Drugs of abuse array ii

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The Evidence Drugs of Abuse Array II (DOA II) Assays are in-vitro diagnostic tests for the qualitative determination of the parent molecule and metabolites of drugs in human urine. They are competitive enzyme immunoassays run on the automated biochip array analyser, Evidence.

The Evidence DOA assays provide only a pliminary analytical test result. A more specific alternative chemical method must be used to obtain a confirmed analytical result. Gas Chromatography/mass spectrometry (GC/MS) is the pferred confirmatory method (1). Other chemical confirmation methods are available. Clinical consideration and professional judgement should be applied to any drug of abuse test result, particularly when pliminary positive results are used.

CLINICAL SIGNIFICANCE

Drug abuse in any form gives rise to serious negative consequences not only for the abuser by devastating their mental and physical health, but also to the whole of society. It is an indirect and direct cause of many crimes and also in the spad of diseases. It is very costly, with costs related to crimes, medical care, treatment and welfare programs for addicted individuals and wasted working hours. Also attracting nationwide attention is the steadily rising problem of pscription drug abuse by the general public and in patients suffering chronic pain. Urine drug testing is a tool that can be used to detect drug users and to monitor compliance of subjects in recovery programs(2-4).

PRINCIPLE

The Evidence analyser is a fully automated Biochip Array System. It performs simultaneous detection of multiple analytes from a single patient sample. The core technology is the Randox Biochip, a solid-state device containing an array of discrete test regions containing immobilised antibodies specific to different DOA compound classes. A competitive chemiluminescent immunoassay is employed for the DOA assays with the drug in the specimen and drug labelled with horseradish peroxidase (HRP) being in direct competition for the antibody binding sites. Increased levels of drug in a specimen will lead to reduced binding of drug labelled with HRP and thus a reduction in chemiluminescence being emitted.

The light signal generated from each of the test regions on the biochip is detected using digital imaging technology and compared to that from a stored calibration curve. A normalised value is calculated as a percentage of the signal intensity emitted from the cut-off point on the calibration curve relative to the signal intensity emitted from the sample test region.

Samples producing a response value greater than, or equal to, the response value of the calibrator cut-off are considered positive (normalised result ≥100).

Samples producing a response value less than the response value of the calibrator cut-off are considered negative (normalised result <100).

REFERENCES

1. Hawks RL. Analytical Methodology from Urine Testing for Drugs of Abuse, National Institute on Drug Abuse (NIDA), Research Monograph, 1986; 73:30-41.

2. Vetulani, J. (2001) Drug addiction. PartI. Psychoactive substances in the past and psence. Pol J Pharmacol. 53(3): 201-14.

3. Manchikanti, L. (2006) pscription drug abuse: what is being done to address this new drug epidemic? Testimony before the Subcommittee on Criminal Justice, Drug Policy and Human Resources. Pain Physician. 9(4): 287-321.

4. Saxon AJ, Calsyn DA, Haver VM, Delaney CJ. (1988) Clinical evaluation and use of urine screening for drug abuse. West J Med. 149(3): 296-303.

5. NCCLS, Urinalysis and Collection, Transportation, and pservation of Urine Specimens: Approved Guidelines, December 1995: vol 15.

 

Bupnorphine (BUP) Assay

INTENDED USE

The Evidence Bupnorphine (BUP) Assay has been designed for use only on the Evidence analyser for the qualitative detection of bupnorphine in urine using a cut-off concentration of 2ng/mL.

