PEDIATRICS Vol. 115 No. 1 January 2005, pp. 95-101 (doi:10.1542/10.1542/peds.2004-0516)
Trends in Prenatal Diagnosis, Pregnancy Termination, and Perinatal Mortality of Newborns With Congenital Heart Disease in France, 1983–2000: A Population-Based Evaluation
* Paris Registry of Congenital Malformations, Epidemiological Research Unit on Perinatal and Women's Health, INSERM U149, Villejuif, France
Service de Cardiologie Pédiatrique, Hôpital Necker-Enfants Malades, Paris, France
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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Objective. To examine population-based overall and malformation-specific trends in the prenatal diagnosis, pregnancy termination, and perinatal mortality for congenital heart disease (CHD) during a period of rapid progress in prenatal diagnosis and medical management of CHD and to explore the impact of prenatal diagnosis on early neonatal mortality for specific (isolated) cardiac malformations.
Methods. A total of 1982 cases of CHD, which were not associated with a known chromosomal anomaly, were obtained from the Paris Registry of Congenital Malformations. Main outcome measures were trends in the proportions diagnosed and terminated before birth, stillbirth, and early (<1 day, 1-week) neonatal mortality for (1) all cases; (2) all cases excluding isolated ventricular septal defects; and (3) malformation-specific trends for transposition of great arteries, hypoplastic left heart syndrome, coarctation of aorta, and tetralogy of Fallot. Analyses included cusum and binomial regression models for analysis of the trends during 1983–2000.
Results. Prenatal diagnosis rates for CHD increased from 23.0% (95% confidence interval [CI]: 19.0–27.4) in 1983–1988 to 47.3% (95% CI: 43.8–50.8) in 1995–2000. Termination rates increased between 1983 and 1989 (9.9%; 95% CI: 7.2–13.2) and 1989 and 1994 (14.7%; 95% CI: 12.3–17.4) but seemed to remain stable thereafter. Other than for hypoplastic left heart syndrome, pregnancy termination was exceptional for the other 3 specific malformations examined. Early neonatal mortality decreased to less than one third in the period 1995–2000 as compared with 1983–1989 (risk ratio, first-week mortality: 0.31; 95% CI: 0.18–0.53). First-week mortality was significantly lower for cases of transposition of great arteries that were diagnosed before birth (risk difference: 15.4%; 95% CI: 4.0–26.7).
Conclusions. Progress in clinical management, together with policies for increased access to prenatal diagnosis, has resulted in both a substantial increase in the prenatal diagnosis and considerable reductions in early neonatal mortality of CHD in the Parisian population.
Key Words: congenital heart disease • prenatal diagnosis • France • mortality
Abbreviations: CHD, congenital heart disease • HLHS, hypoplastic left heart syndrome • TGA, transposition of great arteries • ICD-9, International Classification of Disease, Ninth Revision • CI, confidence interval • RR, risk ratio
Congenital heart disease (CHD) is the most common congenital anomaly1,2 and a major cause of mortality and morbidity in the perinatal period.3 The reported prevalence of CHD is subject to a great deal of variation across different populations and registries, presumably for the most part because of differences in the inclusion of milder anomalies.2,4 However, the reported prevalence of severe CHD seems to be fairly constant across different populations and is 
3.0 per 1000 live births. Differences exist, however, in the rates of prenatal diagnosis and termination of CHD across populations5,6 and over time,4,7,8 which can have an impact on the livebirth prevalence of the more severe cases of CHD,9 particularly for hypoplastic left heart syndrome (HLHS).10
France pursues an active policy of antenatal surveillance, particularly for prenatal diagnosis of congenital anomalies.11,12 Prenatal diagnosis of structural CHD with transabdominal ultrasonography began in the early 1980s and became widespread in the late 1980s.13 Detection rates for structural heart defects have been shown to be higher in France than in other European countries5,6,14 or the United States.7 However, the impact of prenatal diagnosis on the outcomes of newborns with structural heart disease has been difficult to evaluate,15 mostly because of problems related to selection bias as cases that are more likely to be diagnosed prenatally tend to be the more severe cases. Hence, not surprising, previous studies often have found overall poorer outcomes in cases of CHD that are diagnosed prenatally.7,16–18 The impact of prenatal diagnosis has been shown to vary considerably across different malformations with improved outcomes reported for prenatally diagnosed cases of coarctation of aorta and transposition of great arteries (TGA).17,19–23 Nevertheless, even findings from the studies that have assessed the same set of anomalies have not been consistent.19–22 Moreover, few population-based studies7,18,24 have evaluated the impact of prenatal diagnosis on neonatal outcomes, and none has examined the entire period that spans the introduction of screening in the 1980s until the most recent period.
