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Genetic Regulation of Surfactant Deficiency

NCT00828243 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 525

Last updated 2021-06-07

No results posted yet for this study

Summary

Inherited deficiencies in any one of 3 genes (surfactant protein B, surfactant protein C, and ATP-binding cassette transporter A3) can cause neonatal respiratory distress syndrome by disrupting metabolism of the pulmonary surfactant. The investigators will use state of the art methods to link specific changes in the genetic code of each of these genes with disruption of discrete steps in the metabolism of the pulmonary surfactant in human newborn infants. These studies will lead to improved diagnostic capabilities and suggest novel strategies to correct surfactant deficiency in newborn infants.

Conditions

  • Respiratory Distress Syndrome, Newborn

Interventions

DRUG

Nutrient

We administer stable isotopically labeled precursors of surfactant phospholipids (\[1-13C1\] acetate) and of surfactant protein-B (\[5,5,5-2H3\] leucine) to infants with neonatal respiratory distress syndrome. Using mass spectrometry, we measure incorporation of stable isotopically labeled precursors in tracheal aspirates and compare surfactant phospholipid and surfactant protein-B turnover.

Sponsors & Collaborators

  • National Heart, Lung, and Blood Institute (NHLBI)

    collaborator NIH

  • Washington University School of Medicine

    lead OTHER

Principal Investigators

  • F. S. Cole, M.D. · Washington University School of Medicine

Eligibility

Min Age
1 Day
Max Age
6 Months
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2007-11-30
Primary Completion
2013-03-31
Completion
2013-03-31
FDA Drug
Yes

Countries

  • United States

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT00828243 on ClinicalTrials.gov