Using umbilical cord tissue to detect fetal exposure to illicit drugs: a multicentered study in Utah and New Jersey.

OBJECTIVE: We assessed umbilical cord tissue as a means of detecting fetal exposure to five classes of drugs of abuse. STUDY DESIGN: In a multicentered study in Utah and New Jersey, we collected umbilical cord tissue when high-risk criteria were met for maternal illicit drug use. The deidentified umbilical cord specimens were analyzed for five drug classes: methamphetamine, opiates, cocaine, cannabinoids and phencyclidine. For each umbilical cord specimen, an enzyme-linked immunosorbent assay (ELISA)-based screening test was compared with a 'gold standard' test, consisting of gas or liquid chromatography tandem mass spectrometry. RESULT: A total of 498 umbilical cord samples were analyzed of which 157 (32%) were positive using mass spectrometric detection. The sensitivity and specificity of the ELISA-based test for each class of drugs tested were as follows: methamphetamine 97 and 97%, opiates 90 and 98%, cocaine 90 and 100%, cannabinoids 96 and 98% and phencyclidine (only 1 of the 498 umbilical cord sample was positive for phencyclidine) 100 and 100%. CONCLUSION: We judge that the performances of the ELISA-based tests are sufficient for clinical testing of fetal exposure to methamphetamine, opiates, cocaine and cannabinoids. Studies obtained on umbilical cord tissue can result in a more rapid return to the clinician than meconium testing, because waiting for meconium to be passed sometimes requires many days. Moreover, in some cases the meconium is passed in utero making collection impossible, whereas umbilical cord tissue should always be available for drug testing.

nNOS inhibitors attenuate methamphetamine-induced dopaminergic neurotoxicity but not hyperthermia in mice.

Methamphetamine (METH)-induced dopaminergic neurotoxicity is associated with hyperthermia. We investigated the effect of several neuronal nitric oxide synthase (nNOS) inhibitors on METH-induced hyperthermia and striatal dopaminergic neurotoxicity. Administration of METH (5 mg/kg; q. 3 h x 3) to Swiss Webster mice produced marked hyperthermia and 50-60% depletion of striatal dopaminergic markers 72 h after METH administration. Pretreatment with the nNOS inhibitors S-methylthiocitrulline (SMTC; 10 mg/kg) or 3-bromo-7-nitroindazole (3-Br-7-NI; 20 mg/kg) before each METH injection did not affect the persistent hyperthermia produced by METH, but afforded protection against the depletion of dopaminergic markers. A low dose (25 mg/kg) of the nNOS inhibitor 7-nitroindazole (7-NI) did not affect METH-induced hyperthermia, but a high dose (50 mg/kg) produced significant hypothermia. These findings indicate that low dose of selective nNOS inhibitors protect against METH-induced neurotoxicity with no effect on body temperature and support the hypothesis that nitric oxide (NO) and peroxynitrite have a major role in METH-induced dopaminergic neurotoxicity.