NSIDRC Journal Article Alert — March 20, 2009

Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University.

Past issues of Resource Center journal alerts are available at http://www.sidscenter.org.
Availability of full-text journal articles is often limited to subscribers or through inter-library loan. Please see your local library for copies of these articles, or view PubMed's How to Get the Journal Article for more details.

Sudden Infant Death

1. Osawa M, Kimura R, Hasegawa I, Mukasa N, Satoh F

SNP association and sequence analysis of the NOS1AP gene in SIDS

Leg Med (Tokyo). 2009 Mar 14. [Epub ahead of print]

Department of Forensic Medicine, Tokai University School of Medicine, Isehara, Kanagawa 259-1193, Japan.

One of the speculated causes for sudden infant death syndrome (SIDS) is hereditary disease, in which long QT in electrocardiogram has been investigated in the view of mutations in various ion channel genes. In the present study, a novel QT interval determinant of SNP (rs10494366) in NOS1AP is genotyped in SIDS subjects (n=42) and the control group (n=210). Subjects carrying TT genotype was significantly associated with SIDS, compared with those carrying the TG of GG genotype (95% confidence interval 1.28-8.45). Sequence analysis revealed that one non-synonymous substitution in exon 8 (rs12817159) was observed in one subject, in addition to six common SNPs in exons and introns. This postmortem association study showed variations in NOS1AP might be involved in occurrence of SIDS.

2. Krous HF, Ferandos C, Masoumi H, Arnold J, Haas EA, Stanley C, Grossfeld PD

Myocardial Inflammation, Cellular Death, And Viral Detection In Sudden Infant Death Caused By SIDS, Suffocation, Or Myocarditis

Pediatr Res. 2009 Mar 12. [Epub ahead of print]

Department of Pathology [H.F.K.], Department of Pediatrics [P.D.G.], University of California, San Diego, La Jolla, CA, 92037; Rady Children's Hospital [H.F.K., H.M., E.A.H., P.D.G.], San Diego, CA, 92123; Pediatric Infectious Disease [J.A.], Naval Medical Center San Diego, San Diego, CA, 92134; San Diego County Medical Examiner Office [C.S.], San Diego, CA, 92123.

The significance of minor myocardial inflammatory infiltrates and viral detection in SIDS is controversial. We retrospectively compared the demographic profiles, myocardial inflammation, cardiomyocyte necrosis, and of myocardial virus detection in infants who died of SIDS in a safe sleep environment, accidental suffocation, or myocarditis. Formalin-fixed, paraffin-embedded myocardial sections were semiquantitatively assessed for CD3 lymphocytes and CD68 macrophages using immunohistochemistry and for cardiomyocyte cell death in H and E stained sections. Enteroviruses and adenoviruses were searched for using PCR technology. The means of lymphocytes, macrophages, and necrotic cardiomyocytes were not statistically different in SIDS and suffocation cases. Enterovirus, not otherwise specified, was detected in one suffocation case and was the only virus detected in the three groups. Very mild myocardial lymphocyte and macrophage infiltration and scattered necrotic cardiomyocytes in SIDS are not pathologic, but may occur after the developing heart is exposed to environmental pathogens, including viruses.

3. Madea B

Sudden death, especially in infancy - improvement of diagnoses by biochemistry, immunohistochemistry and molecular pathology

Leg Med (Tokyo). 2009 Mar 10. [Epub ahead of print]

Institute of Forensic Medicine, University of Bonn, Stiftsplatz 12, D-53111 Bonn, Germany.

One of the problems in the diagnosis of the cause of death in cases of sudden death, especially in infancy, is the rapidity of death and that the morphological correlates of the underlying diseases and cause of death may be scarce or even completely missing. This is especially true for functional disorders causing death (e.g. arrhythmias) or cases where death occurs in an initial stage of disease with still lacking morphological findings (e.g. myocarditis). Molecular pathological techniques, which were initially of great importance for identification, today contribute also to the determination of the cause and manner of death, especially in cases, where classical methods do not reveal a clear anatomical cause of death. This will be addressed on the basis of several case groups, especially cases of sudden infant death syndrome (SIDS). Using immunohistochemical methods with qualification and quantification of interstitial leucocytes, PCR and Rt-PCR methods for identifying virus genome within the myocardium, it is possible to identify in about 25% of SIDS cases a myocarditis as cause of death. However, proposed limit values for the diagnosis of myocarditis have to be seen with caution since they lack any statistical power. The value of immunohistochemical and molecular pathological methods to identify the cause of death will also be addressed in cases of sudden death of young adults. At last pharmacogenomic investigations, e.g. on the metabolism of tramadol will be addressed which are of importance to declare adverse events, or even lethal outcome during medication.