CLINICAL SIGNIFICANCE

Bupnorphine is a highly lipophylic derivative of thebaine(1) and is a powerful partial agonist analgesic(1,2). It is effective in treating pain and is 25 to 40 times more potent than morphine. Since the 1980s it has been widely pscribed for the treatment of moderate to severe pain and in anaesthiology for pmedication and/or anaesthetic induction(2). Soon after bupnorphine became clinically available there were reports of abuse as it was frequently used as the drug of choice when there was a shortage of heroin supplies(1). Studies then showed that when bupnorphine was used for opiate dependence treatment the withdrawal syndrome on discontinuing bupnorphine was milder than methadone and that fewer symptoms emerge during detoxification with bupnorphine. Therefore bupnorphine hydrochloride in a sublingual tablet was developed and registered for opiate dependence treatment. Another sublingual pparation contains naloxone as well as bupnorphine. The naloxone is added to the bupnorphine to pvent diversion and abuse(3). In the United Kingdom General Practice doctors are able to pscribe bupnorphine for opiate dependence treatment with initial supervised consumption. Once the patient is thought to be sufficiently stable take home doses can be given (4). However, this is not the case in all countries, as in France sublingual tablets may be ordered by any physician, supplied by any pharmacist with supervised consumption not required(2). There is potential for misuse of the sublingual tablets by intravenous injection and it has been reported that in France this has happened regularly in 10-15% of the cases with irregular use in as many as 20-30% of patients. The Misuse of Drugs Act 1971 has defined Bupnorphine as a Class C drug and it falls within Schedule III of the Misuse of Drugs Regulations2001(4).

PRINCIPLE

The Evidence Bupnorphine Assay is a competitive chemiluminescent immunoassay for the detection of bupnorphine in urine.

REFERENCES

1. Debrabandere, L., Van Boven, M. and Daenens, P. (1995) Development of a fluoroimmunoassay for the detection of bupnorphine in urine. J Forensic Sci. 40(2): 250-3.

2. Cirimele, V., Kintz, P., Lohner, S. and Ludes, B. (2003) Enzyme immunoassay validation for the detection of bupnorphine in urine. J Anal Toxicol. 27(2): 103-5.

3. Euro-Methwork Quest for Quality Bupnorphine critical questions examined. (Rev. 17-Oct-05) (http://www.q4q.nl/methwork/BPN/bpn.htm)

4. Guidance for the use of bupnorphine for the treatment of opioid dependence in primary care. SMMGP. RoyalCollege of General Practitioners. (Rev. 2nd Ed. 2004) (http://www.smmgp.org.uk/download/guidance/guidance010.pdf)

 

Ketamine (KET) Assay

INTENDED USE

The Evidence Ketamine (KET) Assay has been designed for use only on the Evidence analyser for qualitative detection of the ketamine in urine using a cut-off concentration of 75 ng/mL.

CLINICAL SIGNIFICANCE

Ketamine was first synthesized in 1962 and subsequently marketed as an anaesthetic drug for human and animal use(1,2). It is a dissociative medical anaesthetic agent that is structurally and pharmacologically similar to phencyclidine (PCP)(3). Although less toxic than PCP, ketamine possesses similar hallucinogenic properties at sub-anaesthetic doses(1). Unlike other anaesthetics ketamine stimulates rather than depsses the cardiovascular system and has comparatively mild respiratory depssant effects. As it possesses bronchodilator activity ketamine can also be used on emergency room patients in status asthmaticus. In Canada ketamine is the sole anaesthetic agent in some short duration surgical procedures. It is also used for the induction of anaesthesia prior to the administration of other general anaesthetic agents or to supplement low potency anaesthetics (3). Ketamine became a drug of abuse shortly after it was introduced to clinical use(1) and is becoming increasingly popular especially as a 'club drug' at 'rave' parties(2,3). The illicit popularity of ketamine is due to its induction of dream-like hallucinations and floating sensations which give an 'out of body' experience(4). Ketamine has also been used as a date-rape drug as it produces sedation, stupor and memory impairment in the victim(2). It has a very short half-life and rapid clearance so abusers administer sequential doses. Routes of administration for abusers include insufflation, intramuscular and intravenous injection(3). In the United States the Drug Enforcement Agency have placed Ketamine into Schedule III of the Controlled Substances Act(4,5).

