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• W2043449639 abstract "Background & Aims: Studies of maternal celiac disease (CD) and fetal outcome are inconsistent, and low statistical power is likely to have contributed to this inconsistency. We investigated the risk of adverse outcomes in women with CD diagnosed prior to pregnancy and in women who did not receive a diagnosis of CD until after the delivery. Methods: A national register-based cohort study restricted to women aged 15–44 years with singleton live born infants was used. We identified 2078 offspring to women who had received a diagnosis of CD (1964–2001): 1149 offspring to women diagnosed prior to birth and 929 offspring to women diagnosed after infant birth. Main outcome measures were: intrauterine growth retardation, low birth weight (<2500 g), very low birth weight (<1500 g), preterm birth (<37 gestational weeks), very preterm birth (<30 gestational weeks), and caesarean section. Results: Undiagnosed CD was associated with an increased risk of intrauterine growth retardation (OR = 1.62; 95% CI: 1.22–2.15), low birth weight (OR = 2.13; 95% CI: 1.66–2.75), very low birth weight (OR = 2.45; 95% CI: 1.35–4.43), preterm birth (OR = 1.71; 95% CI: 1.35–2.17), and caesarean section (OR = 1.82; 95% CI: 1.27–2.60). In contrast, a diagnosis of CD made before the birth was not associated with these adverse fetal outcomes. Conclusions: Undiagnosed maternal CD is a risk factor for unfavorable fetal outcomes, but the risks are reduced when CD has been diagnosed. CD diagnosed prior to pregnancy does not constitute a great a risk as undiagnosed CD. Background & Aims: Studies of maternal celiac disease (CD) and fetal outcome are inconsistent, and low statistical power is likely to have contributed to this inconsistency. We investigated the risk of adverse outcomes in women with CD diagnosed prior to pregnancy and in women who did not receive a diagnosis of CD until after the delivery. Methods: A national register-based cohort study restricted to women aged 15–44 years with singleton live born infants was used. We identified 2078 offspring to women who had received a diagnosis of CD (1964–2001): 1149 offspring to women diagnosed prior to birth and 929 offspring to women diagnosed after infant birth. Main outcome measures were: intrauterine growth retardation, low birth weight (<2500 g), very low birth weight (<1500 g), preterm birth (<37 gestational weeks), very preterm birth (<30 gestational weeks), and caesarean section. Results: Undiagnosed CD was associated with an increased risk of intrauterine growth retardation (OR = 1.62; 95% CI: 1.22–2.15), low birth weight (OR = 2.13; 95% CI: 1.66–2.75), very low birth weight (OR = 2.45; 95% CI: 1.35–4.43), preterm birth (OR = 1.71; 95% CI: 1.35–2.17), and caesarean section (OR = 1.82; 95% CI: 1.27–2.60). In contrast, a diagnosis of CD made before the birth was not associated with these adverse fetal outcomes. Conclusions: Undiagnosed maternal CD is a risk factor for unfavorable fetal outcomes, but the risks are reduced when CD has been diagnosed. CD diagnosed prior to pregnancy does not constitute a great a risk as undiagnosed CD. Celiac disease (CD) is characterized by an immune response to gliadin in genetically predisposed individuals.1Koning F. The molecular basis of celiac disease.J Mol Recognit. 2003; 16: 333-336Crossref PubMed Scopus (42) Google Scholar Over the years, there has been an increasing awareness of the nongastrointestinal manifestations of CD such as osteoporosis,2West J. Logan R.F. Card T.R. Smith C. Hubbard R. Fracture risk in people with celiac disease a population-based cohort study.Gastroenterology. 2003; 125: 429-436Abstract Full Text Full Text PDF PubMed Scopus (169) Google Scholar cancer,3Askling J. Linet M. Gridley G. Halstensen T.S. Ekstrom K. Ekbom A. Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpetiformis.Gastroenterology. 2002; 123: 1428-1435Abstract Full Text Full Text PDF PubMed Scopus (403) Google Scholar and infertility.4Meloni G.F. Dessole S. Vargiu N. Tomasi P.A. Musumeci S. The prevalence of coeliac disease in infertility.Hum Reprod. 1999; 14: 2759-2761Crossref PubMed Scopus (121) Google Scholar, 5Collin P. Vilska S. Heinonen P.K. Hallstrom O. Pikkarainen P. Infertility and coeliac disease.Gut. 1996; 39: 382-384Crossref PubMed Scopus (173) Google Scholar Here, we consider the potential influence of maternal CD on pregnancy outcomes. CD affects 1 of 100–200 adolescents and adults,6Ivarsson A. Persson L.A. Juto P. Peltonen M. Suhr O. Hernell O. High prevalence of undiagnosed coeliac disease in adults a Swedish population-based study.J Intern Med. 1999; 245: 63-68Crossref PubMed Scopus (165) Google Scholar, 7Bingley P.J. Williams A.J. Norcross A.J. Unsworth D.J. Lock R.J. Ness A.R. Jones R.W. Undiagnosed coeliac disease at age seven population based prospective birth cohort study.BMJ. 2004; 328: 322-323Crossref PubMed Scopus (206) Google Scholar, 8Greco L. Veneziano A. Di Donato L. Zampella C. Pecoraro M. Paladini D. Paparo F. Vollaro A. Martinelli P. Undiagnosed coeliac disease does not appear to be associated with unfavourable outcome of pregnancy.Gut. 2004; 53: 149-151Crossref PubMed Scopus (64) Google Scholar, 9Maki M. Mustalahti K. Kokkonen J. Kulmala P. Haapalahti M. Karttunen T. Ilonen J. Laurila K. Dahlbom I. Hansson T. Hopfl P. Knip M. Prevalence of celiac disease among children in Finland.N Engl J Med. 2003; 348: 2517-2524Crossref PubMed Scopus (828) Google Scholar and it is known to affect at least 1 of 100 pregnant women.8Greco L. Veneziano A. Di Donato L. Zampella C. Pecoraro M. Paladini D. Paparo F. Vollaro A. Martinelli P. Undiagnosed coeliac disease does not appear to be associated with unfavourable outcome of pregnancy.Gut. 2004; 53: 149-151Crossref PubMed Scopus (64) Google Scholar, 10Martinelli P. Troncone R. Paparo F. Torre P. Trapanese E. Fasano C. Lamberti A. Budillon G. Nardone G. Greco L. Coeliac disease and unfavourable outcome of pregnancy.Gut. 2000; 46: 332-335Crossref PubMed Scopus (165) Google Scholar To what extent CD is associated with an increased risk for adverse fetal outcome is not adequately described because the influence of maternal CD and fetal outcome has only been investigated in studies of limited size, consisting of at most some few hundred patients with CD.8Greco L. Veneziano A. Di Donato L. Zampella C. Pecoraro M. Paladini D. Paparo F. Vollaro A. Martinelli P. Undiagnosed coeliac disease does not appear to be associated with unfavourable outcome of pregnancy.Gut. 2004; 53: 149-151Crossref PubMed Scopus (64) Google Scholar, 10Martinelli P. Troncone R. Paparo F. Torre P. Trapanese E. Fasano C. Lamberti A. Budillon G. Nardone G. Greco L. Coeliac disease and unfavourable outcome of pregnancy.Gut. 2000; 46: 332-335Crossref PubMed Scopus (165) Google Scholar, 11Ciacci C. Cirillo M. Auriemma G. Di Dato G. Sabbatini F. Mazzacca G. Celiac disease and pregnancy outcome.Am J Gastroenterol. 1996; 91: 718-722PubMed Google Scholar, 12Norgard B. Fonager K. Sorensen H.T. Olsen J. Birth outcomes of women with celiac disease a nationwide historical cohort study.Am J Gastroenterol. 1999; 94: 2435-2440Crossref PubMed Google Scholar, 13Ludvigsson J.F. Ludvigsson J. Coeliac disease in the father affects the newborn.Gut. 2001; 49: 169-175Crossref PubMed Scopus (73) Google Scholar, 14Ferguson R. Holmes G.K. Cooke W.T. Coeliac disease, fertility, and pregnancy.Scand J Gastroenterol. 