4. Dettmeyer R

Immunohistochemical and molecular-pathological diagnosis of myocarditis in cases of suspected sudden infant death syndrome (SIDS) - A multicenter study

Leg Med (Tokyo). 2009 Mar 10. [Epub ahead of print]

Institute of Forensic Medicine, University of Giessen, Frankfurter Street 58, D-35392 Giessen, Germany.

Virus-induced myocarditis is a common disease even in infants and children, but diagnosis can be difficult according to the Dallas-criteria, which have been criticised as being too unreliable. The diagnosis has been substantially improved due to immunohistochemical techniques for characterization and quantification of myocardial inflammatory reactions as well as molecular-pathological methods for viral genome detection. The published studies report on post-mortem samples from SIDS victims and controls which were prospectively investigated. Pediatric cases of unnatural deaths served as controls. The results demonstrate a clearly higher prevalence of viral myocardial infections in cases of suspected SIDS. Preliminary criteria for cellular immunohistochemical diagnosis of viral myocardial affections derived from these findings were suggested.

Other Infant Death

1. Johansson AL, Dickman PW, Kramer MS, Cnattingius S

Maternal Smoking and Infant Mortality: Does Quitting Smoking Reduce the Risk of Infant Death?

Epidemiology. 2009 Mar 13. [Epub ahead of print]

From the aDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and bDepartments of Pediatrics and of Epidemiology and Biostatistics, McGill University Faculty of Medicine, Montreal, Canada.

BACKGROUND:: Maternal smoking has repeatedly been associated with increased infant mortality rates. No study has investigated whether smoking cessation influences the risk of infant death. This study estimates infant mortality after the second pregnancy in relation to smoking behavior in both the first and the second pregnancy. METHODS:: We used the Swedish Medical Birth Register to identify women who delivered their first and second singleton infants during 1983-2002. Maternal smoking during the 2 pregnancies was categorized into (1) never smoker, (2) quitter, (3) starter, and (4) persistent smoker. In the second pregnancy, 555,046 live births (of at least 22 completed gestational weeks) were followed for infant death within 1 year. Cox regression was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). RESULTS:: Compared with infants born to never smokers, the HR (95% CI) of infant mortality in the second pregnancy was 2.0 (1.7-2.4) among infants born to persistently heavy smokers, whereas among women who stopped smoking in the second pregnancy, the HRs were 1.4 (1.0-2.0) among those who had been heavy smokers in the first pregnancy, and 1.0 (0.8-1.2) among those who had been light smokers. The association of smoking during pregnancy with infant mortality was modified by infant's age, and was strongest at 4-15 weeks after birth. The smoking effect on neonatal mortality, but not postneonatal mortality, was mediated by gestational age. CONCLUSIONS:: Smoking cessation reduced the risk of infant death. The smoking-related risk of neonatal mortality appears to be mediated by smoking effects on gestational age, a factor that only partly explains the association between smoking and postneonatal mortality.

Miscarriage/Stillbirth/Prenatal Issues

1. McClure EM, Goldenberg RL

Infection and stillbirth

Semin Fetal Neonatal Med. 2009 Mar 11. [Epub ahead of print]

Department of Epidemiology, UNC Global School of Public Health, Chapel Hill, North Carolina, USA.

Infection may cause stillbirth by several mechanisms, including direct infection, placental damage, and severe maternal illness. Various organisms have been associated with stillbirth, including many bacteria, viruses, and protozoa. In developed countries, between 10% and 25% of stillbirths may be caused by an infection, whereas in developing countries, which have much higher stillbirth rates, the contribution of infection is much greater. In developed countries, ascending bacterial infection, both before and after membrane rupture, with organisms such as Escherichia coli, group B streptococci, and Ureaplasma urealyticum is usually the most common infectious cause of stillbirth. However, in areas where syphilis is prevalent, up to half of all stillbirths may be caused by this infection alone. Malaria may be an important cause of stillbirth in women infected for the first time in pregnancy. The two most important viral causes of stillbirth are parvovirus and Coxsackie virus, although a number of other viral infections appear to be causal. Toxoplasma gondii, Listeria monocytogenes, and the organisms that cause leptospirosis, Q fever, and Lyme disease have all been implicated as etiologic for stillbirth. In certain developing countries, the stillbirth rate is high and the infection-related component so great that achieving a substantial reduction in stillbirth should be possible by reducing maternal infections. However, because infection-related stillbirth is uncommon in developed countries, and because those that do occur are caused by a wide variety of organisms, reducing this etiologic component of stillbirth much further will be difficult.