PRINCIPLE

The Evidence Ketamine Assay is a competitive chemiluminescent immunoassay for the detection of ketamine in urine.

REFERENCES

1. Lua, A.C. and Lin, H.R. (2004) A rapid and sensitive ESI-MS screening procedure for ketamine and norketamine in urine samples. J Anal Toxicol. 28(8): 680-4.

2. Negrusz, A., Adamowicz, P., Saini, B.K., Webster, D.E., Juhascik, M.P., Moore, C.M. and Schlemmer, R.F. (2005) Detection of ketamine and norketamine in urine of nonhuman primates after a single dose of ketamine using microplate enzyme-linked immunosorbent assay (ELISA) and NCI-GC-MS. J Anal Toxicol. 29(3): 163-8.

3. Lalonde, B.R. and Wallage, H.R. (2004) Postmortem blood ketamine distribution in two fatalities. J Anal Toxicol. 28(1): 71-4.

4. Rofael, H.Z. and Abdel-Rahman, M.S. (2002) Development and validation of a high-performance liquid chromatography method for the determination of cocaine, its metabolites and ketamine. J Appl Toxicol. 22(2): 123-8.

5. Code of Federal Regulations; Title 21 - Food and Drugs; Volume 9, Chapter II - Drug Enforcement Administration, Department of Justice; Part 1308 - Schedules of Controlled Substances; Section 13 - Schedule III. (21CFR1308.13).

 

Lysergic acid diethylamide (LSD) Assay

INTENDED USE

The Evidence Lysergic acid diethylamide (LSD) assay has been designed for use only on the Evidence analyser for qualitative detection of LSD in urine using a cut-off concentration of 500 pg/mL.

CLINICAL SIGNIFICANCE

Lysergic acid diethylamide (LSD) is a highly potent hallucinogenic drug(1). It was first synthesized in 1938 from lysergic acid which was derived from ergot, a fungus found growing wild on rye and other grasses(2,3). In the 1950s and 1960s it was used in the United States and United Kingdom on mentally ill patients and also unsuccessfully by the US military as a 'truth drug'. By the 1960s LSD was being abused so much that it was made illegal in the UK in 1966 with medical use also being stopped and prohibited by the Misuse of Drugs Act when it came into force in 1973(3). LSD is usually sold in the form of impgnated paper but can also be in tablets, thin squares of gelatine or sugar cubes and rarely in liquid form(2). The effects of LSD are unpdictable, and may vary with the amount taken, the user's personality, mood, expectations and surroundings in which the drug is taken(1). Devastating psychological effects can be experienced by some users during a trip which can persist after the trip has ended producing a long-lasting psychotic-like state(4). LSD is not considered an addictive drug but it does produce tolerance, which means users who take the drug repeatedly must take progressively higher doses. This is extremely dangerous due to the unpdictability of the drug(1). Although LSD use has varied over the years it is still a significant drug of abuse(2). A sensitive method of detection of LSD in body fluids of users is required as the typical dose is very small and the metabolism rapid and extensive(5,6).

PRINCIPLE

The Evidence LSD Assay is a competitive chemiluminescent immunoassay for the detection of LSD in urine.

REFERENCES

1. NIDA InfoFacts on LSD (18-Apr-07) (http://www.drugabuse.gov/infofacts/lsd.html)

2. US Drug Enforcement Administration LSD Information (18-Apr-07) (http://www.usdoj.gov/dea/concern/lsd_factsheet.html)

3. DrugScope (UK's leading independent centre of expertise on drugs - LSD information (http://www.drugscope.org.uk/druginfo/drugsearch/ds_results.asp?file=\wip\11\1\1\lsd.html) (18-Apr-07)

4. NIDA Research Report Series - Hallucinogens and dissociative drugs (Vers. Mar-01) (http://www.nida.nih.gov/ResearchReports/Hallucinogens/Hallucinogens.html)

5. Li, Z., McNally, A.J., Wang, H. and Salamone, S.J. (1998) Stability study of LSD under various storage conditions. J Anal Toxicol. 22(6): 520-5.

