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Vol. 301, Issue 2, 594-598, May 2002
From the Division of Clinical Pharmacology and Experimental
Therapeutics, Medical Service, San Francisco General Hospital Medical
Center, the Departments of Medicine, Psychiatry, and Biopharmaceutical
Sciences, University of California, San Francisco, San Francisco,
California
Cigarette smoking is the foremost modifiable risk factor for adverse
pregnancy outcomes. Nicotine is a suspected fetal neuroteratogen. There
is concern that nicotine may achieve toxic levels during pregnancy if
nicotine replacement therapies are prescribed at doses used in the
nonpregnant state. Ten healthy, volunteer, pregnant smokers
received infusions of deuterium-labeled nicotine and cotinine during
pregnancy and again postpartum. From blood and urine measurements, the
following were determined: clearance (renal and nonrenal) of nicotine
and cotinine, clearance of nicotine via the cotinine pathway (an
indicator of CYP2A6 activity), and daily intake of nicotine from
smoking. The clearance of nicotine and cotinine was significantly
higher (60 and 140%, respectively), and the half-life of cotinine was
much shorter (8.8 versus 16.6 h, P < 0.01)
during pregnancy. Although plasma levels of cotinine were lower during
pregnancy (119 versus 202 ng/ml, P < 0.05), daily intake of nicotine from smoking was similar during pregnancy and postpartum. For a given level of intake, the pharmacologic and toxicologic effects of nicotine during pregnancy are anticipated to be
less than expected from nicotine metabolism data in nonpregnant women.
Our data indicate that no downward dose adjustment needs to be made for
nicotine replacement therapy during pregnancy. Conversely, higher than
usual doses of nicotine may be necessary to optimize efficacy. Lower
cotinine levels observed during pregnancy do not necessarily reflect
less smoke exposure, and cut-off levels used to classify nonsmokers,
passive smokers, and active smokers need to be established for pregnancy.
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