NSIDRC Journal Article Alert — January 11, 2012
Prepared by the National SUID/SIDS Resource Center at Georgetown University.
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Sudden Infant Death
1. Pediatrics. 2012 Jan 9. [Epub ahead of print]
The Sudden Unexpected Infant Death Case Registry: A Method to Improve Surveillance.
Shapiro-Mendoza CK, Camperlengo LT, Kim SY, Covington T.
Source
aDivision of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, Georgia; and.
Abstract
This article describes a multistate population-based surveillance system for monitoring sudden unexpected infant deaths (SUIDs) known as the SUID Case Registry pilot program. The pilot program represents collaboration between the Centers for Disease Control and Prevention and the National Center for Child Death Review (NCCDR), which is funded by the Health Resources and Services Administration. The SUID Case Registry builds on existing child death review system activities and protocols. The objectives of the SUID Case Registry are to collect accurate and consistent population-based data about the circumstances and events associated with SUID cases, to improve the completeness and quality of SUID case investigations, and to use a decision-making algorithm with standardized definitions to categorize SUID cases. States who participate in the pilot program commit to review all SUID cases in their state by using their multidisciplinary state and local child death review teams. These teams request and review data from death scene investigators, medical examiners and coroners, law enforcement, social services, pediatric and obstetric providers, and public health per usual, but as part of the pilot program, supplement their SUID case reviews by discussing additional medical, environmental, and behavioral factors, and entering this data using the NCCDR Web-based Case Reporting System. This new surveillance system aims to improve knowledge of factors surrounding SUID events and improve investigation practices. The surveillance system will allow researchers and program planners to create prevention strategies and interventions, ultimately reducing SUIDs and injury-related infant deaths.
2. Circulation. 2011 Dec 16. [Epub ahead of print]
Connexin43 Mutation Causes Heterogeneous Gap Junction Loss and Sudden Infant Death.
Van Norstrand DW, Asimaki A, Rubinos C, Dolmatova E, Srinivas M, Tester DJ, Saffitz JE, Duffy HS, Ackerman MJ.
Source
1 Mayo Clinic, Rochester, MN, United States;
Abstract
BACKGROUND:
An estimated 10-15% of sudden infant death syndrome (SIDS) may stem from channelopathy-mediated lethal arrhythmias. Loss of the GJA1-encoded gap junction channel protein connexin43 (Cx43) is known to underlie formation of lethal arrhythmias. GJA1 mutations have been associated with cardiac diseases including atrial fibrillation. Therefore, GJA1 is a plausible candidate gene for premature sudden death.
METHODS AND RESULTS:
GJA1 open reading frame mutational analysis was performed using PCR, DHPLC, and direct DNA sequencing on DNA from 292 SIDS cases. Immunofluorescence and dual whole cell patch-clamp studies were performed to determine functionality of mutant gap junctions. Immunostaining for gap junction proteins was performed on SIDS-associated paraffin-embedded cardiac tissue. Two rare, novel missense mutations, E42K and S272P, were detected in 2 of 292 SIDS cases, a 2-month-old white male and a 3-month-old white female, respectively. Analysis of the E42K victim's parental DNA demonstrated a de novo mutation. Both mutations involved highly conserved residues and were absent in over 1000 ethnic-matched reference alleles. Immunofluorescence demonstrated no trafficking abnormalities for either mutation and S272P demonstrated wildtype junctional conductance. However, junctional conductance measurements for the E42K mutation demonstrated a loss-of-function not rescued by wildtype. Moreover, the E42K victim cardiac tissue demonstrated a mosaic immunostaining pattern for Cx43 protein.
CONCLUSIONS:
This study provides the first molecular and functional evidence implicating a GJA1 mutation as a novel pathogenic substrate for SIDS. E42K-Cx43 demonstrated a trafficking-independent reduction in junctional coupling in vitro as well as demonstrating a mosaic pattern of mutational DNA distribution in deceased cardiac tissue, suggesting a novel mechanism of Cx43-associated sudden death.
3. Curr Microbiol. 2011 Dec 17. [Epub ahead of print]
A Possible Murine Model for Investigation of Pathogenesis of Sudden Infant Death Syndrome.
Bettelheim KA, Luke RK, Johnston N, Pearce JL, Goldwater PN.
Source
Department of Agricultural Sciences, La Trobe University, Bundoora, VIC, 3086, Australia.
