosteroids among subjects who were not already taking regular oral corticosteroids.
A secondary analysis was performed on all subjects for whom maternal height and prepregnancy weight were available. Prepregnancy maternal BMI was calculated for each patient (weight in kilograms divided by height in meters2). Body mass index was analyzed as both a continuous variable and as a dichotomous variable—nonobese (BMI < 30 kg/m2) and obese (BMI 30 kg/m2).24 The primary outcome was the rate of maternal pulmonary and nonpulmonary complications compared by BMI and asthma status. Maternal pulmonary complications included prevalence of asthma exacerbations, hospitalizations or use of steroids, and change (deterioration or improvement) in asthma severity during pregnancy. Maternal nonpulmonary complications included the incidence of gestational diabetes, preeclampsia (including both preeclampsia and gestational hypertension), cesarean delivery, and preterm delivery (less than 37 weeks). Women with chronic hypertension and pregestational diabetes were excluded from the analysis of pregnancy complications. Rates of pulmonary complications were compared among the asthma patients by asthma severity and maternal BMI, whereas the rate of nonpulmonary complications was compared between asthma patients and controls by maternal BMI. The data regarding nonpulmonary complications were obtained at postpartum chart reviews and were based on clinical diagnosis.
Statistical analyses were performed using the SAS 8.2 software (SAS Institute, Cary, NC). Categorical variables were compared using the 
2 and Fisher exact tests, and continuous variables were compared using the Wilcoxon test. The independent risks associated with obesity were analyzed both using the Mantel-Haenszel test for stratification and logistic models using obesity, asthma severity class (control, mild, moderate-severe), maternal age, chronic hypertension, pregestational diabetes, African-American ethnicity, Hispanic ethnicity, and parity as covariates. Nominal two-tailed P values are reported with statistical significance defined as P < .05. No adjustments were made for multiple comparisons.
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RESULTS |
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30 kg/m2) was higher among cases with asthma compared with controls without asthma (30.7% compared with 25.5% respectively, P = .006). Thirty-two percent of the women in the moderate-severe asthma group (271/843), and 29.2% of the women (250/856) in the mild group (P = .19) were obese, compared with 25.5% (221/867) in the control group (P = .002). Obese women were older, more educated, more likely multiparous and of African-American ethnicity compared with nonobese women, among the asthmatic patients as well as among the controls. However, the difference in maternal age (mean difference of 1–2 years) did not carry a clinical significance. Obese women were also more likely to be hypertensive or diabetic before pregnancy. There were no differences between the obese and nonobese groups in the type of insurance, rate of smoking, or marital status (Table 1). There was no difference in gestational age at delivery when compared between obese and nonobese women in the asthma or in the control groups as well as in birth weight when compared between obese and nonobese women among the control participants. The infants of obese asthmatic women weighed more at birth compared with nonobese asthmatic women; however this difference (70 grams) was not of clinical significance. (Table 2)
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The following describes the association of obesity with nonpulmonary complications among asthma patients and controls: There was no difference between obese and nonobese asthmatic patients as well as among the controls in the rate of preterm birth before 37 weeks or before 32 weeks. Among asthma patients (mild and moderate-severe), as well as among the controls, obese gravidas had more cesarean deliveries, a higher rate of preeclampsia or gestational hypertension, and a higher rate of gestational diabetes compared with nonobese women (Table 2). The magnitude of the association between obesity and these complications was consistent among the groups categorized by severity of asthma and controls without asthma (Fig. 1). There was no difference between asthma and control women in the rates of cesarean delivery, preeclampsia, and gestational diabetes when compared within obese and within nonobese women separately.
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After adjustment for confounding variables, obesity was associated with increased odds for cesarean delivery (odds ratio [OR] –1.6, 95% confidence interval [CI] 1.3–2.0), preeclampsia (OR 1.7, 95% CI 1.3–2.3), and gestational diabetes mellitus (OR 4.2, 95% CI 2.8–6.3), but not with preterm birth (OR 0.8, 95% CI 0.6–1.0, P = .1). There was no interaction between asthma and obesity in a regression model for the association with nonpulmonary pregnancy complications.
Obesity was associated with an increase in asthma exacerbations during pregnancy but not with other indicators of asthma severity, including steroid treatment (Table 2). Women requiring hospitalization for asthma had a higher mean BMI than women who did not require hospitalization (28.7 ± 8.4 compared with 27.1 ± 7.4 kg/m2, P < .001). However, when these patients were dichotomized to obese and nonobese, there was no difference in asthma-associated hospitalizations during pregnancy (Table 2).