2. Cacciatore J, Schnebly S, Froen JF

The effects of social support on maternal anxiety and depression after stillbirth

Health Soc Care Community. 2009 Mar;17(2):167-76

College of Human Services, Arizona State University, Glendale, AZ 85306, USA. joanne.cacciatore@asu.edu

While most births result in a live baby, stillbirth (the birth of a dead baby) occurs in nearly 1 in 110 pregnancies. This study examined whether levels of maternal anxiety and depression are lower amongst mothers who received social support after stillbirth. Using non-probability sampling, data were collected from 769 mothers residing within the USA who experienced a stillbirth within the past 18 months and for whom we have complete data. The study Maternal Observations and Memories of Stillbirth and the website http://www.momstudy.com containing the questionnaire were open in the period 8 February 2004-15 September 2005. Congruent with the family stress and coping theory, mothers of stillborn babies who perceived family support in the period after stillbirth experienced levels of anxiety and depression that were notably lower than those of their counterparts. Nurses, physicians and support groups also were important sources of support after a stillbirth; however, these sources of support alone were not statistically significant in reducing anxiety and depression in grieving mothers. Community interventions should focus on the grieving mother and her family system, including her partner and surviving children.

3. Guosheng L, Hongmei S, Chuan N, Haiying L, Xiaopeng Z, Xianqiong L

The relationship of serum AGE levels in diabetic mothers with adverse fetal outcome

J Perinatol. 2009 Mar 12. [Epub ahead of print]

1Department of Pediatrics, First Affiliated Hospital of Jinan University, Guangzhou, China.

Objective:To investigate changes in serum-advanced glycosylation end product (AGE) levels in gestation diabetic mothers (GDMs) and its relationship with adverse fetal outcome.Study Design:A total of 60 GDMs in mid-gestation and 72 late-gestation GDMs fulfilling the inclusion criteria were recruited. Seventy-two mid-gestation and 80 late-gestation mothers with no pregnancy complications acted as controls. Fasting blood glucose and serum AGE levels were analyzed in each group. Clinical data on these women and their perinatal outcomes were collected. Maternal serum AGE levels and changes in blood glucose between mid-gestation groups and late-gestation groups were compared. Factors, including AGE levels, affecting the prevalence of complications of fetal outcome in GDMs were investigated.Result:Mid-gestation and late-gestation GDMs had significantly higher serum AGE levels and fasting blood glucose than their respective controls (P<0.001 and P<0.05, respectively). After treatment mid-gestation GDMs had significantly lower blood glucose levels at late gestation (P<0.05), but their serum AGE levels remained relatively high. There were no significant changes in serum AGE levels from mid- to late gestation. Women with GDM who had abnormal fetal outcomes had significantly higher maternal serum AGE levels than controls with normal fetal outcome (P<0.05). Particularly, those pregnancies that resulted in birth asphyxia, congenital malformations or stillbirth had higher serum AGEs (P<0.05). Logistic regression analysis showed elevated AGEs as a predictor of adverse perinatal outcome in GDMs, OR=6.285 (P<0.001, 95% CI 2.561to15.534).Conclusion:High-serum AGE is an adverse factor in perinatal outcomes in GDMs. Sustained high AGE levels from mid- to late gestation could be an indicator of adverse perinatal outcomes.Journal of Perinatology advance online publication, 12 March 2009; doi:10.1038/jp.2009.12.

Prepared by the
National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center
Georgetown University
2115 Wisconsin Avenue, N.W., Suite 601
Washington, DC 20007
(866) 866-7437 toll free
(202) 687-7466 local
(202) 784-9777 fax
info@sidscenter.org
http://www.sidscenter.org