Abstract
Several studies have indicated a possible causative role of toxigenic bacteria in sudden infant death syndrome (SIDS). This study examined the effect of toxigenic E. coli on pregnant and infant mice to determine if these animals could be used as a model for SIDS pathogenesis. Strains of E. coli from the intestinal contents of infants who have died of SIDS or other causes and from the faeces of healthy infants were collected over a broad time scale. The isolates were tested for their ability to produce then known toxins of E. coli and were serotyped (O and H antigens). Certain serotypes (e.g. O1:H- and O25:H1) emerged significantly more frequently from cases of SIDS than from healthy infants and isolates of these types were generally toxigenic in Vero-cell cultures but whose verotoxicity was not related to classical Shiga or other known toxins. This mouse model was developed to test the effects of these toxigenic and also non-toxigenic strains. Four apparently healthy pups aged between 17 and 21 days died unobserved overnight but no pups of the 54 control mice died suddenly (P = 0.0247, Fisher's exact test). These were considered to represent sudden unexpected deaths. Pathological effects compatible with those in SIDS were observed in mouse pups exposed to toxigenic strains indicating this model may be suitable for further study into the pathogenesis of unexpected deaths in infancy. Providing an animal model of SIDS would promote a much better avenue for studying the pathogenesis of this enigmatic condition.
4. Toxicol Appl Pharmacol. 2011 Dec 15;257(3):396-404. Epub 2011 Oct 6.
Effects of cigarette smoke exposure on nicotinic acetylcholine receptor subunits α7 and β2 in the sudden infant death syndrome (SIDS) brainstem.
Machaalani R, Say M, Waters KA.
Source
Department of Medicine, The University of Sydney, NSW 2006, Australia. rita.machaalani@sydney.edu.au
Abstract
It is postulated that nicotine, as the main neurotoxic constituent of cigarette smoke, influences SIDS risk through effects on nicotinic acetylcholine receptors (nAChRs) in brainstem nuclei that control respiration and arousal. This study compared α7 and β2 nAChR subunit expression in eight nuclei of the caudal and rostral medulla and seven nuclei of the pons between SIDS (n=46) and non-SIDS infants (n=14). Evaluation for associations with known SIDS risk factors included comparison according to whether infants had a history of exposure to cigarette smoke in the home, and stratification for sleep position and gender. Compared to non-SIDS infants, SIDS infants had significantly decreased α7 in the caudal nucleus of the solitary tract (cNTS), gracile and cuneate nuclei, with decreased β2 in the cNTS and increased β2 in the facial. When considering only the SIDS cohort: 1-cigarette smoke exposure was associated with increased α7 in the vestibular nucleus and increased β2 in the rostral dorsal motor nucleus of the vagus, rNTS and Cuneate, 2-there was a gender interaction for α7 in the gracile and cuneate, and β2 in the cNTS and rostral arcuate nucleus, and 3-there was no effect of sleep position on α7, but prone sleep was associated with decreased β2 in three nuclei of the pons. In conclusion, SIDS infants demonstrate differences in expression of α7 and β2 nAChRs within brainstem nuclei that control respiration and arousal, which is independent on prior history of cigarette smoke exposure, especially for the NTS, with additional differences for smoke exposure (β2), gender (α7 and β2) and sleep position (β2) evident.
Copyright © 2011 Elsevier Inc. All rights reserved.
5. Acta Paediatr. 2012 Jan;101(1):8-13. doi: 10.1111/j.1651-2227.2011.02464.x. Epub 2011 Oct 10.
Can home monitoring reduce mortality in infants at increased risk of sudden infant death syndrome? A systematic review.
Strehle EM, Gray WK, Gopisetti S, Richardson J, McGuire J, Malone S.
Source
North Tyneside General Hospital, Rake Lane, North Shields, Tyne and Wear, UK.
Abstract
Aim: To conduct a systematic review to evaluate the effectiveness of home monitoring devices in the prevention of sudden infant death syndrome (SIDS). Methods: Systematic literature review to June 30, 2010. Results: Eleven unique studies were identified. Only one of these studies involved a comparison of home monitoring with a control intervention and so could be deemed level I evidence. The remaining studies constituted level III evidence. Conclusions: There is no high-level evidence that home monitoring may be of use in preventing SIDS; further research is needed.
© 2011 The Author(s)/Acta Paediatrica © 2011 Foundation Acta Paediatrica.