6. Wiegand, R.F., Klette, K.L., Stout, P.R. and Gehlhausen, J.M. (2002) Comparison of EMIT II, CEDIA, and DPC RIA assays for the detection of lysergic acid diethylamide in forensic urine samples. J Anal Toxicol. 26(7): 519-23.

 

3,4 methylenedioxymethamphetamine (MDMA) Assay

INTENDED USE

The Evidence 3,4 methylenedioxymethamphetamine (MDMA) assay has been designed for use only on the Evidence analyser for qualitative detection of the MDMA in urine using a cut-off concentration of 500ng/mL.

CLINICAL SIGNIFICANCE

3,4 methylenedioxymethamphetamine (MDMA) is a ring substituted analogue of amphetamine commonly referred to as Ecstasy(1,2). It was first synthesized in 1914 as an anorectic but was never marketed as such because of its side-effects. During the 1970s psychotherapists became interested in using MDMA as a therapeutic agent as it was reported to produce a pleasant state of introspection and reduced anxiety which would facilitate the therapeutic process. Widespad abuse of the drug began in the early 1980s(2) and in 1988 MDMA became a Schedule I controlled substance under Federal Controlled Substances Act(1). At low doses Ecstasy produces euphoria, increased self-awareness and an increased sense of trust with higher doses thought to be hallucinogenic. Toxic effects include anxiety, depssion, tachycardia, elevated blood pssure, cardiac arrhythmias, pupil dilation and sleep disorders(2). Many deaths associated with Ecstasy use have been reported. Many of these deaths have resulted from hyperpyrexia brought on by high levels of exertion, high ambient temperatures and inadequate fluid intake. Death from Ecstasy use has also been attributed to sudden cardiac arrest, suicide, acute intoxication and accident secondary to Ecstasy use(2). Ecstasy is usually ingested in tablet form but can also be crushed and snorted or injected(3). Psychotherapists have again become interested in using MDMA as a therapeutic agent and it was reported in 2002 that the FDA and the Spanish Ministry of Health have concluded that the risk/benefit ratio is favourable under certain circumstances for clinical studies investigating MDMA assisted psychotherapy. Worldwide these studies are the only ones into therapeutic use of MDMA(4). In the UK Ecstasy is a Class A drug under the Misuse of Drugs Act(5).

PRINCIPLE

The Evidence MDMA Assay is a competitive chemiluminescent immunoassay for the detection of MDMA in urine.

REFERENCES

1. US Drug Enforcement Administration MDMD (Ecstasy) Information. (Rev. Aug 06) (http://www.usdoj.gov/dea/concern/mdma.html)

2. Kunsman, G.W., Levine, B., Kuhlman, J.J., Jones, R.L., Hughes, R.O., Fujiyama, C.I. and Smith, M.L. (1996) MDA-MDMA concentrations in urine specimens. J Anal Toxicol. 20(7): 517-21.

3. MDMA (Ecstasy) US DEA Office of Diversion Control Information. (http://www.deadiversion.usdoj.gov/drugs_concern/mdma/mdma.htm) (Rev. Jun 06)

4. Doblin, R. (2002) A clinical plan for MDMA (Ecstasy) in the treatment of posttraumatic stress disorder (PTSD): partnering with the FDA. J Psychoactive Drugs. 34(2): 185-94.

5. Home Office Website, Misuse of Drugs Act (http://www.drugs.gov.uk/drugs-laws/misuse-of-drugs-act/) (18-Apr-07)

 

Methaqualone (MTQ) Assay

INTENDED USE

The Evidence Methaqualone (MTQ) Assay has been designed for use only on the Evidence analyser for qualitative detection of the methaqualone in urine using a cut-off concentration of 300ng/mL.