In this study, we examine overall and malformation-specific trends in the prenatal diagnosis, pregnancy termination, and perinatal mortality as a result of CHD using population-based data from the Paris Registry of Congenital Malformations for the years 1983–2000. We also assess trends in the timing of prenatal diagnosis and pregnancy termination. In addition, we explore the impact of prenatal diagnosis on early neonatal mortality for HLHS and TGA, for which previous hospital-based studies have reported conflicting results.19–22
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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A total of 2440 cases of CHD were obtained from the Paris Registry of Congenital Malformations for the years 1983–2000. The base study population corresponded to births and terminations of pregnancy to women who were residents of Paris and gave birth or had a termination of pregnancy in a Parisian maternity unit during the period 1983–2000 (total number of births: 452 867). Data for the registry are collected from multiple sources of information, including maternity units, neonatology services, and cytogenetic and pathology services, to allow high case ascertainment for malformations and chromosomal abnormalities. Registration is essentially complete for cases that are identified during the initial hospitalization for delivery or for those that are identified in the postmortem examination. The registration, including mortality outcomes, are not complete, however, for late diagnoses or for mortality outcomes beyond the early (first week) neonatal period.
The diagnosis for each case was based on either an evaluation by a pediatric cardiologist as documented in the medical chart or postmortem examination. Cases were classified following the International Classification of Disease, Ninth Revision and included (1) bulbus cordis anomalies and anomalies of cardiac septal closure (ICD-9 code 745), (2) other congenital anomalies of the heart (ICD-9 code 746), and (3) other congenital anomalies of circulatory systems (ICD-9 code 747). Cardiac anomalies associated with a known chromosomal anomaly composed 18.1% (N = 458) of cases. These cases were excluded from additional analyses. Hence, the study population comprised 1982 cases of CHD. In addition, 13 (0.7%) cases had missing information on prenatal diagnosis and were excluded from the analyses of trends in prenatal diagnosis.
Main outcome measures for the study were trends in the proportion diagnosed and/or terminated before birth, perinatal (stillbirth plus early neonatal mortality), and early (<24 hours, 1-week) neonatal mortality of cases not associated with a chromosomal anomaly. Trends were examined for (1) all cases; (2) all cases excluding isolated ventricular septal defects; and (3) malformation-specific trends for isolated cases of TGA, HLHS, coarctation of aorta, and tetralogy of Fallot. We also assessed timing of prenatal diagnosis and pregnancy termination by examining trends in the median gestational age at diagnosis and at termination.
Analyses that excluded isolated ventricular septal defects and the malformation-specific analyses were undertaken to (1) partially control for the potential selection bias as a result of increasing diagnosis of less severe cases over time and (2) examine heterogeneities in prenatal diagnosis and outcomes for 4 major anomalies. To assess the impact of associated malformations on study outcomes, we examined the prenatal diagnosis, pregnancy termination, and perinatal mortality of the isolated cases of CHD for the most recent period (1995–2000). For this analysis, isolated cases of CHD were defined as those that were not associated with another major, noncardiac malformation. During this period, 17% of cases (among those without a known chromosomal anomaly) were associated with at least 1 other major noncardiac malformation.
Statistical Analysis
We report proportions with 95% binomial exact confidence intervals (CI). We used cusums for nonparametric analysis of time trends in binary variables.25 This technique allows detection of significant monotonic (always increasing/decreasing) and nonmonotonic (eg, quadratic) trends. Inverted U-shaped curves of cusums over time suggest a monotonically increasing trend in proportions over time, whereas U-shaped curves suggest a monotonically decreasing trend. We also used binomial regression models26 for analysis of maternal age–adjusted trends in the study outcomes. Maternal age was considered a potential confounding variable in the analyses of trends because (1) there has been a consistent trend toward delayed childbearing in the Parisian population and (2) the prenatal surveillance of older women might be different from their younger counterparts, as older women are at higher risk for adverse pregnancy outcomes including congenital anomalies. The Kruskal-Wallis test was done to test the statistical significance of trends in the timing of prenatal diagnosis and pregnancy termination.
