The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Original Article
PreviousPrevious
Volume 334:821-827 March 28, 1996 Number 13
NextNext

The Relation of Transient Hypothyroxinemia in Preterm Infants to Neurologic Development at Two Years of Age
Mary Lynne Reuss, M.D., M.P.H., Nigel Paneth, M.D., M.P.H., Jennifer A. Pinto-Martin, Ph.D., John M. Lorenz, M.D., and Mervyn Susser, M.B., B.Ch., D.P.H.

 Sign up for free e-toc
 

This Article
-Full Text
- PDF

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
ABSTRACT

Background Transient hypothyroxinemia, a common finding in premature infants, is not thought to have long-term sequelae or to require treatment. We investigated whether hypothyroxinemia in premature infants is a cause of subsequent motor and cognitive abnormalities.

Methods In this historical cohort study, we retrieved blood thyroxine values, obtained on routine screening in the first week of life, from state screening records of children who weighed 2000 g or less at birth, who were born at 33 weeks' gestation or earlier, and who were enrolled in a population-based study of the late sequelae of neonatal brain hemorrhage. We investigated the relation of these values to the odds for disabling cerebral palsy among 463 subjects for whom data were available and to the mental-development score on the Bayley Scales of Infant Development or the Stanford–Binet Intelligence Scales for Children at the age of two years in 400 subjects. The effects of severe hypothyroxinemia, defined as a blood thyroxine value more than 2.6 SD below the mean for New Jersey newborns, were assessed before and after adjustment for gestational age and potentially confounding variables.

Results In analyses adjusted for gestational age, infants with severe hypothyroxinemia had a risk of disabling cerebral palsy that was nearly 11 times that of infants without hypothyroxinemia (odds ratio, 10.8; 95 percent confidence interval, 3.0 to 39.3) and a mean mental-development score at the age of two that was 15.4 points lower (95 percent confidence interval, 8.1 to 22.6 points) than the mean score of children with normal neonatal blood thyroxine concentrations. After adjustment for gestational age and multiple prenatal, perinatal, and early and late neonatal variables, severe hypothyroxinemia was still associated with an increased risk of disabling cerebral palsy (odds ratio, 4.4; 95 percent confidence interval, 1.0 to 18.6) and a reduction of nearly 7 points (95 percent confidence interval, 0.3 to 13.2 points) in the mental-development score.

Conclusions Severe hypothyroxinemia in preterm infants may be an important cause of problems in neurologic and mental development detected at the age of two years.


Source Information

From the Sergievsky Center (M.L.R., M.S.) and the Department of Obstetrics and Gynecology (M.L.R.), Columbia University, New York; the Program in Epidemiology (N.P.) and the Department of Pediatrics and Human Genetics (N.P., J.M.L.), the College of Human Medicine, Michigan State University, East Lansing; and the School of Nursing, University of Pennsylvania, Philadelphia (J.A.P.-M.).

Address reprint requests to Dr. Reuss at 2 Beach Ct., Saratoga Springs, NY 12866.

Full Text of this Article


This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.