CLINICAL SIGNIFICANCE

Methaqualone is one of the most potent quinazolines(1), first synthesized in 1951 and introduced in Europe in 1956. It was marketed in the United States in 1965(2) as a safe barbiturate substitute(3), with nonaddictive sedative-hypnotic properties(2). As early as 1966 there were reports of both physical and psychological dependence(4). By 1972 abuse of methaqualone in the US had reached epidemic proportions(2). Abuse of methaqualone in the US at this time was called 'luuding out' and involved taking the methaqualone orally with alcohol. Apart from sedative hypnotic properties methaqualone has anti-convulsant, antispasmodic, anaesthetic and antihistamine actions(1). At therapeutic dosages it can produce a sensual, euphoric state and a relaxed intimate mood(2). When used excessively it leads to tolerance dependence and withdrawal symptoms(3). As the addictive nature of methaqualone became clear it was withdrawn from many developed markets and was made a Schedule I drug in the US in 1984(1,3). Since 1973 the oral use of methaqualone as a drug of abuse has decreased dramatically in western countries(2). However the practice of smoking methaqualone is a serious public health problem in South Africa, other parts of Africa and India. When smoked the methaqualone is combined with cannabis and tobacco in a process called 'white pipe' giving rise to an intensely euphoric rush(1). The South African Police Service report that the production, trafficking, and abuse of methaqualone are of particular forensic importance to South Africa as it remains the synthetic drug of choice amongst South African drug abusers(5).

PRINCIPLE

The Evidence Methaqualone Assay is a competitive chemiluminescent immunoassay for the detection of methaqualone in urine.

REFERENCES

1. McCarthy, G., Myers, B. and Siegfried, N. (2005) Treatment for methaqualone dependence in adults. Cochrane Database Syst Rev. (2):CD004146.

2. Peat, M.A. and Finkle, B.S. (1980) Determination of methaqualone and its major metabolite in plasma and saliva after single oral doses. J Anal Toxicol. 4(3): 114-8.

3. US Drug Enforcement Administration Glutethimide & Methaqualone Information (18-Apr-07) (http://www.dea.gov/concern/glutethimide.html)

4. Brenner, C., Hui, R., Passarelli, J., Wu, R., Brenneisen, R., Bracher, K., ElSohly, M.A., Ghodoussi, V.D. and Salamone, S.J. (1996) Comparison of methaqualone excretion patterns using Abuscreen ONLINE and EMIT II immunoassays and GC/MS. Forensic Sci Int. 79(1): 31-41.

5. South African Police Service Department of Safety and Security Background Information on Methaqualone (18-Apr-07) (http://www.saps.gov.za/drugs/drugs/bground.htm)

 

Fentanyl (FENT) Assay

INTENDED USE

The Evidence Fentanyl (FENT) assay has been designed for use only on the Evidence analyser for qualitative detection of the fentanyl in urine using a cut-off concentration of 1ng/mL.

CLINICAL SIGNIFICANCE

Fentanyl was first synthesized in Belgium in the late 1950s and in the 1960s was introduced into medical practice as an intravenous anaesthetic. Other analogues of fentanyl have been synthesized and introduced into medical practice with fentanyls now being extensively used in anaesthesia and analgesia(1). Fentanyl is a synthetic opioid, a specific μ-agonist and as an analgesic it has approximately 80 times the potency of morphine. Fentanyl in high doses causes euphoria, marked muscular rigidity and respiratory depssion(2). In view of the fact that the effects of acting fentanyls are indistinguishable from those produced by nasal inhalation of street heroin, except that fentanyl is much more potent, fentanyl has high abuse potential(3). Illicit pharmaceutical use of fentanyl appeared first in the mid-1970s primarily in the medical professions and continues to be a problem in the United States(1). A number of deaths have been reported with a fentanyl transdermal patch that is used for chronic pain management(4). In the late 1970s fentanyl appeared in the illicit drug market with over 12 different analogues of fentanyl having been produced clandestinely and identified in the US drug traffic(1). These fentanyl analogues can be sold as synthetic heroine or China white(2). Intravenous administration is most commonly used but fentanyl can also be smoked or snorted(1).