1982; 17: 65-68Crossref PubMed Scopus (95) Google Scholar, 15Ogborn A.D. Pregnancy in patients with coeliac disease.Br J Obstet Gynaecol. 1975; 82: 293-296Crossref PubMed Scopus (27) Google Scholar, 16Gasbarrini A. Torre E.S. Trivellini C. De Carolis S. Caruso A. Gasbarrini G. Recurrent spontaneous abortion and intrauterine fetal growth retardation as symptoms of coeliac disease.Lancet. 2000; 356 (letter): 399-400Abstract Full Text Full Text PDF PubMed Scopus (117) Google Scholar Maternal CD may influence fetal development in several ways. Gliadin can induce cytokine production in peripheral blood mononuclear cells,17O’Keeffe J. Mills K. Jackson J. Feighery C. T-cell proliferation, MHC class II restriction and cytokine products of gliadin-stimulated peripheral blood mononuclear cells (PBMC).Clin Exp Immunol. 1999; 117: 269-276Crossref Scopus (35) Google Scholar which may affect the fetus. Mucosal inflammation can cause nonoptimal nutrient intake—so can associated abdominal symptoms and anorexia—leading to intrauterine growth retardation among pregnant women. If CD influences fetal growth, this may be of interest because nonoptimal fetal growth is associated with increased risk of immediate disease18Battaglia F.C. Intrauterine growth retardation.Am J Obstet Gynecol. 1970; 106: 1103-1114Abstract Full Text PDF PubMed Scopus (57) Google Scholar and chronic disease in adult life.19Godfrey K.M. Barker D.J. Fetal nutrition and adult disease.Am J Clin Nutr. 2000; 71: 1344S-1352SPubMed Google Scholar The aims of this study were to assess the impact of CD in the mother and the risk of adverse fetal outcome by use of Swedish register data. By separating mothers with a diagnosis before birth from those with a diagnosis after birth, we could investigate to what extent a gluten-free diet influenced fetal outcome. In this context, undiagnosed CD implies the presence of a metabolically active and untreated CD, whereas women with diagnosed CD were more likely to be treated and on a gluten-free diet at time of giving birth. We calculated the risk of adverse fetal outcome on the basis of prospectively collected data in a large study of more than 2000 births to women with CD compared with some 2.8 million births to women without a diagnosis of CD. We did so while adjusting for a number of factors, which have previously been linked to CD or adverse fetal outcome, among them smoking20Snook J.A. Dwyer L. Lee-Elliott C. Khan S. Wheeler D.W. Nicholas D.S. Adult coeliac disease and cigarette smoking (see comments).Gut. 1996; 39: 60-62Crossref PubMed Scopus (108) Google Scholar and diabetes mellitus.21Collin P. Reunala T. Pukkala E. Laippala P. Keyrilainen O. Pasternack A. Coeliac disease—associated disorders and survival.Gut. 1994; 35: 1215-1218Crossref PubMed Scopus (425) Google Scholar We defined CD according to the following international classification of disease (ICD) codes: ICD-7: 286.00; ICD-8: 269.00, 269.98; ICD-9: 579A; ICD-10: K90.0. Women with a hospital-based discharge diagnosis of CD between 1964 and 2001 were identified through the Swedish national inpatient register. This individual-based information was obtained from the Swedish National Board of Health and Welfare. The national inpatient register has been described by Askling et al.3Askling J. Linet M. Gridley G. Halstensen T.S. Ekstrom K. Ekbom A. Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpetiformis.Gastroenterology. 