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NSIDRC Journal Article Alert — September 11, 2009
Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University.
These articles have been selected from PubMed, a service of the National Library of Medicine that includes over 19 million citations from MEDLINE and other life science journals for biomedical articles back to 1948. PubMed includes links to full text articles and other related resources.
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. Duncan JR, Garland M, Myers MM, Fifer WP, Yang M, Kinney HC, Stark RI
Prenatal Nicotine-Exposure Alters Fetal Autonomic Activity and Medullary Neurotransmitter Receptors: Implications for Sudden Infant Death Syndrome
J Appl Physiol. 2009 Sep 3. [Epub ahead of print]
Childrens Hospital.
During pregnancy, exposure to nicotine and other compounds in cigarette smoke increases the risk of the sudden infant death syndrome (SIDS) 2-5-fold. Serotonergic (5-HT) abnormalities are found in infants that die of SIDS in regions of the medulla oblongata known to modulate cardiorespiratory function. Using a baboon model, we tested the hypothesis that prenatal exposure to nicotine alters 5-HT receptor and/or transporter binding in the fetal medullary 5-HT system in association with cardiorespiratory dysfunction. At 87 (mean) days gestation (dg) mothers were continuously infused with saline (n=5) or nicotine (n=5) at 0.5 mg/hr. Fetuses were surgically instrumented at 129 dg for cardiorespiratory monitoring. Cesarean section delivery and retrieval of fetal medulla were performed at 161 (mean) dg for autoradiographic analyses of nicotinic and 5-HT receptor and transporter binding. In nicotine-exposed fetuses, high frequency heart rate variability was increased 55%, possibly reflecting increases in the parasympathetic control of heart rate. This effect was more pronounced with greater levels of fetal breathing and age. These changes in heart rate variability were associated with increased 5-HT1A receptor binding in the raphé obscurus (p=0.04) and increased nicotinic receptor binding in the raphé obscurus and vagal complex (p<0.05) in the nicotine-exposed animals compared to controls (n=6). The shift in autonomic balance in the fetal primate toward parasympathetic predominance with chronic exposure to nicotine may be related in part to abnormal 5-HT-nicotine alterations in the raphé obscurus. Thus increased risk for SIDS due to maternal smoking may be partly related to the effects of nicotine on 5-HT and/or nicotinic receptors. Key words: Cardiorespiratory function, Nicotinic receptors, Parasympathetic activity, Raphé obscurus.
Other Infant Death
Miscarriage/Stillbirth/Prenatal Issues
1. Erez O, Gotsch F, Mazaki-Tovi S, Vaisbuch E, Kusanovic JP, Kim CJ, Chaiworapongsa T, Hoppensteadt D, Fareed J, Than NG, Nhan-Chang CL, Yeo L, Pacora P, Mazor M, Hassan SS, Mittal P, Romero R.
Evidence of maternal platelet activation, excessive thrombin generation, and high amniotic fluid tissue factor immunoreactivity and functional activity in patients with fetal death
J Matern Fetal Neonatal Med. 2009 Aug;22(8):672-87
Perinatology Research Branch, NICHD, NIH, DHHS, Bethesda, Maryland, USA.