PRINCIPLE

The Evidence Fentanyl Assay is a competitive chemiluminescent immunoassay for the detection of fentanyl in urine.

REFERENCES

1. US Drug Enforcement Administration Fentanyl Information (18-Apr-07) (http://www.dea.gov/concern/fentanyl.html)

2. Ruangyuttikarn, W., Law, M.Y., Rollins, D.E. and Moody, D.E. (1990) Detection of fentanyl and its analogs by enzyme-linked immunosorbent assay. J Anal Toxicol. 14(3): 160-4.

3. Skulska, A., Kala, M. and Parczewski, A. (2005) Fentanyl and its analogues in clinical and forensic toxicology. Przegl Lek. 62(6):581-4.

4. Raymond, B. and Morawiecka, I. (2004) Transdermal fentanyl (Duragesic): respiratory arrest in adolescents. Canadian Adverse Reaction Newsletter 14(4):1-2.

 

Oxycodone 1, 2 (OXYC1 and 2) and Generic Opioids (OPDS) Assays

INTENDED USE

The Evidence Oxycodone 1, 2 (OXYC1 and 2) and Generic Opioids (OPDS) Assays have been designed for use only on the Evidence analyser for qualitative detection of oxycodone in urine using a cut-off concentration of 100ng/mL.

CLINICAL SIGNIFICANCE

Oxycodone is a semi-synthetic opioid structurally related to other members of the opioid class(1) and derived from the opium alkaloid thebaine (2). It has both analgesic and anti-tussive properties(3) and has been used for the treatment of moderate to severe postoperative or cancer related pain(4). In analgesic potency it is comparable to morphine with its most dangerous potential side-effect being respiratory depssion. It causes respiratory depssion by direct action on brain stem respiratory centres(2). Oxycodone is classified in the United Kingdom under the Misuse of Drugs Act as a Class A drug and as Schedule II in the United States(5). It has been marketed as a slow release formulation called OxyContin® and in the US OxyContin® is the most commonly pscribed Schedule II controlled narcotic. US researchers reported that 6.9 million pscriptions for OxyContin® were written from May 2000 to May 2001(3,6). Abuse of oxycodone has been an issue in the United States since the 1960s but the recent exponential increase in the number of addicts has been linked to the widespad availability of OxyContin®. Oxycodone causes activation of μ-receptors which causes euphoria and analgesia and when the slow-release polymer of OxyContin® is destroyed a heroin like high can be achieved. Fatalities due to oxycodone overdose are usually due to respiratory depssion to the level of respiratory arrest. In 2002 the Drug Abuse Warning Network survey identified oxycodone abuse as a major contributor to overdose death throughout the United States(6,7,8). Hydromorphone which is detected by the Generic Opioids assay is a semi-synthetic opioid agonist and a hydrogenated ketone of morphine(9). It is about 8 times more potent than morphine and since it was first introduced into clinical practice it has been used to treat cancer pain and post-operative pain. It is a useful alternative to morphine in patients who have adverse side effects with morphine such as nausea, sedation and myoclonus. Hydromorphone hydrochloride is five times more water soluble than morphine sulphate which is important when concentrated pparations or small delivery volumes are required(10). All hydromorphone products are Schedule II of the Controlled Substance Act(11) and Schedule 2 on the Misuse of Drugs Act 1971(12). Hydromorphone like other Schedule II opioids has high abuse and dependence potential and produces tolerance(13). It is much sought after by narcotic addicts and is usually obtained by the abuser through fraudulent pscriptions and theft. The tablets are often dissolved and injected as a substitute for heroin(11).

