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Maternal Disease (maternal + disease)

Distribution by Scientific Domains

Medical Sciences	62%
Life Sciences	37%

Selected Abstracts

OPINION: Some Severe Maternal Diseases Might be Caused by Fetal-Versus-Maternal Disease (FVMD)

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010
Lei Yan
Citation Yan L, Zuo C, Wei D, Zhao X. Some severe maternal diseases might be caused by fetal-versus-maternal disease (FVMD). Am J Reprod Immunol 2010; 63: 189,192 Pregnancy-related disease is a common challenging clinical problem. From our review and clinical experience, we hypothesize that many severe pregnancy-related complications might be caused by a fetal-versus-maternal disease (FVMD), based on the fact that maternal disease is related to immunity and that fetal cells are present in maternal blood. Fetus is a semi-antigen and can be considered as a tumor or graft. The pathophysiology of FVMD must be complex. We speculate it to be a three-step process: impaired maternal immunological function, fetal T-cell activation and injury of target organs. More experiments and research will be needed to prove our hypothesis. [source]

Role of a fetal defence mechanism against oxidative stress in the aetiology of preeclampsia

HISTOPATHOLOGY, Issue 1 2009
Christoph Jan Wruck
Aims:, Increasing evidence suggests that oxidative stress may play a key role in the aetiology of preeclampsia (PE). The aim of this study was to elucidate the placental defence mechanisms employed against oxidative stress and, in particular, the specific role of nuclear factor erythroid 2-related factor 2 (Nrf2). Methods and results:, Expression of Nrf2 in third-trimester placental tissue was compared in preeclamptic and normal gestation-matched controls. PE was associated with increased Nrf2 activity within cytotrophoblastic nuclei. Nrf2 expression was restricted to proliferative and early post-proliferative cytotrophoblast only. Syncytiotrophoblast was immunonegative for Nrf2 in both controls and preeclamptic placentas. Conclusions:, Nrf2 is exclusively active within cytotrophoblast, strongly suggesting that these cells are the origin of Nrf2-dependent gene products. Syncytiotrophoblast is transcriptionally inactive; therefore in times of oxidative stress essential cytoprotective enzymes must be derived from the cytotrophoblast. Excessive cytotrophoblastic turnover causes disproportionate release of toxic placental factors, manifesting as PE and endangering maternal health. Increased cytotrophoblastic proliferation/fusion could thus be interpreted as a fetal defence mechanism, initiated in response to the requirements of vulnerable syncytiotrophoblast. We therefore propose a direct relationship between fetal defence against oxidative stress and consequent placental toxicity as part of the aetiology of this complex maternal disease. [source]

Diagnostic accuracy of verbal autopsies in ascertaining the causes of stillbirths and neonatal deaths in rural Ghana

PAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 5 2008
Karen M. Edmond
Summary This study evaluated the diagnostic accuracy of a verbal autopsy (VA) tool in ascertaining the causes of stillbirths and neonatal deaths in rural Ghana and was nested within a community-based maternal vitamin A supplementation trial (ObaapaVitA trial). All stillbirths and neonatal deaths between 1 January 2003 and 30 June 2004 were prospectively included. Community VAs were carried out within 6 months of death and were classified with a primary cause of death by three experienced paediatricans. The reference standard diagnosis was obtained by the study paediatrician in 4 district hospitals in the study area. There were 20 317 deliveries, 661 stillbirths and 590 neonatal deaths with a VA diagnosis in the study population. A total of 311 stillbirths and 191 neonatal deaths had both a VA and a hospital reference standard diagnosis. The VA performed poorly for stillbirth diagnoses such as congenital abnormalities and maternal haemorrhage. Accuracy was higher for intrapartum obstetric complications and antepartum maternal disease. For neonatal deaths, sensitivity was >60% for all major causes; specificity was 76% for birth asphyxia but >85% for prematurity and infection. Overall, VA diagnostic accuracy was higher than expected in this rural African setting. Our classification system was based on the expected public health importance of the individual causes of death, differing implications for intervention and the ability to distinguish between the individual causes in low-resource settings. We believe this system was easier to use than traditional approaches and resulted in high precision and accuracy. However, further simplifications are needed to allow use of the World Health Organisation VA in routine child health programmes. The diagnostic accuracy of the VA tool should also be assessed in other regions and in multicentre studies. [source]