6. Matern Child Health J. 2012 Jan;16(1):72-82.
Racial differences in trends and predictors of infant sleep positioning in South Carolina, 1996-2007.
Smith MG, Liu JH, Helms KH, Wilkerson KL.
Source
Office of Public Health Statistics and Information Systems, South Carolina Department of Health and Environmental Control, 2600 Bull St., Columbia, SC, USA, smithm4@dhec.sc.gov.
Abstract
This paper examines racial differences in trends and predictors of prone and lateral infant sleep positioning among South Carolina mothers and infants. Pregnancy Risk Assessment Monitoring System data were used to analyze linear trends in prone, lateral, and supine infant sleep positioning among 14,648 mother-infant pairs from 1996 to 2007. Logistic regression models were used to examine the predictors of prone and lateral positioning among 9,015 mother-infant pairs from 2000 to 2007. From 1996 to 2007, white infants experienced a reduction in both prone and lateral positioning and an increase in supine positioning (28.2-66.7%), while black infants had smaller decreases in prone and lateral positioning and a smaller increase in supine positioning (22.6-47.1%) than white infants. Compared to births in 2000-2005, births after the explicit recommendation that infants not be placed in the lateral sleep position (2006-2007) were associated with decreased odds of lateral positioning among white infants (odds ratio [OR]: 0.66; 95% confidence interval [CI]: 0.51, 0.87) but not among black infants. The significant predictors of white infants being placed in the prone position were different from the predictors for black infants. Additionally, with regard to lateral sleep positioning, more significant predictors were observed among white infants than black infants. These findings suggest that efforts are warranted to increase the prevalence of supine sleep positioning, especially among black infants. Race-specific programs may efficiently reduce non-supine sleep positioning to help narrow racial gaps in sudden infant death syndrome.
Miscarriage/Stillbirth/Prenatal Issues
1. J Reprod Immunol. 2011 Dec 21. [Epub ahead of print]
The basis and value of currently used immunomodulatory therapies in recurrent miscarriage.
Bansal AS, Bajardeen B, Thum MY.
Source
Department of Immunology, St Helier Hospital, Carshalton, Surrey SM5 1AA, England, United Kingdom.
Abstract
Recurrent miscarriage (RM) without an obvious identifiable cause may arise from excessive maternal T and natural killer (NK) cell activity against the trophoblast or early embryo. Impaired regulatory T cell function leading to increased pro-inflammatory Th17 and NK cell cytotoxicity may be central. Ongoing subclinical endometrial infection and/or inflammation with increased secretion of TNFα and stimulation of autoimmunity to heat shock proteins may also be contributory. Therapies with a varying theoretical basis and clinical evidence aimed at reducing excessive endometrial immune activity have been used non-selectively in women with RM with variable success. Recent work has now improved our understanding of the role of the different immune cells and proteins that are important at each stage of a normal pregnancy. The vulnerability of the early embryo to T and NK cell-mediated rejection suggests that immune-based therapies need to be maximally effective during early pregnancy. Targeting RM women with demonstrable T and NK cell activity may improve the overall clinical efficacy of these treatments. It may also prevent costly and possibly harmful use in women who are unlikely to respond, and make better use of scarce resources. This report describes the underlying principles behind the use of the different immune-based therapies. The broad evidence supporting their efficacy is also described, as are the possible adverse consequences. Suggestions are also made on how the maternal immune system may be positively modulated using current, widely available treatments that have minimal or no side effects.
Copyright © 2011. Published by Elsevier Ireland Ltd.
2. Thromb Res. 2011 Dec 16. [Epub ahead of print]
The association of antiphospholipid antibodies with intrauterine fetal death: A case-control study.
Helgadottir LB, Skjeldestad FE, Jacobsen AF, Sandset PM, Jacobsen EM.
Source
Department of Haematology, Oslo University Hospital Ullevål, Oslo, Norway; Department of Obstetrics and Gynaecology, Oslo University Hospital Ullevål, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Abstract
INTRODUCTION:
Over the past few decades it has been recognized that antiphospholipid antibodies are associated with pregnancy loss. Other placenta-mediated pregnancy complications have also been associated with the presence of antiphospholipid antibodies. Most studies have measured antiphospholipid antibodies near the time of the event investigated.
OBJECTIVES:
To investigate the association of antiphospholipid antibodies and a history of intrauterine fetal death (IUFD) in a case-control design.
