Document Detail

The interrelationship of maternal stress, endocrine factors and inflammation on gestational length.
MedLine Citation:
PMID:  12775946     Owner:  NLM     Status:  MEDLINE    
Preterm birth rates continue to rise in the United States despite the advent of tocolytic agents and the identification of risk factors for preterm birth, such as vaginal infection and a shortened cervix. Although improvement in gestational-age-related survival of preterm infants has occurred as a result of the use of antenatal corticosteroids, neonatal surfactant therapy, and regionalization of perinatal care, there has been no reduction in the incidence of preterm birth. Recently, investigators have appreciated that the etiology of preterm birth is heterogeneous, perhaps accounting for one reason for the failure of current interventions to improve pregnancy outcome. Both abnormal maternal hormonal homeostasis and intrauterine inflammatory responses appear to contribute to a significant proportion of the cases of preterm birth, and the interaction of the maternal endocrine and immunologic systems may contribute to the pathophysiology of this condition. An important modulator of endocrine and immune function is perceived emotional and social stress. Maternal stress has been strongly associated with preterm birth, but the links between maternal stress and resultant aberrations of maternal endocrine and immune function remain difficult to quantify and investigate. However, new insights into the role of perceived maternal stress on gestational length suggest that specific interventions to alleviate stress could contribute to an increase in gestational length and a decrease in the risk for preterm birth. This review addresses the role of maternal stress on the regulation of maternal hormone and inflammatory responses and how aberrations in these systems may lead to preterm birth.
Roberta J Ruiz; Judith Fullerton; Donald J Dudley
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Obstetrical & gynecological survey     Volume:  58     ISSN:  0029-7828     ISO Abbreviation:  Obstet Gynecol Surv     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-05-30     Completed Date:  2003-10-01     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  0401007     Medline TA:  Obstet Gynecol Surv     Country:  United States    
Other Details:
Languages:  eng     Pagination:  415-28     Citation Subset:  IM    
Department of Family Nursing Care, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas 78229, USA.
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MeSH Terms
Cytokines / genetics
Endocrine System / physiopathology
Ethnic Groups
Gestational Age
Infant, Newborn
Infant, Premature
Inflammation / physiopathology
Obstetric Labor, Premature / ethnology,  immunology,  physiopathology*,  psychology
Polymorphism, Genetic
Social Support
Stress, Psychological
Reg. No./Substance:

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