Influence of maternal systemic lupus erythematosus on first-trimester combined screening for chromosomal abnormalities

PRENATAL DIAGNOSIS, Issue 7 2007
J. Heinig
Abstract Objective To explore the effect of maternal systemic lupus erythematosus (SLE) on first-trimester screening markers for Down syndrome. Methods A retrospective study was conducted on 1150 normal singleton fetuses that underwent first-trimester combined screening for Down syndrome. Fetal delta nuchal translucency (NT), maternal serum PAPP-A and free ,-hCG were compared between pregnancies with SLE (n = 10) and without preexisting maternal disease (n = 1140). Results The medians ± SD for delta NT, log10 MoM of PAPP-A and free ,-hCG ± SD in pregnancies with SLE and without maternal disease were , 0.18 ± 0.29 versus , 0.18 ± 0.33, 0.005 ± 0.32 versus 0.02 ± 0.26, and 0.22 ± 0.19 versus , 0.014 ± 0.28, with a p value of 0.7, 0.98 and 0.03, respectively. Conclusions Patients with preexisting SLE have increased maternal serum-free ,-hCG levels in the first-trimester. But, because of the multimodal procedure of risk calculation there is no significant difference in the screen-positive rate after the combined first-trimester screening for trisomy 21. Copyright © 2007 John Wiley & Sons, Ltd. [source]

OPINION: Some Severe Maternal Diseases Might be Caused by Fetal-Versus-Maternal Disease (FVMD)

Etiology, pathogenesis and prevention of neural tube defects

CONGENITAL ANOMALIES, Issue 2 2006
Rengasamy Padmanabhan
ABSTRACT Spina bifida, anencephaly, and encephalocele are commonly grouped together and termed neural tube defects (NTD). Failure of closure of the neural tube during development results in anencephaly or spina bifida aperta but encephaloceles are possibly post-closure defects. NTD are associated with a number of other central nervous system (CNS) and non-neural malformations. Racial, geographic and seasonal variations seem to affect their incidence. Etiology of NTD is unknown. Most of the non-syndromic NTD are of multifactorial origin. Recent in vitro and in vivo studies have highlighted the molecular mechanisms of neurulation in vertebrates but the morphologic development of human neural tube is poorly understood. A multisite closure theory, extrapolated directly from mouse experiments highlighted the clinical relevance of closure mechanisms to human NTD. Animal models, such as circle tail, curly tail, loop tail, shrm and numerous knockouts provide some insight into the mechanisms of NTD. Also available in the literature are a plethora of chemically induced preclosure and a few post-closure models of NTD, which highlight the fact that CNS malformations are of hetergeneitic nature. No Mendelian pattern of inheritance has been reported. Association with single gene defects, enhanced recurrence risk among siblings, and a higher frequency in twins than in singletons indicate the presence of a strong genetic contribution to the etiology of NTD. Non-availability of families with a significant number of NTD cases makes research into genetic causation of NTD difficult. Case reports and epidemiologic studies have implicated a number of chemicals, widely differing therapeutic drugs, environmental contaminants, pollutants, infectious agents, and solvents. Maternal hyperthermia, use of valproate by epileptic women during pregnancy, deficiency and excess of certain nutrients and chronic maternal diseases (e.g. diabetes mellitus) are reported to cause a manifold increase in the incidence of NTD. A host of suspected teratogens are also available in the literature. The UK and Hungarian studies showed that periconceptional supplementation of women with folate (FA) reduces significantly both the first occurrence and recurrence of NTD in the offspring. This led to mandatory periconceptional FA supplementation in a number of countries. Encouraged by the results of clinical studies, numerous laboratory investigations focused on the genes involved in the FA, vitamin B12 and homocysteine metabolism during neural tube development. As of today no clinical or experimental study has provided unequivocal evidence for a definitive role for any of these genes in the causation of NTD suggesting that a multitude of genes, growth factors and receptors interact in controlling neural tube development by yet unknown mechanisms. Future studies must address issues of gene-gene, gene-nutrient and gene,environment interactions in the pathogenesis of NTD. [source]