2002; 123: 1428-1435Abstract Full Text Full Text PDF PubMed Scopus (403) Google Scholar This study was approved by the research ethics committee of the Karolinska Institute. None of the participants was contacted. Patient information was anonymized prior to the analyses. To exclude the possibility that the findings were due to the presence of diabetes mellitus among women with CD, adjustment was made for the presence of diabetes mellitus in a separate analysis. Diabetes mellitus was defined as follows (according to the Swedish medical birth register): women who gave birth 1973–1994 and were identified as having diabetes using the definition “current diabetes mellitus during pregnancy”; women who gave birth 1973–1989 were identified as having diabetes if this was recorded using the relevant ICD code or if the woman had a diagnosis of diabetes mellitus; and women who gave birth 1994–2001 were identified as having diabetes if they had either received a diagnosis of diabetes mellitus at the antenatal visit or if they were known to suffer from chronic diabetes mellitus. In Sweden, more than 99% of all live births are registered in the medical birth register.22Cnattingius S. Ericson A. Gunnarskog J. Kallen B. A quality study of a medical birth registry.Scand J Soc Med. 1990; 18: 143-148PubMed Google Scholar The medical birth register was established in 1973 and contains standardized information on both mother and child. This is collected at the first antenatal visit, throughout pregnancy, and at birth and provided to the Swedish National Board of Health and Welfare (which maintains the medical birth register). Mothers and children in this cohort study were identified through their national civil registration numbers recorded in the medical birth register. The national civil registration number is a unique number assigned to over 99.9% of all Swedish residents at birth or immigration.23Lunde A.S. Lundeborg S. Lettenstrom G.S. Thygesen L. Huebner J. The person-number systems of Sweden, Norway, Denmark, and Israel.Vital Health Stat 2. 1980; 2: 1-59Google Scholar The subjects of this study consisted of all live-born singleton infants who were born in Sweden during the period 1973 to 2001 to mothers aged between 15 and 44 years. Some mothers contributed more than 1 child to the study. The exposed cohort was defined as those infants whose mother had a diagnosis of CD. Measures from the birth register included infant sex; maternal age at delivery (15–19, 20–24, 25–29, 30–34, 35–40, 41–44 years); parity (defined as the number of previous births, including stillbirths: 0, 1, ≥2); nationality (citizens of Nordic countries were coded as “1,” all other women as “0”); calendar period (1964–1982, 1983–1995, 1996–2001); smoking (0, 1–9 cigarettes per day, ≥10 cigarettes per day); and a diagnosis of diabetes mellitus. Between 1973 and 2001, we identified 10,678 women with a diagnosis of diabetes mellitus at time of infant birth. Data on smoking are available from 1983 onward. Placental weight was recorded between 1982 and 1989. Our main outcome measures were low birth weight (LBW; <2500 g), very low birth weight (VLBW; <1500 g), preterm birth (<37 gestational weeks), very preterm birth (<30 gestational weeks), low Apgar score at 5 minutes (<7), caesarean section, and intrauterine growth retardation (IUGR). IUGR was defined according to national growth curves with IUGR corresponding to a weight for age below −2 standard deviations from the mean.24Marsal K. Persson P.H. Larsen T. Lilja H. Selbing A. Sultan B. Intrauterine growth curves based on ultrasonically estimated foetal weights.Acta Paediatr. 