Oxycodone is N-demethylated to noroxycodone, and O-demethylated in the psence of the cytochrome P450 2D6 enzyme to produce oxymorphone(1). The oxycodone 1, oxycodone 2 andGeneric Opioids assays are standardised to oxycodone, each showing 100% specificity to oxycodone. In addition to specificity to oxycodone the oxycodone 1 assay also shows specificity to Noroxycodone and hydrocodone and Generic Opioids assay shows specificity to hydromorphone, hydrocodone and codeine.

PRINCIPLE

The Evidence Oxycodone 1,2 and Generic Opioids Assays are competitive chemiluminescent immunoassays for the detection of oxycodone in urine.

REFERENCES

1. Baldacci, A., Caslavska, J., Wey, A.B. and Thormann, W. (2004) Identification of new oxycodone metabolites in human urine by capillary electrophoresis-multiple-stage ion-trap mass spectrometry. J Chromatogr A. 1051(1-2): 273-82.

2. Le, N.L., Reiter, A., Tomlinson, K., Jones, J. and Moore, C. (2005) The detection of oxycodone in meconium specimens. J Anal Toxicol. 29(1): 54-7.

3. Moore, K.A., Ramcharitar, V., Levine, B. and Fowler, D. (2003) Tentative identification of novel oxycodone metabolites in human urine. J Anal Toxicol. 27(6): 346-52.

4. Poyhia, R., Seppala, T., Olkkola, K.T. and Kalso, E. (1992) The pharmacokinetics and metabolism of oxycodone after intramuscular and oral administration to healthy subjects. Br J Clin Pharmacol. 33(6): 617-21.

5. Drugscope Oxycodone Information (http://www.drugscope.org.uk/druginfo/) (18-Apr-07)

6. Abadie, J.M., Allison, K.H., Black, D.A., Garbin, J., Saxon, A.J. and Bankson, D.D. (2005) Can an immunoassay become a standard technique in detecting oxycodone and its metabolites? J Anal Toxicol. 29(8): 825-9.

7. Narconon pscription drug rehabilitation information (http://www.pscription-drug-rehab.com/narconon_program01.html) (18-Apr-07)

8. "Oxycodone explained" by Luke Skrebowski, The Observer, Sunday March 24(th) 2002.

9. Murray, A. and Hagen, N.A. (2005) Hydromorphone. J Pain Symptom Manage. 29 (5 Suppl): S57-66

10. Zheng, M., McErlane, K.M. and Ong, M.C. (2002) Hydromorphone metabolites: isolation and identification from pooled urine samples of a cancer patient. Xenobiotica. 32(5): 427-39

11. US Drug Enforcement Administration Briefs & Background Internet Information on Hydromorphone (18-Apr-07) (http://www.dea.gov/concern/hydromorphone.html)

12. UK Home Office Website, Controlled Drugs List. (Rev. 27-Jan-06) (http://www.drugs.gov.uk/publication-search/drug-licences/controlled-list)

13. US Drug Enforcement Administration Office of Diversion Control Drugs and Chemicals of Concern Hydromorphone (Rev. Jun-06) (http://www.deadiversion.usdoj.gov/drugs_concern/hydromorphone.htm)

 

Propoxyphene (PPX) Assay

INTENDED USE

The Evidence Propoxyphene (PPX) Assay has been designed for use only on the Evidence analyser for qualitative detection of propoxyphene in urine using a cut-off concentration of 300 ng/mL.

