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The use of fatty acid ethyl esters in neonatal hair to identify infants affected by prenatal alcohol exposure: a baseline study
Author(s) -
Caprara D. L.,
Klein J.,
Koren G.
Publication year - 2004
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2003.11.095
Subject(s) - in utero , meconium , prenatal alcohol exposure , fetal alcohol , fetus , alcohol , physiology , pregnancy , medicine , chemistry , obstetrics , biochemistry , biology , genetics
The identification of prenatal alcohol exposure is difficult due to the lack of a clear and consistent diagnostic marker. The usefulness of Fatty Acid Ethyl Esters (FAEE) as biomarkers for in utero alcohol exposure has been well established for meconium, however by extending the use of FAEE into neonatal hair, we can increase the window of detection for maternal drinking up to three months after birth. Using solid phase extraction and GC‐MS in CI mode, we have successfully developed and validated a method for the quantitative analysis of FAEE in hair that can discriminate between adult heavy drinkers and non‐drinkers. We now extend the use of this assay into neonatal hair. Baseline establishment for FAEE levels in neonatal hair is currently in progress to account for any endogenous FAEE levels found in the body. Hair samples were collected from non‐drinking mothers and their neonates and analyzed for FAEE. Low levels of selected FAEE were detected in neonatal samples of our preliminary baseline cohort (n=13; mean cumulative FAEE=0.709±0.805 pmol/mg). Detection limits ranged from 0.01 to 0.04 pmol/mg. A baseline for the quantitative analysis of FAEE in neonatal hair will help define a reliable positive screening cut‐off for in utero alcohol exposure. This novel neonatal hair test will aid a physician's ability to diagnose fetal alcohol spectrum disorder and provide intervention at stages where the effects of pre‐natal alcohol exposure can be minimized or prevented. Clinical Pharmacology & Therapeutics (2004) 75 , P25–P25; doi: 10.1016/j.clpt.2003.11.095

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