Drug of Abuse, Opiates Confirmation, Urine
Detection and quantification of codeine, hydrocodone, oxycodone, morphine, hydromorphone, and oxymorphone in urine
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Codeine is converted by hepatic metabolism to morphine and norcodeine with a half-life of 2 to 4 hours. If codeine is ingested, the ratio of codeine to morphine generally exceeds 1.0 in urine during the first 24 hours. The ratio may fall below 1.0 after 24 hours and after 30 hours, only morphine may be detected.
Morphine is a naturally occurring narcotic analgesic obtained from the poppy plant, Papaver somniferum. Morphine is converted by hepatic metabolism to normorphine with a half-life of 2 to 4 hours. The presence of morphine in urine can indicate exposure to morphine, heroin, or codeine within 2 to 3 days. Ingestion of bakery products containing poppy seeds can also cause morphine to be excreted in urine. If excessively large amounts are consumed, this can result in urine morphine concentrations up to 2,000 ng/mL for a period of 6 to 12 hours after ingestion.
Hydrocodone exhibits a complex pattern of metabolism including O-demethylation, N-demethylation, and 6-keto reduction to the 6 beta hydroxymetabolites. Hydromorphone is a metabolite of hydrocodone. The presence of hydrocodone >100 ng/mL indicates exposure within 2 to 3 days prior to specimen collection.
Hydromorphone is metabolized primarily in the liver and is excreted primarily as the glucuronidated conjugate, with small amounts of parent drug and minor amounts of 6 hydroxy reduction metabolites. The presence of hydromorphone >100 ng/mL indicates exposure within 2 to 3 days prior to specimen collection. Hydromorphone is also a metabolite of hydrocodone; therefore, the presence of hydromorphone could also indicate exposure to hydrocodone.
Oxycodone is metabolized to noroxycodone, oxymorphone, and their glucuronides and is excreted primarily via the kidney. The presence of oxycodone >100 ng/mL indicates exposure to oxycodone within 2 to 3 days prior to specimen collection.
Oxymorphone is metabolized in the liver and excreted via the kidney primarily as the glucuronide conjugates. Oxymorphone is also a metabolite of oxycodone and, therefore, the presence of oxymorphone could also indicate exposure to oxycodone.
The detection interval for the opiates is generally 2 to 3 days after last ingestion.
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.
Positive cutoff concentrations
Codeine: <100 ng/mL
Hydrocodone: <100 ng/mL
Hydromorphone: <100 ng/mL
Morphine: <100 ng/mL
Oxycodone: <100 ng/mL
Oxymorphone: <100 ng/mL
This procedure reports the total urine concentration; this is the sum of the unconjugated and conjugated forms of the parent drug.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
This test detects drugs structurally similar to morphine. Other drugs in the opioid class such as fentanyl, meperidine, methadone, and opiate antagonists such as naloxone, are not detected.
The presence of meperidine in a very high concentration (overdose proportions) will result in a positive screen report. The liquid chromatography-tandem mass spectrometry report will be negative for opiates.
While 6-monoacetylmorphine (6-MAM) is metabolized to morphine, the presence of morphine alone is not sufficient evidence to prove heroin use. 6-MAM is the only definitive metabolite of heroin.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Hardman JG, Limbird LE, Gilman AG: Goodman and Gilman's. The Pharmacological Basis of Therapeutics. 10th edition. New York, McGraw-Hill, 2001, pp 569-619
2. Baselt RC: Disposition of Toxic Drugs and Chemicals in Man. Sixth edition. Foster City, CA, Biomedical Publications, 2002
3. Porter WH, Moyer TP: Clinical toxicology. In Tietz Fundamentals of Clinical Chemistry. Fifth edition. Edited by CA Burtis, ER Ashwood, Philadelphia, WB Saunders Company, 2001, pp 636-679