Amphetamine-Type Stimulants, Confirmation, Meconium
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Several stimulants and hallucinogens chemically related to phenylethylamine are referred to collectively as the amphetamine-type stimulants (amphetamines). Generally, this refers to the prescription and illicit amphetamines including amphetamine; methamphetamine; 3,4-methylenedioxymethamphetamine (Ecstasy, MDMA); 3,4-methylenedioxyamphetamine (MDA); and 3,4-methylenedioxyethylamphetamine (MDEA).(1) Methamphetamine has become a drug of choice among stimulant abusers because of its availability and ease to synthesize.
The metabolism of amphetamine consists of hydroxylation and deamination followed by conjugation with glucuronic acid. Methamphetamine is metabolized to amphetamine; both should be present in urine after methamphetamine use. Both MDMA and MDEA are metabolized to MDA.(1)
The disposition of drug in meconium is not well understood. The proposed mechanism is that the fetus excretes drug into bile and amniotic fluid. Drug accumulates in meconium either by direct deposit from bile or through swallowing of amniotic fluid.(2) The first evidence of meconium in the fetal intestine appears at approximately the 10th to 12th week of gestation, and slowly moves into the colon by the 16th week of gestation.(3) Therefore, the presence of drugs in meconium has been proposed to be indicative of in utero drug exposure during the final 4 to 5 months of pregnancy, a longer historical measure than is possible by urinalysis.(2)
Intrauterine drug exposure to amphetamines has been associated with maternal abruption, prematurity, and decreased growth parameters such as low-birth weight.(4) Some intrauterine amphetamine-exposed infants may develop hypertonia, tremors, and poor feeding and abnormal sleep patterns.(5)
Detection of in utero drug exposure up to 5 months before birth
The presence of any 1 of the following: amphetamine; methamphetamine; 3,4-methylenedioxyamphetamine; 3,4-methylenedioxymethamphetamine; or 3,4-methylenedioxyethylamphetamine at >50 ng/g is indicative of in utero exposure up to 5 months before birth.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Since the evidence of illicit drug use during pregnancy can be cause for separating the baby from the mother, a kit is available that includes all materials necessary to complete chain-of-custody to ensure that the test results are appropriate for legal proceedings.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
Positives are reported with a quantitative LC-MS/MS result.
Amphetamine by LC-MS/MS: >50 ng/g
Methamphetamine by LC-MS/MS: >50 ng/g
3,4-Methylenedioxyamphetamine by LC-MS/MS: >50 ng/g
3,4-Methylenedioxyethylamphetamine by LC-MS/MS: >50 ng/g
3,4-Methylenedioxymethamphetamine by LC-MS/MS: >50 ng/g
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Baselt RC: Disposition of Toxic Drugs and Chemical in Man. Edited by RC Baselt. Foster City, CA, Biochemical Publications, 2008:83-86;947-952;993-999
2. Ostrea EM Jr, Brady MJ, Parks PM, et al: Drug screening of meconium in infants of drug-dependent mothers: and alternative to urine testing. J Pediatr 1989;115:474-477
3. Ahanya SN, Lakshmanan J, Morgan BL, Ross MG: Meconium passage in utero: mechanisms, consequences, and management. Obstet Gynecol Surv 2005;60:45-56
4. Kwong TC, Ryan RM: Detection of intrauterine illicit drug exposure by newborn drug testing. National Academy of Clinical Biochemistry. Clin Chem 1997;43:235-242
5. Dixon SD: Effects of transplacental exposure to cocaine and methamphetamine on the neonate. West J Med 1989;150:436-442