Objective. Fetal death can lead to disseminated intravascular coagulation or fetal death syndrome. However, currently it is not clear what are the changes in the coagulation system in patients with a fetal death without the fetal death syndrome. This study was undertaken to determine: (1) whether fetal death in the absence of fetal death syndrome is associated with changes in hemostatic markers in maternal plasma and amniotic fluid; and (2) whether maternal hypertension or placental abruption are associated with further changes in the hemostatic profile of these patients. Methods. A cross-sectional study included the following: (1) determination of changes in markers of coagulation and platelet activation in patients with a normal pregnancy (n = 71) and patients with fetal demise (FD) without disseminated intravascular coagulation (n = 65); (2) determination of the amniotic fluid (AF)-tissue factor concentration and activity, as well as the concentrations of thrombin-antithrombin III (TAT) complexes in patients with a normal pregnancy (n = 25) and those with a FD (n = 36) who underwent amniocentesis. Plasma and AF concentrations of TAT complexes and TF (an index of thrombin generation), as well as maternal plasma concentrations of sCD40L (a marker of platelet activation), tissue factor pathway inhibitor (TFPI) and prothrombin fragments (PF) 1 + 2 (also an indicator of in vivo thrombin generation) were measured by ELISA. TF and TFPI activity were measured using chromogenic assays. Results. (1) patients with FD without hypertension had a higher median maternal plasma sCD40L concentration than normal pregnant women (P < 0.001); (2) patients with FD had a higher median maternal plasma TAT III complexes than women with a normal pregnancy (P < 0.001); (3) the median AF-TF concentration and activity were higher in the FD group than in the normal pregnancy group (P < 0.001 for both); (4) patients with preeclampsia and FD had a higher median maternal plasma immunoreactive TF concentration than both normotensive patients with FD and women with normal pregnancies (P < 0.001 and P = 0.001, respectively); (5) the median plasma TF activity was higher in patients with preeclampsia and FD than that of women with normal pregnancies (P = 0.003); (6) among patients with a FD, those with placental abruption had a higher median AF-TAT complexes concentration than those without abruption (P = 0.0004). Conclusions. Our findings indicate that: (1) mothers with a FD have evidence of increased in vivo thrombin generation and platelet activation than women with normal pregnancies; (2) patients with a FD and hypertension had a higher degree of TF activation than those with fetal death but without hypertension; (3) the AF of women with a FD had a higher median TF concentration and activity than that of normal pregnant women. AF can be a potential source for tissue factor and it participates in the development of fetal death syndrome in patients with a retained dead fetus.
2. de Vienne CM, Creveuil C, Dreyfus M
Does young maternal age increase the risk of adverse obstetric, fetal and neonatal outcomes: A cohort study
Eur J Obstet Gynecol Reprod Biol. 2009 Sep 3. [Epub ahead of print]
Department of Obstetrics and Gynecology, University Hospital of Caen, France.
OBJECTIVE: To determine whether young maternal age is associated with increased risks of adverse obstetric, fetal and perinatal outcomes. STUDY DESIGN: Register-based study using the data from a computerized database of a University Hospital for the years 1994-2001. The study population included 8514 primiparous women aged less than 31 who delivered a singleton infant. Using maternal age as a continuous variable, crude and adjusted relative risks (RRs) were estimated for each maternal and perinatal outcome. RESULTS: Crude and adjusted RRs of anaemia during pregnancy and fetal death consistently increased with younger maternal age. After adjustment for confounding factors, RRs (95% confidence interval) of fetal death and anaemia were respectively 1.37 (1.09-1.70) and 1.27 (1.15-1.40) for a 16-year-old compared to a 20-year-old mother. Younger mothers had significantly decreased risks of obstetric complications (preeclampsia, caesarean section, operative vaginal delivery and post-partum haemorrhage). Higher prevalence of prematurity and low birth weight in infants born to teenagers were not attributable to young maternal age after adjustment for confounding factors. CONCLUSION: In our population, younger maternal age was significantly and consistently associated to greater risks of fetal death and anaemia and to lower risks of adverse obstetric outcomes.
3. Pollack AZ, Buck Louis GM, Sundaram R, Lum KJ
Caffeine consumption and miscarriage: a prospective cohort study
Fertil Steril. 2009 Sep 2. [Epub ahead of print]
Epidemiology Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockville; Epidemiology Department, Johns Hopkins School of Public Health, Baltimore, Maryland.
Caffeine consumption has been equivocally associated with miscarriage, despite an absence of prospective longitudinal measurement of caffeine intake during sensitive windows of human development. In response to this critical data gap, we analyzed daily caffeine consumption while attempting pregnancy through 12 menstrual cycles at risk for pregnancy and found that caffeine consumption did not increase the risk or hazard of miscarriage, even after adjusting for relevant covariates.
Prepared by the
National Sudden and Unexpected Infant/Child Death and Pregnancy
Loss Resource Center
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