1996; 85: 843-848Crossref PubMed Scopus (1348) Google Scholar We also looked at birth weight and pregnancy duration. To explore the reasons for birth weight differences, we assessed placental weight in a subset of women. All data on fetal outcome were obtained from the medical birth register. The validity of the medical birth register is high,22Cnattingius S. Ericson A. Gunnarskog J. Kallen B. A quality study of a medical birth registry.Scand J Soc Med. 1990; 18: 143-148PubMed Google Scholar and the register will only accept gestational age data from 22 through <46 weeks and birth weight data in the range of 300–7000 g. Placental weights <200 g or >1500 g were regarded as coding errors and excluded from all analyses (3557 births corresponding to 0.6% of all births with data on placental weight were hence excluded). We compared proportions of offspring with adverse fetal outcome in mothers with CD compared with mothers who never had a diagnosis of CD (unexposed) in relation to the date of the first discharge diagnosis of CD. We compared the following groups of women with unexposed women: (1) women diagnosed prior to infant birth and presumably treated at time of infant birth and (2) women with undiagnosed CD, receiving their diagnosis after infant birth. Categorical independent variables were tested against our outcome measures using the Pearson χ2 test (with Yates correction) (or Fisher exact test when the expected value of any cells was less than 5). Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95% CI) for each fetal outcome in relation to presence of CD in the mother. 95% Confidence intervals for odds ratios not including 1.00 were considered statistically significant. In multivariate model I, we analyzed the risk of adverse fetal outcome in relation to CD adjusting simultaneously for infant sex, parity, maternal age at delivery, nationality, and calendar period. In multivariate model II (births from 1983 and onward), we also adjusted for smoking. We compared infant birth weight, pregnancy duration, and placental weight between women with CD and women who never had CD using the Student t test and multiple linear regression analyses when adjusting for infant sex, parity, maternal age at delivery, nationality, and calendar period (and in separate analyses also for smoking). We modeled the interaction of smoking with CD, adjusted for the main effects (smoking and CD) as well as for all the other potential confounding factors. This was done through the creation of a variable that was the sum of smoking and CD and looked at its association with the dependent variable outcomes after adjustment for the main effects (smoking and CD). Each mother could potentially contribute several separate births to the study, so not all births were independent of each other. To assess whether this potential nonindependence influenced the reported associations, we performed additional analyses restricted to 1 birth per mother (the first birth recorded between 1973 and 2001). Statistics were calculated using SPSS 11.0 (2002; SPSS Inc, Chicago, IL). Most women were 20–34 years of age when giving birth (Table 1). Few women reported smoking during pregnancy, and almost all women were of Nordic nationality. Among the 2078 women with CD, 1149 were diagnosed before birth, and 929 were undiagnosed (255 had a hospital discharge diagnosis of CD within less than 5 years after infant birth, and 674 received a hospital discharge diagnosis 5 years or more after infant birth). Only 3.8% of offspring to mothers with undiagnosed CD were born during the last calendar period; this was due to insufficient follow-up time. The calculations of placental weight were based on 593,532 births (among them were 207 offspring to women with undiagnosed CD and 112 offspring to women with diagnosed CD).Table 1Characteristics of Mothers to Participating InfantsCharacteristicsNo CD N (%)Undiagnosed N (%)Diagnosed N (%)Total2,822,8059291,149Maternal age (yr)15–19104,730 (3.7)39 (4.2)73 (6.4)20–24659,692 (23.4)237 (25.5)370 (32.2)25–291,043,915 (37.0)316 (34.0)454 (39.5)30–34709,186 (25.1)243 (26.2)177 (15.4)35–40278,910 (9.9)83 (8.9)69 (6.0)40–4426,372 (0.9)11 (1.2)6 (0.5)Data not available0 (0.0)0 (0.0)0 (0.0)Parity0a“0” indicates no previous children before the birth included in this