Binomial regression was also used for analysis of time period–adjusted effect of prenatal diagnosis on neonatal mortality of infants who were born with TGA. This was done to control for the potentially confounding effect of time. Such confounding could arise because (1) the rate of prenatal diagnosis of TGA has increased over time, (2) the spectrum of severity of cases diagnosed might have changed over time, and (3) the clinical treatment (medical as well as surgical) of infants who are born with TGA has in all likelihood improved over time (in ways that might not be related directly or indirectly to prenatal diagnosis of the anomaly).
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RESULTS |
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Prenatal Diagnosis
The proportion of CHD cases that were diagnosed prenatally increased from 23.0% (95% CI: 19.0–27.4) in 1983–1988 to 47.3% (95% CI: 43.8–50.8) in 1995–2000 (Table 1). Cusum analysis suggested a monotonically increasing time trend in the proportion of cases that were diagnosed before birth (P < .001; Fig 1). This was true both for all cases and for all cases excluding isolated ventricular septal defects (Table 1). Compared with the period 1983–1988, there was an increase of 34% in maternal age–adjusted probability of prenatal diagnosis for CHD in 1989–1994 (age-adjusted risk ratio (RR) 1.34; 95% CI: 1.09–1.65) and a 2-fold increase (age-adjusted RR: 1.99; 95% CI: 1.64–2.41) in the prenatal diagnosis of CHD in 1995–2000 (Table 2). Analysis of prenatal diagnosis rates for isolated cases only during the most recent period (1995–2000) suggested essentially the same prenatal diagnosis rates; the proportion of isolated cases with a prenatal diagnosis was 45.4% (95% CI: 41.4–49.5) as compared with 47.3% (95% CI: 43.8–50.8) for all cases.
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Trends in prenatal diagnosis differed substantially across the 4 specific malformations examined (Table 3). However, for all 4 malformations, there were significant increases in the proportion of cases that were diagnosed prenatally over time. By the most recent period, approximately three fourths of the cases of the TGA (72.5%; 95% CI: 56.1–85.4), 90% of the cases of HLHS (88.9%; 95% CI: 70.8–97.6), 40% of the cases of coarctation of aorta (42.4%; 95% CI: 25.5–60.8), and 70% of cases of tetralogy of Fallot (69.7%; 95% CI: 51.3–84.4) were diagnosed prenatally.
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Gestational age at prenatal diagnosis decreased significantly over time (Kruskal-Wallis test, P = .001). The median gestational age at diagnosis was 27 weeks during the period 1983–1988, 25 weeks in 1989–1994, and 23 weeks in 1995–2000. Gestational age at diagnosis also decreased significantly for cases that were terminated; median gestational age at diagnosis was 24 weeks in 1983–1988, 23 weeks in 1989–1995, and 22 weeks in 1995–2000 (P = .0005). In particular, timing of prenatal diagnosis decreased significantly for cases of HLHS: 24 weeks, 23 weeks, and 21 weeks of gestation for the 3 periods, respectively (P = .04).
Pregnancy Termination
The proportion of cases of CHD that were terminated before birth increased between 1983–1988 and 1989–1994 but seemed to remain stable thereafter (Tables 1 and 2). Overall, 15% of the cases were terminated in 1995–2000 (15.4%; 95% CI: 13.0–18.1). The pregnancy termination rates for the isolated cases seemed to be somewhat lower (12.2%; 95% CI: 9.7–15.1) during this same period. This difference did not reach statistical significance, however.
During the most recent period, almost half of the cases that were terminated (45.4%; 95% CI: 33.5–57.3) were accounted for by "complex" CHD involving at least 2 distinct anomalies (ICD-9 codes). During this same period, the most frequent cases of CHD terminated involved HLHS; univentricular heart; and, to a lesser extent, pulmonary valve abnormalities (eg, pulmonary atresia), atrioventricular septal defect, and congenital aortic valve stenosis.
Other than for HLHS, termination of pregnancy was exceptional in the case of the other 3 specific malformations examined (Table 3). In contrast, >60% of the cases of HLHS were terminated in the more recent periods: 72.4% (95% CI: 52.8–87.3) in 1989–1994 and 63.0% (95% CI: 42.4–80.6) in 1995–2000.