CLINICAL SIGNIFICANCE

Dextropropoxyphene, which is usually called propoxyphene, was first marketed in 1957 under the trade name of Darvon(® 1,2). It is a synthetic opiate with mild analgesic properties and structurally related to methadone(3). Propoxyphene does not seem to have any significant antipyretic, anti-inflammatory or anti-tussive actions(2) with its oral analgesic potency one-half to one-third that of codeine. It is reported that more than 100 tonnes of propoxyphene are produced in the US annually and more than 30 million pscriptions are written for the products(1). As propoxyphene is so widely pscribed it is prone to abuse. Propoxyphene by itself or in conjunction with other drugs or alcohol can be toxic and is associated with a large number of fatalities(4). Overdose can result in stupor, coma, convulsions, respiratory depssion, cardiac arrhythmias, hypotension, pulmonary oedema and circulatory collapse. It is among the most commonly encountered drugs associated with emergency department visits(2). The United States Drug Enforcement Administration report that propoxyphene is among the top 10 drugs reported by medical examiners in drug abuse deaths(1). Propoxyphene deaths occur rapidly and have been reported to have occurred in as little as twice the therapeutic blood level(3). Oral ingestion is the most common route of administration in abuse and peak plasma levels occur within 1-2 hours after a single oral dose(4).

PRINCIPLE

The Evidence Propoxyphene Assay is a competitive chemiluminescent immunoassay for the detection of propoxyphene in urine.

REFERENCES

1. US Drug Enforcement Administration Propoxyphene (18-Apr-07) (http://www.dea.gov/concern/dextroproxyphene.html)

2. Poklis, A., Poklis, J.L., Tarnai, L.D. and Backer, R.C. (2004) Evaluation of the Triage PPY on-site testing device for the detection of dextropropoxyphene in urine. J Anal Toxicol. 28(6): 485-8.

3. K-Pharm Research and Consulting Review of Propoxyphene Products for Inclusion within Alberta's Triplicate pscription Program August 29, 2003. (http://www.cpsa.ab.ca/collegeprograms/attachments_tpp/Propoxyphene%20Report.pdf)

4. Wu, R.S., McNally, A.J., Pilcher, I.A., Salamone, S.J. and Rashid, S. (1997) Synthesis of new d-propoxyphene derivatives and the development of a microparticle-based immunoassay for the detection of propoxyphene and norpropoxyphene. Bioconjug Chem. 8(3): 385-90.

 

Creatinine (dilution marker in urine)

INTENDED USE

The Evidence Dilution Marker Creatinine-CREAT Assay has been designed for use only on the Evidence analyser for qualitative detection of the creatinine in urine using a cut-off concentration of 20 mg/dL.

CLINICAL SIGNIFICANCE

Creatinine is psent in all body secretions and is a by-product of muscle metabolism, formed by a spontaneous and irreversible conversion from creatine and creatine phosphate. The formation of creatinine is proportional to total muscle mass, and approximately to body weight. The production rate shows minimal daily variations, unless the muscle mass changes, with 2% of whole body creatine being transformed every 24 hours. (1)

Since creatinine is excreted at a relatively constant rate, measurement of urinary creatinine can indicate if the urinary concentration has been adjusted by in vivo or in vitro dilution. (3) Measurement of creatinine can be useful in drug screen urine analysis to detect false negative samples, as the ingestion of large volumes of fluid can dilute the concentration of a drug to a point below a level determined to be positive (2, 3). A creatinine value < 20 mg/dL should be used as a cut off, to evaluate the urine and the validity of the drug screening result (4). A level below this indicates that the sample may be falsely negative (4).

PRINCIPLE

The Evidence Dilution Marker Assay is a competitive chemiluminescent immunoassay for the detection of creatinine in urine.

REFERENCES

1. Spenser K; Analytical reviews in clinical biochemistry: the estimation of creatinine; Annals of Clinical Biochemistry; 23: 1-25 (1986).

2. Lafolie P, Beck O, Blennow G, et al; Importance of creatinine analyses of urine when screening for abused drugs, Clinical Chemistry; 37/11: 1927-1931 (1991).

3. Needleman S. B., Porvaznik M, Ander D; Creatinine analysis in single collection urine specimens, Journal of Forensic Sciences; 37/4: 1125-1133 (1992).

4. Frazer A.D., Zamecnik J., Keravel J., McGrath L., Wells J.; Experience with urine drug testing by the Correctional Service of Canada, Forensic Science International; 121(1-2): 16-22 (2001).