dataset.1,191,666 (42.2)361 (38.9)622 (54.1)1–21,457,101 (51.6)489 (52.6)478 (41.6)≥3173,938 (6.2)78 (8.4)49 (4.3)Data not available100 (<0.1)1 (0.1)0 (0.0)NationalityNordic country2,651,823 (93.9)900 (96.9)1,136 (98.9)Other country170,982 (6.1)29 (3.1)13 (1.1)Data not available0 (0.0)0 (0.0)0 (0.0)Infant sexBoys1,451,035 (51.4)470 (50.6)560 (48.7)Girls1,371,770 (48.6)459 (49.4)589 (51.3)Data not available0 (0.0)0 (0.0)0 (0.0)Calendar periodbThe large difference in proportions of pregnancies exposed to “diagnosed celiac disease” as opposed to “undiagnosed celiac disease” is a time-related phenomenon. For example, a woman giving birth during 1999 is only followed for another 2 years; hence, there is little chance of her receiving a diagnosis of celiac disease in 2000 or 2001. This explains the low proportion of undiagnosed celiac disease among mothers giving birth in 1996–2001.1964–1982958,128 (33.9)558 (60.1)71 (6.2)1983–19951,354,082 (48.0)336 (36.2)454 (39.5)1996–2001510,595 (18.1)35 (3.8)624 (54.3)Data not available0 (0.0)0 (0.0)0 (0.0)Smoking habitsNon smoker1,396,002 (49.5)262 (28.2)770 (67.0)1–9 cigarettes/day249,178 (8.8)71 (7.6)178 (15.5)≥10 cigarettes/day148,691 (5.3)39 (4.2)72 (6.3)Data not available1,028,934 (36.5)557 (60.0)129 (11.2)*Mothers may occur more than once as each pregnancy is counted as one independent event.NOTE: CD, Celiac disease.a “0” indicates no previous children before the birth included in this dataset.b The large difference in proportions of pregnancies exposed to “diagnosed celiac disease” as opposed to “undiagnosed celiac disease” is a time-related phenomenon. For example, a woman giving birth during 1999 is only followed for another 2 years; hence, there is little chance of her receiving a diagnosis of celiac disease in 2000 or 2001. This explains the low proportion of undiagnosed celiac disease among mothers giving birth in 1996–2001. Open table in a new tab *Mothers may occur more than once as each pregnancy is counted as one independent event. NOTE: CD, Celiac disease. Offspring to women with undiagnosed CD had on average a lower birth weight than unexposed offspring (−170 g; 95% CI: −215 to −127 g; P < .001). Also offspring to women with diagnosed CD weighed less than those born to women without CD (−53 g; 95% CI: −92 to −14 g; P = .004). Adjusting for all of the measures except smoking, offspring to women with undiagnosed CD had a mean adjusted birth weight of 165 g below that of unexposed offspring (95% CI: −200 to −129 g; P < .001) (adding smoking: −178 g; 95% CI: −233 to −123 g; P < .001). Also, offspring to women with diagnosed CD were smaller than unexposed offspring (adjusted birth weight difference: −62 g; 95% CI: −94 to −30 g; P < .001). After adjustment for all of the measures except smoking, women with undiagnosed CD gave birth to smaller children than women with diagnosed CD (−87 g; 95% CI: −154 to −20 g; P < .011). Women with undiagnosed CD were more likely to have offspring with LBW and VLBW (Table 2, Table 3). No risk increase for LBW and VLBW was found among offspring to women with diagnosed CD (Table 2, Table 3).Table 2Fetal Outcomes in Offspring to Women With Celiac DiseaseProportion with adverse fetal outcome N (%)Odds ratio; 95% CI ORP valueAdjusted ORaAdjusted for maternal age, parity, nationality, calendar period, and infant sex. See text for further explanation of covariates.; 95% CI AORP valueIUGRbIntrauterine growth retardation: weight for age below −2 standard deviations.No CD88,073/2,806,297 (3.1)1.001.00Undiagnosed CD51/923 (5.5)1.80; 1.36–2.39<.0011.62; 1.22–2.15.001Diagnosed CD39/1,141 (3.4)1.09; 0.79–1.50.5881.29; 0.94–1.78.115Data not available16,522Low birth weightcLow birth weight <2500 g.No CD95,531/2,814,664 (3.4)1.001.00Undiagnosed