	Home :: A - Z Index: A B C D E F G H I J K L M N O P Q R S T U V W X Y Z :: Search
	Center Resources Bereavement Support Child Care and SIDS Definitions En Español First Responders For Families Infant Mortality Injury and Violence Prevention Journal Alerts MCH Alert Multimedia Pregnancy Loss Professional Resources Program Manual and Trainer's Guide Publications Research Bibliographies Safe Sleep Environment State Links Statistics Training Toolkit Partner Centers About the SUID Consortium Program Support Center at First Candle Project IMPACT National Center for Cultural Competence Other Partners Site Tools About Contact FAQs Site Map For more information on maternal and child health topics, visit the MCH Library	NSIDRC Journal Article Alert — March 20, 2009 Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University. Past issues of Resource Center journal alerts are available at http://www.sidscenter.org. Availability of full-text journal articles is often limited to subscribers or through inter-library loan. Please see your local library for copies of these articles, or view PubMed's How to Get the Journal Article for more details. Sudden Infant Death 1. Osawa M, Kimura R, Hasegawa I, Mukasa N, Satoh F SNP association and sequence analysis of the NOS1AP gene in SIDS Leg Med (Tokyo). 2009 Mar 14. [Epub ahead of print] Department of Forensic Medicine, Tokai University School of Medicine, Isehara, Kanagawa 259-1193, Japan. One of the speculated causes for sudden infant death syndrome (SIDS) is hereditary disease, in which long QT in electrocardiogram has been investigated in the view of mutations in various ion channel genes. In the present study, a novel QT interval determinant of SNP (rs10494366) in NOS1AP is genotyped in SIDS subjects (n=42) and the control group (n=210). Subjects carrying TT genotype was significantly associated with SIDS, compared with those carrying the TG of GG genotype (95% confidence interval 1.28-8.45). Sequence analysis revealed that one non-synonymous substitution in exon 8 (rs12817159) was observed in one subject, in addition to six common SNPs in exons and introns. This postmortem association study showed variations in NOS1AP might be involved in occurrence of SIDS. 2. Krous HF, Ferandos C, Masoumi H, Arnold J, Haas EA, Stanley C, Grossfeld PD Myocardial Inflammation, Cellular Death, And Viral Detection In Sudden Infant Death Caused By SIDS, Suffocation, Or Myocarditis Pediatr Res. 2009 Mar 12. [Epub ahead of print] Department of Pathology [H.F.K.], Department of Pediatrics [P.D.G.], University of California, San Diego, La Jolla, CA, 92037; Rady Children's Hospital [H.F.K., H.M., E.A.H., P.D.G.], San Diego, CA, 92123; Pediatric Infectious Disease [J.A.], Naval Medical Center San Diego, San Diego, CA, 92134; San Diego County Medical Examiner Office [C.S.], San Diego, CA, 92123. The significance of minor myocardial inflammatory infiltrates and viral detection in SIDS is controversial. We retrospectively compared the demographic profiles, myocardial inflammation, cardiomyocyte necrosis, and of myocardial virus detection in infants who died of SIDS in a safe sleep environment, accidental suffocation, or myocarditis. Formalin-fixed, paraffin-embedded myocardial sections were semiquantitatively assessed for CD3 lymphocytes and CD68 macrophages using immunohistochemistry and for cardiomyocyte cell death in H and E stained sections. Enteroviruses and adenoviruses were searched for using PCR technology. The means of lymphocytes, macrophages, and necrotic cardiomyocytes were not statistically different in SIDS and suffocation cases. Enterovirus, not otherwise specified, was detected in one suffocation case and was the only virus detected in the three groups. Very mild myocardial lymphocyte and macrophage infiltration and scattered necrotic cardiomyocytes in SIDS are not pathologic, but may occur after the developing heart is exposed to environmental pathogens, including viruses. 3. Madea B Sudden death, especially in infancy - improvement of diagnoses by biochemistry, immunohistochemistry and molecular pathology Leg Med (Tokyo). 2009 Mar 10. [Epub ahead of print] Institute of Forensic Medicine, University of Bonn, Stiftsplatz 12, D-53111 Bonn, Germany. One of the problems in the diagnosis of the cause of death in cases of sudden death, especially in infancy, is the rapidity of death and that the morphological correlates of the underlying diseases and cause of death may be scarce or even completely missing. This is especially true for functional disorders causing death (e.g. arrhythmias) or cases where death occurs in an initial stage of disease with still lacking morphological findings (e.g. myocarditis). Molecular pathological techniques, which were initially of great importance for identification, today contribute also to the determination of the cause and manner of death, especially in cases, where classical methods do not reveal a clear anatomical cause of death. This will be addressed on the basis of several case groups, especially cases of sudden infant death syndrome (SIDS). Using immunohistochemical methods with qualification and quantification of interstitial leucocytes, PCR and Rt-PCR methods for identifying virus genome within the myocardium, it is possible to identify in about 25% of SIDS cases a myocarditis as cause of death. However, proposed limit values for the diagnosis of myocarditis have to be seen with caution since they lack any statistical power. The value of immunohistochemical and molecular pathological methods to identify the cause of death will also be addressed in cases of sudden death of young adults. At last pharmacogenomic investigations, e.g. on the metabolism of tramadol will be addressed which are of importance to declare adverse events, or even lethal outcome during medication. 