MATERIALS AND METHODS:
A case-control study of 105 women with a history of IUFD after 22 gestational weeks and 262 controls with live births. The prevalence of lupus anticoagulant, anticardiolipin- and anti-β2-glycoprotein 1 antibodies were measured 3-18years after the event of IUFD.
RESULTS:
Total 9.5% of women with a history of IUFD and 5.0% of controls had at least one positive test for antiphospholipid antibodies (OR 2.0; 95% confidence interval (CI) 0.9-4.8). Women with a history of IUFD were significantly more often positive for lupus anticoagulant compared to controls (OR 4.3; 95% CI 1.0-18.4). The association of lupus anticoagulant with a history of IUFD was confined to women positive for other antiphospholipid antibodies in addition to lupus anticoagulant. Being positive for anti-β2-glycoprotein 1 or anticardiolipin antibodies alone was not significantly associated with a history of IUFD.
CONCLUSIONS:
Women with a history of IUFD after 22 gestational weeks were more often lupus anticoagulant positive. The association was confined to women with multiple positivity for antiphospholipid antibodies, although firm conclusions on the importance of multiple positivity cannot be made from this study.
Copyright © 2011 Elsevier Ltd. All rights reserved.
3. JAMA. 2011 Dec 14;306(22):2469-79.
Association between stillbirth and risk factors known at pregnancy confirmation.
Stillbirth Collaborative Research Network Writing Group.
Collaborators (16)
Source
Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, 301 University Blvd, Galveston, TX 77555, USA.
Abstract
CONTEXT:
Stillbirths account for almost half of US deaths from 20 weeks' gestation to 1 year of life. Most large studies of risk factors for stillbirth use vital statistics with limited data.
OBJECTIVE:
To determine the relation between stillbirths and risk factors that could be ascertained at the start of pregnancy, particularly the contribution of these factors to racial disparities.
DESIGN, SETTING, AND PARTICIPANTS:
Multisite population-based case-control study conducted between March 2006 and September 2008. Fifty-nine US tertiary care and community hospitals, with access to at least 90% of deliveries within 5 catchment areas defined by state and county lines, enrolled residents with deliveries of 1 or more stillborn fetuses and a representative sample of deliveries of only live-born infants, oversampled for those at less than 32 weeks' gestation and those of African descent.
MAIN OUTCOME MEASURE:
Stillbirth.
RESULTS:
Analysis included 614 case and 1816 control deliveries. In multivariate analyses, the following factors were independently associated with stillbirth: non-Hispanic black race/ethnicity (23.1% stillbirths, 11.2% live births) (vs non-Hispanic whites; adjusted odds ratio [AOR], 2.12 [95% CI, 1.41-3.20]); previous stillbirth (6.7% stillbirths, 1.4% live births); nulliparity with (10.5% stillbirths, 5.2% live births) and without (34.0% stillbirths, 29.7% live births) previous losses at fewer than 20 weeks' gestation (vs multiparity without stillbirth or previous losses; AOR, 5.91 [95% CI, 3.18-11.00]; AOR, 3.13 [95% CI, 2.06-4.75]; and AOR, 1.98 [95% CI, 1.51-2.60], respectively); diabetes (5.6% stillbirths, 1.6% live births) (vs no diabetes; AOR, 2.50 [95% CI, 1.39-4.48]); maternal age 40 years or older (4.5% stillbirths, 2.1% live births) (vs age 20-34 years; AOR, 2.41 [95% CI, 1.24-4.70]); maternal AB blood type (4.9% stillbirths, 3.0% live births) (vs type O; AOR, 1.96 [95% CI, 1.16-3.30]); history of drug addiction (4.5% stillbirths, 2.1% live births) (vs never use; AOR, 2.08 [95% CI, 1.12-3.88]); smoking during the 3 months prior to pregnancy (<10 cigarettes/d, 10.0% stillbirths, 6.5% live births) (vs none; AOR, 1.55 [95% CI, 1.02-2.35]); obesity/overweight (15.5% stillbirths, 12.4% live births) (vs normal weight; AOR, 1.72 [95% CI, 1.22-2.43]); not living with a partner (25.4% stillbirths, 15.3% live births) (vs married; AOR, 1.62 [95% CI, 1.15-2.27]); and plurality (6.4% stillbirths, 1.9% live births) (vs singleton; AOR, 4.59 [95% CI, 2.63-8.00]). The generalized R(2) was 0.19, explaining little of the variance.