Median gestational age at termination did not change significantly over time; median age at termination was 25 weeks in 1983–1988 and 1989–1994 and 24 weeks in 1995–2000 (P = .18). Timing of pregnancy termination did not appreciably change for the cases of HLHS either.
Perinatal Mortality
Perinatal mortality decreased substantially for CHD over time to almost one third in 1995–2000 (maternal age–adjusted RR: 0.38; 95% CI: 0.27–0.57) as compared with 1983–1988 (Table 2). Cusum analysis suggested a monotonically decreasing trend over time (P < .001; Fig 2). Stillbirth and first-day and first-week neonatal mortality all decreased substantially over time; however, the trends seemed to be greater for neonatal mortality than for stillbirth (Table 1). Stillbirth rate decreased by approximately one half (maternal age–adjusted RR: 0.49; 95% CI: 0.27–0.87), whereas early neonatal mortality of newborns with CHD decreased to less than one third in the period 1995–2000 as compared with 1983–1989 (Table 2): first-day mortality (maternal age–adjusted RR: 0.30; 95% CI: 0.11–0.82) and first-week mortality (adjusted RR: 0.31; 95% CI: 0.18–0.53).
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Analysis of mortality outcomes for isolated cases showed comparable perinatal and neonatal mortality rates. For example, the perinatal mortality rates for all cases was 6.4% (95% CI: 4.7–8.5) during 1995–2000 as compared with 5.1% (95% CI: 3.4–7.4) for isolated cases. Similarly, the first-week mortality was 3.3% (95% CI: 2.1–5.0) for all cases during 1995–2000 as compared with 3.7% (95% CI: 2.2–5.7) for the isolated cases. In general, as isolated cases accounted for the overwhelming majority (>80%) of cases, their outcomes determined to a large extent the overall outcomes for the cases of CHD.
There was a substantial decrease in perinatal mortality as a result of TGA and HLHS over time (Table 3); however, differences did not reach statistical significance for the latter (P = .10). For TGA, first-week neonatal mortality decreased from 19% in 1983–1988 (18.8%; 95% CI: 4.0–45.6) to 3% (2.6%; 95% CI: 0.1–13.5) in 1995–2000 (P = .04). For coarctation of aorta and tetralogy of Fallot, the number of isolated cases was not sufficient to assess trends over time.
Finally, first-week mortality was significantly lower for cases of TGA that were diagnosed before birth (Fischer exact test, P = .01); the mortality rate was 15.4% for cases that were diagnosed after birth (N = 39) as compared with 0% for cases that were diagnosed before birth (N = 39; risk difference: 15.4%; 95% CI: 4.0–26.7). This difference decreased slightly but remained statistically significant after adjustment for time period (time period–adjusted risk difference: 12.8%; 95% CI: 0.002–25.3%). However, we did not find any evidence of a significant impact of prenatal diagnosis on early neonatal mortality for HLHS; the first-week neonatal mortality rate was 69.2% for prenatally diagnosed cases (n = 13) and 73.9% for cases diagnosed postnatally (n = 23).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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In summary, we found substantial increases in prenatal diagnosis of CHD in the Parisian population during the study period. Currently, >50% of the cases of CHD that are not associated with a known chromosomal anomaly are likely to be diagnosed prenatally. Prenatal diagnosis occurred at a significantly earlier time during the study period, in particular for cases that were terminated. Trends varied substantially across different malformations examined. Our results suggest that almost 90% of the cases of HLHS are diagnosed prenatally and that 60% are terminated before birth. Overall, termination rates increased between 1983–1988 and 1989–1994 but seemed to remain stable thereafter. Timing of pregnancy termination did not appreciably change during the study period.
By the end of 1990s, perinatal mortality as a result of CHD decreased to approximately one third its rate in the 1980s. This was particularly the case for TGA, for which early neonatal mortality decreased to approximately one sixth. Prenatal diagnosis of TGA was associated with a substantially lower first-week neonatal mortality. This effect of prenatal diagnosis remained significant after adjustment for time period. Conversely, we did not find a significant effect for prenatal diagnosis on early neonatal mortality of HLHS.