4. Dettmeyer R Immunohistochemical and molecular-pathological diagnosis of myocarditis in cases of suspected sudden infant death syndrome (SIDS) - A multicenter study Leg Med (Tokyo). 2009 Mar 10. [Epub ahead of print] Institute of Forensic Medicine, University of Giessen, Frankfurter Street 58, D-35392 Giessen, Germany. Virus-induced myocarditis is a common disease even in infants and children, but diagnosis can be difficult according to the Dallas-criteria, which have been criticised as being too unreliable. The diagnosis has been substantially improved due to immunohistochemical techniques for characterization and quantification of myocardial inflammatory reactions as well as molecular-pathological methods for viral genome detection. The published studies report on post-mortem samples from SIDS victims and controls which were prospectively investigated. Pediatric cases of unnatural deaths served as controls. The results demonstrate a clearly higher prevalence of viral myocardial infections in cases of suspected SIDS. Preliminary criteria for cellular immunohistochemical diagnosis of viral myocardial affections derived from these findings were suggested. Other Infant Death 1. Johansson AL, Dickman PW, Kramer MS, Cnattingius S Maternal Smoking and Infant Mortality: Does Quitting Smoking Reduce the Risk of Infant Death? Epidemiology. 2009 Mar 13. [Epub ahead of print] From the aDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and bDepartments of Pediatrics and of Epidemiology and Biostatistics, McGill University Faculty of Medicine, Montreal, Canada. BACKGROUND:: Maternal smoking has repeatedly been associated with increased infant mortality rates. No study has investigated whether smoking cessation influences the risk of infant death. This study estimates infant mortality after the second pregnancy in relation to smoking behavior in both the first and the second pregnancy. METHODS:: We used the Swedish Medical Birth Register to identify women who delivered their first and second singleton infants during 1983-2002. Maternal smoking during the 2 pregnancies was categorized into (1) never smoker, (2) quitter, (3) starter, and (4) persistent smoker. In the second pregnancy, 555,046 live births (of at least 22 completed gestational weeks) were followed for infant death within 1 year. Cox regression was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). RESULTS:: Compared with infants born to never smokers, the HR (95% CI) of infant mortality in the second pregnancy was 2.0 (1.7-2.4) among infants born to persistently heavy smokers, whereas among women who stopped smoking in the second pregnancy, the HRs were 1.4 (1.0-2.0) among those who had been heavy smokers in the first pregnancy, and 1.0 (0.8-1.2) among those who had been light smokers. The association of smoking during pregnancy with infant mortality was modified by infant's age, and was strongest at 4-15 weeks after birth. The smoking effect on neonatal mortality, but not postneonatal mortality, was mediated by gestational age. CONCLUSIONS:: Smoking cessation reduced the risk of infant death. The smoking-related risk of neonatal mortality appears to be mediated by smoking effects on gestational age, a factor that only partly explains the association between smoking and postneonatal mortality. Miscarriage/Stillbirth/Prenatal Issues 1. McClure EM, Goldenberg RL Infection and stillbirth Semin Fetal Neonatal Med. 2009 Mar 11. [Epub ahead of print] Department of Epidemiology, UNC Global School of Public Health, Chapel Hill, North Carolina, USA. Infection may cause stillbirth by several mechanisms, including direct infection, placental damage, and severe maternal illness. Various organisms have been associated with stillbirth, including many bacteria, viruses, and protozoa. In developed countries, between 10% and 25% of stillbirths may be caused by an infection, whereas in developing countries, which have much higher stillbirth rates, the contribution of infection is much greater. In developed countries, ascending bacterial infection, both before and after membrane rupture, with organisms such as Escherichia coli, group B streptococci, and Ureaplasma urealyticum is usually the most common infectious cause of stillbirth. However, in areas where syphilis is prevalent, up to half of all stillbirths may be caused by this infection alone. Malaria may be an important cause of stillbirth in women infected for the