CONCLUSION:
Multiple risk factors that would have been known at the time of pregnancy confirmation were associated with stillbirth but accounted for only a small amount of the variance in this outcome.
Comment in
JAMA. 2011 Dec 14;306(22):2506-7.
4. JAMA. 2011 Dec 14;306(22):2459-68.
Causes of death among stillbirths.
Stillbirth Collaborative Research Network Writing Group.
Collaborators (16)
Source
Department of Obstetrics and Gynecology, University of Utah School of Medicine, 30 N 1900 E, Salt Lake City, UT 84132, USA.
Abstract
CONTEXT:
Stillbirth affects 1 in 160 pregnancies in the United States, equal to the number of infant deaths each year. Rates are higher than those of other developed countries and have stagnated over the past decade. There is significant racial disparity in the rate of stillbirth that is unexplained.
OBJECTIVE:
To ascertain the causes of stillbirth in a population that is diverse by race/ethnicity and geography.
DESIGN, SETTING, AND PARTICIPANTS:
A population-based study from March 2006 to September 2008 with surveillance for all stillbirths at 20 weeks or later in 59 tertiary care and community hospitals in 5 catchment areas defined by state and county boundaries to ensure access to at least 90% of all deliveries. Termination of a live fetus was excluded. Standardized evaluations were performed at delivery.
MAIN OUTCOME MEASURES:
Medical history, fetal postmortem and placental pathology, karyotype, other laboratory tests, systematic assignment of causes of death.
RESULTS:
Of 663 women with stillbirth enrolled, 500 women consented to complete postmortem examinations of 512 neonates. A probable cause of death was found in 312 stillbirths (60.9%; 95% CI, 56.5%-65.2%) and possible or probable cause in 390 (76.2%; 95% CI, 72.2%-79.8%). The most common causes were obstetric conditions (150 [29.3%; 95% CI, 25.4%-33.5%]), placental abnormalities (121 [23.6%; 95% CI, 20.1%-27.6%]), fetal genetic/structural abnormalities (70 [13.7%; 95% CI, 10.9%-17.0%]), infection (66 [12.9%; 95% CI, 10.2%-16.2%]), umbilical cord abnormalities (53 [10.4%; 95% CI, 7.9%-13.4%]), hypertensive disorders (47 [9.2%; 95% CI, 6.9%-12.1%]), and other maternal medical conditions (40 [7.8%; 95% CI, 5.7%-10.6%]). A higher proportion of stillbirths in non-Hispanic black women compared with non-Hispanic white and Hispanic ones was associated with obstetric complications (43.5% [50] vs 23.7% [85]; difference, 19.8%; 95% CI, 9.7%-29.9%; P < .001) and infections (25.2% [29] vs 7.8% [28]; difference, 17.4%; 95% CI, 9.0%-25.8%; P < .001). Stillbirths occurring intrapartum and early in gestation were more common in non-Hispanic black women. Sources most likely to provide positive information regarding cause of death were placental histology (268 [52.3%; 95% CI, 47.9%-56.7%]), perinatal postmortem examination (161 [31.4%; 95% CI, 27.5%-35.7%]), and karyotype (32 of 357 with definitive results [9%; 95% CI, 6.3%-12.5%]).
CONCLUSIONS:
A systematic evaluation led to a probable or possible cause in the majority of stillbirths. Obstetric conditions and placental abnormalities were the most common causes of stillbirth, although the distribution differed by race/ethnicity.
Comment in
JAMA. 2011 Dec 14;306(22):2506-7.
5. Pediatrics. 2012 Jan;129(1):e120-7. Epub 2011 Dec 12.
Prognostic models for stillbirth and neonatal death in very preterm birth: a validation study.
Schuit E, Hukkelhoven CW, Manktelow BN, Papatsonis DN, de Kleine MJ, Draper ES, Steyerberg EW, Vergouwe Y.
Source
PhD., The Netherlands Perinatal Registry, Mercatorlaan 1200, PO Box 8588, 3503 RN Utrecht, The Netherlands. chukkelhoven@perinatreg.nl.