The interpretation of our results is subject to several caveats and limitations. One potential source of bias that might lead to overestimation of prenatal diagnosis rates relates to the possibility of incomplete case ascertainment. This might be the case particularly for infants who were born with CHD and had a late diagnosis or those whose CHD was undiagnosed. Some of the latter may comprise less severe cases that remain asymptomatic during the early neonatal period. It is important in general to distinguish sources of bias that concern baseline rates, eg, incomplete case ascertainment because of limited registration that includes only early neonatal period from sources of bias that might be related to trends over time. We are not aware of any reason to expect that case ascertainment in the postnatal period decreased over time. Hence, the time trends that we observed are likely to reflect true increases in prenatal diagnosis of CHD.
Another important potential source of bias relates to the observed increase in number of CHD cases over time. There are 4 potential explanations for such trend: (1) increased prenatal and early postnatal diagnosis of cases over time, in particular increased diagnosis of less severe cases (eg, isolated ventricular septal defects) as a result of progress in cardiac echography; (2) increased postmortem diagnosis of anomalies as the registry data suggest that postmortem examinations for congenital anomalies have increased over time27; (3) referral bias, which we attempted to minimize by including only women who resided in Paris and gave birth at a Parisian maternity unit; and (4) increase in maternal age–related chromosomal anomalies (most important, Trisomy 21) that are associated with CHD. To minimize the last, we excluded all congenital heart defects that were associated with known chromosomal anomalies.
Perhaps the most important source of potential bias that could result in underestimation of mortality rates as a result of CHD over time relates to increased diagnosis and hence inclusion of less severe cases. Such selection bias could potentially explain all or part of the observed trends for lower perinatal mortality over time. We conducted the analyses that excluded isolated ventricular septal defects to control partially for such selection. Indeed, both the baseline outcomes and time trends did differ for the subset of CHD that excluded isolated ventricular septal defects. However, differences in trends for mortality with or without inclusion of isolated ventricular septal defects were most notable between 1983–1988 and 1989–1994. By the most recent period (1995–2000), trends in perinatal mortality were essentially the same for all CHD combined and the subset of CHD that excluded isolated ventricular septal defects.
The absolute number of deaths as a result of CHD also decreased over time, further suggesting that increases in the registered cases of CHD (ie, the denominators for mortality rates) do not entirely explain the observed decreases in mortality over time. Moreover, the malformation-specific trends are presumably less subject to selection bias as a result of inclusion of less severe cases over time. Therefore, for the 4 specific malformations examined, the severity of cases might not have changed substantially over time. In any case, our results regarding trends in mortality rates as a result of CHD cannot be considered definitive as data limitations preclude a complete control for selection bias.
The observed decreases in perinatal mortality might have been in part related to the increases in pregnancy termination for severe cases of CHD. Indeed, termination rates significantly increased between 1983–1988 and 1989–1994. Nevertheless, whereas termination rates remained essentially stable between 1989–1994 and 1995–2000, perinatal mortality, in particular early neonatal mortality, continued to decrease, both overall and for the 4 specific malformations examined.
Our analyses of trends in perinatal mortality were limited to the early neonatal period (first week). Although the Paris Registry includes data on mortality up to 1 year of age, the data beyond the first week are not collected systematically. In our analyses of available data for infant (ie, up to 1 year of age) mortality, we found similar trends as those that we report here for first-week mortality (data available on request). However, a full evaluation of the question of late neonatal and postneonatal mortality of infants who were born with CHD requires population-based data with complete assessment of mortality up to 1 year of age. In addition, we had limited power in assessing trends in perinatal mortality caused by specific malformations, in particular for coarctation of aorta and tetralogy of Fallot.
Our findings on the survival advantage of prenatally diagnosed cases of TGA are consistent with those reported based on a large hospital-series by Bonnet et al19 from a major pediatric cardiology center in Paris. Our results differ, however, from those of Kumar et al.20 Potential explanations for these differences include (1) variations in case ascertainment, in particular, inclusion of deaths as a result of CHD not diagnosed during life, which was done in the study by Bonnet et al and in our study; (2) differences in case mix not accounted for by our control for time period; and (3) clinical management or other factors related to organization of services in the different populations studied.