first time in pregnancy. The two most important viral causes of stillbirth are parvovirus and Coxsackie virus, although a number of other viral infections appear to be causal. Toxoplasma gondii, Listeria monocytogenes, and the organisms that cause leptospirosis, Q fever, and Lyme disease have all been implicated as etiologic for stillbirth. In certain developing countries, the stillbirth rate is high and the infection-related component so great that achieving a substantial reduction in stillbirth should be possible by reducing maternal infections. However, because infection-related stillbirth is uncommon in developed countries, and because those that do occur are caused by a wide variety of organisms, reducing this etiologic component of stillbirth much further will be difficult. 2. Cacciatore J, Schnebly S, Froen JF The effects of social support on maternal anxiety and depression after stillbirth Health Soc Care Community. 2009 Mar;17(2):167-76 College of Human Services, Arizona State University, Glendale, AZ 85306, USA. joanne.cacciatore@asu.edu While most births result in a live baby, stillbirth (the birth of a dead baby) occurs in nearly 1 in 110 pregnancies. This study examined whether levels of maternal anxiety and depression are lower amongst mothers who received social support after stillbirth. Using non-probability sampling, data were collected from 769 mothers residing within the USA who experienced a stillbirth within the past 18 months and for whom we have complete data. The study Maternal Observations and Memories of Stillbirth and the website http://www.momstudy.com containing the questionnaire were open in the period 8 February 2004-15 September 2005. Congruent with the family stress and coping theory, mothers of stillborn babies who perceived family support in the period after stillbirth experienced levels of anxiety and depression that were notably lower than those of their counterparts. Nurses, physicians and support groups also were important sources of support after a stillbirth; however, these sources of support alone were not statistically significant in reducing anxiety and depression in grieving mothers. Community interventions should focus on the grieving mother and her family system, including her partner and surviving children. 3. Guosheng L, Hongmei S, Chuan N, Haiying L, Xiaopeng Z, Xianqiong L The relationship of serum AGE levels in diabetic mothers with adverse fetal outcome J Perinatol. 2009 Mar 12. [Epub ahead of print] 1Department of Pediatrics, First Affiliated Hospital of Jinan University, Guangzhou, China. Objective:To investigate changes in serum-advanced glycosylation end product (AGE) levels in gestation diabetic mothers (GDMs) and its relationship with adverse fetal outcome.Study Design:A total of 60 GDMs in mid-gestation and 72 late-gestation GDMs fulfilling the inclusion criteria were recruited. Seventy-two mid-gestation and 80 late-gestation mothers with no pregnancy complications acted as controls. Fasting blood glucose and serum AGE levels were analyzed in each group. Clinical data on these women and their perinatal outcomes were collected. Maternal serum AGE levels and changes in blood glucose between mid-gestation groups and late-gestation groups were compared. Factors, including AGE levels, affecting the prevalence of complications of fetal outcome in GDMs were investigated.Result:Mid-gestation and late-gestation GDMs had significantly higher serum AGE levels and fasting blood glucose than their respective controls (P<0.001 and P<0.05, respectively). After treatment mid-gestation GDMs had significantly lower blood glucose levels at late gestation (P<0.05), but their serum AGE levels remained relatively high. There were no significant changes in serum AGE levels from mid- to late gestation. Women with GDM who had abnormal fetal outcomes had significantly higher maternal serum AGE levels than controls with normal fetal outcome (P<0.05). Particularly, those pregnancies that resulted in birth asphyxia, congenital malformations or stillbirth had higher serum AGEs (P<0.05). Logistic regression analysis showed elevated AGEs as a predictor of adverse perinatal outcome in GDMs, OR=6.285 (P<0.001, 95% CI 2.561to15.534).Conclusion:High-serum AGE is an adverse factor in perinatal outcomes in GDMs. Sustained high AGE levels from mid- to late gestation could be an indicator of adverse perinatal outcomes.Journal of Perinatology advance online publication, 12 March 2009; doi:10.1038/jp.2009.12. Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center Georgetown University 2115 Wisconsin Avenue, N.W., Suite 601 Washington, DC 20007 (866) 866-7437 toll free (202) 687-7466 local (202) 784-9777 fax info@sidscenter.org http://www.sidscenter.org
	Accessibility • Copyright © Georgetown University • (866) 866-7437 (toll free) • (202) 687-7466 (local) 2115 Wisconsin Avenue, NW, Suite 601 • Washington, DC 20007 • info@sidscenter.org • (202) 784-9777 (fax)

Center Resources

Partner Centers

Site Tools

For more information on maternal and child health topics, visit the MCH Library

NSIDRC Journal Article Alert — March 20, 2009