Abstract
Objectives: To validate externally 2 prognostic models for stillbirth and neonatal death in very preterm infants who are either known to be alive at the onset of labor or admitted for neonatal intensive care. Patients And Methods: All infants, with gestational age 22 to 32 weeks, of European ethnicity, known to be alive at the onset of labor (n = 17 582) and admitted for neonatal intensive care (n = 11 578), who were born in the Netherlands between January 1, 2000, and December 31, 2007. The main outcome measures were stillbirth or death within 28 days for infants known to be alive at the onset of labor and death before discharge from the NICU for infants admitted for intensive care. Model performance was studied with calibration plots and c statistic. Results: Of the infants known to be alive at the onset of labor, 16.7% (n = 2939) died during labor or within 28 days of birth, and 7.8% (n = 908) of the infants admitted for neonatal intensive care died before discharge from intensive care. The prognostic model for infants known to be alive at the onset of labor showed good calibration and excellent discrimination (c statistic 0.92). The prognostic model for infants admitted for neonatal intensive care showed good calibration and good discrimination (c statistic 0.82). Conclusions: The 2 prognostic models for stillbirth and neonatal death in very preterm Dutch infants showed good performance, suggesting their use in clinical practice in the Netherlands and possibly other Western countries.
6. Clin Dev Immunol. 2012;2012:175041. Epub 2011 Sep 29.
Inflammatory cytokines in maternal circulation and placenta of chromosomally abnormal first trimester miscarriages.
Calleja-Agius J, Jauniaux E, Muttukrishna S.
Source
UCL EGA Institute for Women's Health, University College London, 86-96, Chenies Mews, London, WCIE 6HX, UK. jean.calleja-agius@um.edu.mt
Abstract
The impact of abnormal placental karyotype on the inflammatory response within the villous tissue and peripheral circulation of women with miscarriage was evaluated. Villous (n = 38) and venous blood samples (n = 26) were obtained from women with missed miscarriage. Tissue chromosome analysis indicated 23 abnormal and 15 normal karyotypes. Concentration of tumour necrosis factor alpha (TNFα), TNF-R1 and TNF-R2, and interleukin (IL)-10 were measured using flowcytometric bead array in fresh villous homogenate, cultured villous extracts, culture medium, maternal whole blood, and plasma. Plasma TNFα/IL-10 ratios were significantly (P < 0.05) lower in miscarriages with abnormal karyotype. In the abnormal karyotype group, there were significantly higher levels of TNFα (P < 0.01), IL-10 (P < 0.01), TNF-R1 (P < 0.001), and TNF-R2 (P < 0.001) in the villous extracts and culture-conditioned medium compared to normal karyotype group. In miscarriage with abnormal karyotype, there is an exacerbated placental inflammatory response, in contrast to miscarriage of normal karyotype where maternal systemic response is increased.
7. Ann Rheum Dis. 2012 Jan;71(1):61-6. Epub 2011 Sep 6.
Risk of thromboembolic events after recurrent spontaneous abortion in antiphospholipid syndrome: a case-control study.
Martinez-Zamora MA, Peralta S, Creus M, Tassies D, Reverter JC, Espinosa G, Cervera R, Carmona F, Balasch J.
Source
Correspondence to Juan Balasch, Institut Clínic of Gynecology, Obstetrics and Neonatology, Hospital Clínic, Villarroel, 170. 08 Barcelona, Spain; jbalasch@ub.edu.
Abstract
OBJECTIVE:
To investigate whether patients having antiphospholipid syndrome (APS) as the only aetiological factor for recurrent spontaneous abortion (RSA) are at increased risk of thrombosis later in life.
METHODS:
A case-control study at a tertiary university referral centre. The study group consisted of 57 primary APS and RSA women (APS-RSA group). Control groups included: 86 patients with RSA of unknown aetiology (uRSA group), 42 patients with RSA and thrombophilic genetic defects as the only aetiologic factor for RSA (tRSA group) and 30 antiphospholipid antibody (aPL) positive but otherwise healthy women (aPL group). The main measurement was the thrombosis rate after long-term follow-up.
RESULTS:
APS-RSA patients had a significantly higher 12-year cumulative thrombotic incidence rate compared with the three comparator groups (19.3% vs 4.8%, 0.0% and 0.0%, respectively (log rank), p<0.001). Patients in the APS-RSA group had 25.6 thrombotic events per 1000 patient-years (95% CI 12.8 to 45.9). The OR of thrombosis in relation to the presence (APS-RSA group) or absence (uRSA and tRSA groups) of aPL in patients with RSA was 15.06 (95% CI 3.2 to 70.5).
CONCLUSIONS:
Our data indicate that a history of RSA associated with aPL is a risk factor for subsequent thrombosis in the long term.
Prepared by the
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