In conclusion, progress in clinical management, together with policies for increased access to prenatal diagnosis, has resulted in a substantial increase in the prenatal diagnosis and a considerable reduction in perinatal mortality of infants with CHD in the Parisian population. This does not suggest, however, that prenatal diagnosis generally confers a survival advantage to infants who are born with CHD. Findings from our study and the available evidence in the literature suggest that prenatal diagnosis might have improved the outcomes for certain anomalies. Nevertheless, much of the improvement in outcomes for CHD probably came about as a result of progress in postnatal medical and surgical care of newborns with CHD. At the same time, increased prenatal diagnosis of CHD has provided a greater opportunity for consultation between health care professionals and parents and thereby the possibility for more informed decision making for parents and their caregivers.
Our findings need to be corroborated and expanded on using population-based data from a reasonably large cohort of newborns with CHD with sufficient follow-up and detailed assessment of diagnoses and outcomes. In addition, with the improvements in the survival of infants with CHD, it becomes increasingly important to evaluate the role of prognostic factors, including that of prenatal diagnosis, in determining the mortality, morbidity, and in particular neurodevelopmental outcomes of infants with CHD.28 Heterogeneities in outcomes across different cardiac anomalies15,17,19–21,23 and for given anomalies at different centers,19,20,29,30 disparities in outcomes across socioeconomic groups,31,32 and alternative strategies for antenatal screening of CHD33–35 also need to be examined further.
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ACKNOWLEDGMENTS |
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Dr Khoshnood was supported by the Institut National de la Santé et de la Recherche Médicale program of visiting fellowships for foreign researchers and by the Fondation pour la Recherche Médicale.
We thank the staff of the Paris maternity units for their participation in the collection of data used for this analysis. The Paris Registry received financial support from the Institut National de la Santé et de la Recherche Médicale, Direction Générale de la Santé, and Institut de Veille Sanitaire.
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FOOTNOTES |
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Accepted Jun 21, 2004.
Reprint requests to (B.K.) INSERM U149, 16 Ave Paul Vaillant Couturier, 94807 Villejuif Cedex, France. E-mail: khoshnood{at}vjf.inserm.fr
No conflict of interest declared.
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  M. S. Sklansky, D. P. Berman, J. D. Pruetz, and R.-K. R. Chang Prenatal Screening for Major Congenital Heart Disease: Superiority of Outflow Tracts Over the 4-Chamber View J. Ultrasound Med., July 1, 2009; 28(7): 889 - 899. [Abstract] [Full Text] [PDF]
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 J. L. M. McCoyd "I'm not a saint": Burden Assessment as an Unrecognized Factor in Prenatal Decision Making Qual Health Res, November 1, 2008; 18(11): 1489 - 1500. [Abstract] [PDF]
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 J. Skinner, T. Hornung, and E. Rumball Transposition of the great arteries: from fetus to adult Heart, September 1, 2008; 94(9): 1227 - 1235. [Full Text] [PDF]
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 F. Kaguelidou, L. Fermont, Y. Boudjemline, J. Le Bidois, A. Batisse, and D. Bonnet Foetal echocardiographic assessment of tetralogy of Fallot and post-natal outcome Eur. Heart J., June 1, 2008; 29(11): 1432 - 1438. [Abstract] [Full Text] [PDF]
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 S V Rasiah, A K Ewer, P Miller, J G Wright, D J Barron, W J Brawn, and M D Kilby Antenatal perspective of hypoplastic left heart syndrome: 5 years on Arch. Dis. Child. Fetal Neonatal Ed., May 1, 2008; 93(3): F192 - F197. [Abstract] [Full Text] [PDF]
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 J. Davis and J J R. Fernando Successful management of prenatal hydrops fetalis in a mother with HIV Int J STD AIDS, April 1, 2008; 19(4): 281 - 282. [Abstract] [Full Text] [PDF]
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 B. Khoshnood, C. De Vigan, V. Vodovar, G. Breart, F. Goffinet, and B. Blondel Advances in Medical Technology and Creation of Disparities: The Case of Down Syndrome Am J Public Health, December 1, 2006; 96(12): 2139 - 2144. [Abstract] [Full Text] [PDF]
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 M. C M Macintosh, K. M Fleming, J. A Bailey, P. Doyle, J. Modder, D. Acolet, S. Golightly, and A. Miller Perinatal mortality and congenital anomalies in babies of women with type 1 or type 2 diabetes in England, Wales, and Northern Ireland: population based study BMJ, July 22, 2006; 333(7560): 177. [Abstract] [Full Text] [PDF]
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