CD65/926 (7.0)2.15; 1.67–2.76<.0012.13; 1.66–2.75<.001Diagnosed CD47/1147 (4.1)1.22; 0.91–1.63.1371.25; 0.93–1.67.137Data not available8,146Very low birth weightdVery low birth weight <1500 g.No CD14,567/2,814,664 (0.5)1.001.00Undiagnosed CD11/926 (1.2)2.31; 1.28–4.19.0062.45; 1.35–4.43.003Diagnosed CD6/1147 (0.5)1.01; 0.45–2.25.9790.98; 0.44–2.18.956Data not available8146Preterm birthePreterm birth <37 gestational weeks.No CD139,921/2,815,329 (5.0)1.001.00Undiagnosed CD74/925 (8.0)1.66; 1.31–2.11<.0011.71; 1.35–2.17<.001Diagnosed CD72/1,146 (6.3)1.28; 1.01–1.63.0411.25; 0.98–1.59.066Data not available7483Very preterm birthfVery preterm birth <30 gestational weeks.No CD9,548/2,815,329 (0.3)1.001.00Undiagnosed CD6/925 (0.6)1.92; 0.86–4.28.1122.06; 0.92–4.60.078Diagnosed CD4/1146 (0.3)1.03; 0.39–2.75.9540.99; 0.37–2.64.981Data not available7483Low Apgar scoregLow Apgar score: Apgar score at 5 minutes <7.No CD32,423/2,597,696 (1.2)1.001.00Undiagnosed CD13/805 (1.6)1.30; 0.75–2.25.3501.18; 0.68–2.04.563Diagnosed CD11/1,130 (1.0)0.78; 0.43–1.41.4070.86; 0.47–1.56.615Data not available225,252Caesarean sectionNo CD65,510/2,822,693 (2.3)1.001.00Undiagnosed CD32/928 (3.4)1.50; 1.06–2.14.0241.82; 1.27–2.60.001Diagnosed CD17/1149 (1.5)0.63; 0.39–1.02.0600.87; 0.53–1.41.563Data not available113Births with complete data on infant sex, maternal age at delivery, parity, nationality, and calendar period.NOTE. CD, Celiac disease.a Adjusted for maternal age, parity, nationality, calendar period, and infant sex. See text for further explanation of covariates.b Intrauterine growth retardation: weight for age below −2 standard deviations.c Low birth weight <2500 g.d Very low birth weight <1500 g.e Preterm birth <37 gestational weeks.f Very preterm birth <30 gestational weeks.g Low Apgar score: Apgar score at 5 minutes <7. Open table in a new tab Table 3Fetal Outcomes in Offspring to Women With Celiac DiseaseProportion with adverse fetal outcome N (%)Odds ratio; 95% CI ORP valueAdjusted ORaAdjusted for maternal age, parity, nationality, calendar period, infant sex, and smoking. See text for further explanation of covariates.; 95% CI AORP valueIUGRbIntrauterine growth retardation: weight for age below −2 standard deviations.No CD46,285/1,785,448 (2.6)1.001.00Undiagnosed CD14/370 (3.8)1.48; 0.87–2.52.1521.42; 0.83–2.43.203Diagnosed CD36/1016 (3.5)1.38; 0.99–1.92.0581.40; 1.00–1.96.047Data not available1,038,049Low birth weightcLow birth weight <2500 g.No CD57,777/1,787,213 (3.2)1.001.00Undiagnosed CD29/370 (7.8)2.54; 1.74–3.72<.0012.47; 1.68–3.61<.001Diagnosed CD40/1018 (3.9)1.22; 0.89–1.68.2101.22; 0.89–1.68.214Data not available1,036,282Very low birth weightdVery low birth weight <1500 g.No CD8,935/1,787,213 (0.5)1.001.00Undiagnosed CD6/370 (1.6)3.28; 1.46–7.35.0043.24; 1.44–7.26.004Diagnosed CD5/1018 (0.5)0.98; 0.41–2.37.9680.99; 0.41–2.39.988Data not available1,036,282Preterm birthePreterm birth <37 gestational weeks.No CD89,452/1,792,803 (5.0)1.001.00Undiagnosed CD38/372 (10.2)2.17; 1.55–3.03<.0012.12; 1.52–2.97<.001Diagnosed CD63/1019 (6.2)1.26; 0.97–1.62.0811.24; 0.96–1.60.103Data not available1,030,689Very preterm birthfVery preterm birth <30 gestational weeks.No CD5800/1,792,803 (0.3)1.001.00Undiagnosed CD4/372 (1.1)3.35; 1.25–8.97.0163.38; 1.26–9.05.016Diagnosed CD3/1019 (0.3)0.91; 0.29–2.82.8710.91; 0.29–2.84.877Data not available1,030,689Low Apgar scoregLow Apgar score: Apgar score at 5 minutes <7.No CD18,187/1,761,042 (1.0)1.001.00Undiagnosed CD5/366 (1.4)1.33; 0.55–3.21.5301.38; 0.57–3.33.478Diagnosed CD10/1011 (1.0)0.96; 0.52–1.78.8910.91; 0.49–1.70.774Data not available1,062,464Caesarean sectionNo CD59,562/1,793,861 (3.3)1.001.00Undiagnosed CD32/372 (8.6)2.74; 1.91–3.94<.0012.12; 1.47–3.06<.001Diagnosed CD16/1,020 (1.6)0.47; 0.28–0.76.0020.84; 0.51–1.38.491Data not available1,029,630Births with complete data on infant sex, maternal age at delivery, parity, nationality, calendar period, and smoking.NOTE. CD, Celiac disease.a Adjusted for maternal age, parity, nationality, calendar period, infant sex, and smoking. See text for further explanation of covariates.b Intrauterine growth retardation: weight for age below −2 standard deviations.c Low birth weight <2500 g.d Very low birth weight <1500 g.e Preterm birth <37 gestational weeks.f Very preterm birth <30 gestational weeks.g Low Apgar score: Apgar score at 5 minutes <7. Open table in a new tab Births with complete data on infant sex, maternal age at delivery, parity, nationality, and calendar period. NOTE. CD, Celiac disease. Births with complete data on infant sex, maternal age at delivery, parity, nationality, calendar period, and smoking. NOTE. CD, Celiac disease. Women with undiagnosed CD had shorter pregnancy duration than unexposed women (−1.6 days; 95% CI: −2.6 to −0.6 days; P < .001); a decrease in pregnancy duration was also seen in women with diagnosed CD (−1.5 days; 95% CI: −2.4 to −0.6 days; P < .001). Adjustment for all of the measures except smoking yielded similar values for pregnancy duration (undiagnosed CD vs unexposed: −2.0 days; 95% CI: −2.9 to −1.2 days; P < .001) (adding smoking: −3.3 days; 95% CI: −4.6 to −2.0 days; P < .001). In both multivariate models, pregnancy duration was shorter in women with undiagnosed CD as opposed to in women with diagnosed CD (−1.0 day; 95% CI: −1.7 to −0.2 days; P = .012) (adding smoking: −1.0 day; 95% CI: −1.8 to −0.3 days; P = 0.009). Offspring to women with undiagnosed CD suffered an increased risk for preterm and very preterm birth (Table 2, Table 3). Offspring to women with diagnosed CD were not at increased risk for preterm or very preterm birth when adjusting for potential confounders (Table 2, Table 3). The crude risk of IUGR was increased in women with undiagnosed CD and remained statistically significant when adjusting for all of the measures except smoking (Table 2). However, it did not reach statistical significance when adding smoking to the independent variables in a subset of women with available smoking data. The risk of IUGR was significantly increased in offspring to women with diagnosed CD when adjusting for all of the measures including smoking (Table 3). Low Apgar score at 5 minutes (<7) was not linked to undiagnosed or diagnosed CD (Table 2, Table 3). Caesarean section was more common among women with undiagnosed CD than among unexposed women (Table 2, Table 3). Stratifying by nonsmoking and smoking women with undiagnosed CD revealed some apparent differences in the estimates and statistical significance (Table 4). To assess whether these differences between the strata reflected a differential effect of smoking on birth outcomes in mothers with CD, we conducted interaction tests. The interaction of smoking with undiagnosed CD was not evident and did not produce any statistically significant results for any of the outcomes. Therefore, smoking does not appear to modify the effect on birth outcomes of undiagnosed CD. The variation in estimates between the strata (smokers and nonsmokers) reflects the independent effect of smoking and other sources" @default.
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• W2043449639 date "2005-08-01" @default.
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• W2043449639 title "Celiac Disease and Risk of Adverse Fetal Outcome: A Population-Based Cohort Study" @default.
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• W2043449639 doi "https://doi.org/10.1053/j.gastro.2005.05.065" @default.
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