There were no differences in the rates of overall asthma improvement (20.6% compared with 23.6%, P = .36) or deterioration (33.3% compared with 28.8%, P = .20), when compared between obese and nonobese women (Table 2).
After adjustment for confounding variables there remained an association between obesity and asthma exacerbation during pregnancy (OR 1.3, 95% CI 1.1–1.7, P = .01), (Table 3).
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DISCUSSION |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXREFERENCES |
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In this study population there was a higher rate of obesity among asthmatic pregnant women than with controls. After adjustment for confounding variables, obesity in asthmatic patients and not the disease itself was found to be associated with cesarean deliveries (OR –1.6), preeclampsia or gestational hypertension (OR –1.7) and gestational diabetes (OR –4.2). There was no association between either asthma or obesity and preterm deliveries, and there was no interaction between asthma and obesity in a regression model for nonpulmonary complications of pregnancy. The adverse effects of obesity on pregnancy in a general population of women were previously described.23,25 In the study by Sebire25 (n = 287,213) obese gravidas had an OR of 1.7 for gestational diabetes mellitus, 1.4 for proteinuric preeclampsia, and 1.3 for delivery by emergency cesarean delivery. Our results convey further evidence for the lack of association between well-controlled asthma and adverse nonpulmonary pregnancy outcome as was found by Dombrowski et al9 in the same cohorts. However, other studies reported an increased risk for perinatal complications with maternal asthma.6,8 In 36,985 Swedish women, pregnancies in women with asthma were significantly more likely to be complicated by preeclampsia, perinatal mortality, preterm birth, and low birth weight (but not congenital malformations). The study also suggested that patients with more severe asthma are at a greater risk.7 However, these results were not adjusted for maternal BMI. Namazy and Schatz26 postulated recently the possible mechanisms for increased perinatal risks found by previous studies: 1) hypoxia and other physiologic consequences of poorly controlled asthma, 2) medications used to treat asthma, and 3) pathogenic or demographic factors associated with asthma but not actually caused by the disease or its treatment. Obesity is associated with asthma and may be the underlying demographic factor for many of the nonpulmonary complications previously described.
Obesity was found to be associated with asthma exacerbation, even after adjustment for confounding variables. Akerman et al19 found that increased BMI among obese adults was associated with increased severity of asthma; Hakala et al27 found in a small nonrandomized study that weight loss reduces airway obstruction as well as peak expiratory flow variability in obese patients with asthma, and a randomized controlled trial has shown that weight reduction in obese individuals with asthma improves lung function and severity of the disease.21
This secondary analysis has the same limitations as the primary study: the management of asthma was not standardized, and control participants were not rigorously evaluated for absence of asthma. Moreover, the diagnosis of gestational diabetes and preeclampsia was not based on strict criteria but merely on a clinical diagnosis according to the criteria used by each one of the Maternal-Fetal Medicine Units centers. The primary study was not powered to assess the effects of obesity on the severity of asthma, thus the lack of association between some of the pulmonary complications of asthma (steroid treatment, hospitalizations, etc.) and obesity in our population may be due to a small sample size.
Nonpulmonary complications of asthma during pregnancy, including gestational diabetes, gestational hypertension and preeclampsia, and cesarean delivery, are associated with maternal obesity and not with asthma status. Further study is needed to evaluate the effects of obesity on the severity of pulmonary complications of asthma during pregnancy as well as to assess the effects of excess weight gain and weight reduction on the course of asthma during pregnancy.
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APPENDIX |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXREFERENCES |
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Footnotes |
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Supported by grants from the National Institute of Child Health and Human Development (HD19897, HD21410, HD21414, HD21434, HD27869, HD27917, HD27905, HD27889, HD27860, HD27861, HD27915, HD27883, HD34122, HD34116, HD34210, HD34208, HD34136, and HD36801) and the National Heart, Lung, and Blood Institute.
The authors thank Mitchell P. Dombrowski, MD, for his assistance in the design of the study and his role as the Primary Protocol Subcommittee Committee Chair and Elizabeth Thom, PhD, for her role as the Principal Investigator of the Biostatistics Center.
Corresponding author: Israel Hendler, MD, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Hutzel Hospital-Wayne State University, 3990 John R. Street, Detroit, MI, 48201; e-mail: ihendler{at}med.wayne.edu. 
doi:10.1097/01.AOG.0000223180.53113.0f
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