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Drugs of abuse array i (oral fluid) (forensic use only)

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Drugs of abuse array i (oral fluid) (forensic use only) B A T (evidence®) 4x90 (360 biochips) EV3613 POA
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Intended Use

The EvidenceDrugs of Abuse Array I Oral Fluid is used for in-vitro diagnostic tests for the qualitative determination of the parent molecule and metabolites of drugs in human oral fluid.

This product is for forensic use only.

The Evidence DOA I OF Array provides only a preliminary 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 preferred 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 preliminary 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 spread of diseases. It is very costly, with costs related to crimes, medical care, treatment and welfare programs for addicted individuals and wasted working hours (1). Oral fluid can provide a quick and non-invasive specimen for drug testing (2), with its usefulness as an aid in clinical diagnosis and for therapeutic drug monitoring now established (3). It offers the advantage of less potential for sample adulteration and substitution (2 )and in many cases drug in oral fluid represents the physiologically active fraction. Oral fluid testing has been successfully used as an alternative to blood testing in pharmacokinetic and pharmacotoxicologic studies (3).

Principle

The Evidence analyzer 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 immobilized 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 labeled 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 labeled with HRP and thus a reduction in the chemiluminescent signal 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. 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).

The DOA I OF array will qualitatively test for Amphetamine class (AMPH / MAMP), Barbiturates (BARB), Benzodiazepine class (BENZO 1 / BENZO 2), Cocaine (BZG), Methadone (MDONE), Opiates (OPIAT), Phencyclidine (PCP) and Cannabinoids (THC).

REFERENCES

1. Vetulani J. (2001) Drug addiction. PartI. Psychoactive substances in the past and presence. Pol. J. Pharmacol. 53(3):201-214.

2. Drummer O.H. (2006) Drug testing in oral fluid. Clin. Biochem. Rev. 27(3):147-159.

3. Schepers R.J., Oyler J.M., Joseph R.E. Jr, Cone E.J., Moolchan E.T. and Huestis M.A. (2003) Methamphetamine and amphetamine pharmacokinetics in oral fluid and plasma after controlled oral methamphetamine administration to human volunteers. Clin. Chem. 49(1):121-132.

 

Amphetamine Class Assay

Amphetamine (AMPH)

Methamphetamine (MAMP)

Intended Use

The Evidence amphetamine assays have been designed for use only on the Evidence analyzer for qualitative detection of the amphetamine class of compounds in oral fluid using a cut-off concentration of 50 ng/mL.

Clinical Significance

Amphetamines are synthetic drugs, which cause powerful central nervous system (CNS) stimulation resulting in euphoric effects similar to that of cocaine. They can also cause increased alertness, self-confidence and the ability to concentrate (1,2). They are potent sympathomimetic agents with a range of therapeutic applications for example; they can be used to treat mild depression, obesity, narcolepsy, and certain behavioural disorders in children (1,3). Isomeric forms of amphetamine and methamphetamine exist and the D-isomer (dextroamphetamine) is four times as potent as the L-isomer (2).

Abuse of amphetamines is a significant problem, although abuse of amphetamine is not widespread in the US, methamphetamine abuse is, and there has been much concern over 'ice', the solid form of methamphetamine (4). Amphetamine abusers can develop a tolerance for the drug, and the possibility of developing psychological dependence is significant (3). Chronic abuse of amphetamine can lead to weight loss, hallucinations and paranoid psychosis, while acute overdose can cause agitation, hyperthermia, convulsions, coma and respiratory and/or cardiac failure (2). Large quantities of illegally synthesized amphetamines are manufactured (1). Many amphetamine analogues from the illicit market of the 1960s have been reintroduced and new analogues have been synthesized and marketed for their increased potency, altered pharmacological effects and difficulty of detection (1,4).

MDMA (Methylenedioxy-methamphetamine), MDA (Methylenedioxyamphetamine) and MDEA (Methylenedioxyethylamphetamine) are synthetically modified amphetamines (2). MDMA is one of the most common amphetamine analogues on the illicit market. It was previously used as an adjunct to psychotherapy but it was placed on the schedule of controlled substances in 1988. Despite this, it still remains very popular as a recreational drug. MDMA is metabolized to MDA, another drug known for its central stimulant properties. (2,4). Amphetamines are usually taken orally, intravenously or by snorting (3). The half-life of amphetamines in humans is in the range 10 to 30 hours depending on the drug and the amount taken (5). The time course of methamphetamine and metabolite concentrations in oral fluid appears to follow a similar time course as in plasma (6). Studies have suggested that the disposition of methamphetamine in oral fluid is dose-proportional. Oral fluid concentrations of methamphetamine and metabolites have been found to be higher than plasma concentrations (6, 7).

Evidence performs two amphetamine class assays, based on d-amphetamine and methamphetamine in the form of two discrete test regions (DTR) on the Drugs of Abuse (DoA) biochip. By performing both tests simultaneously the main amphetamines, metabolites and analogues can be detected giving a more accurate indication of recent drug use.

Principle

The Evidence Amphetamine Class Assay is a competitive chemiluminescent immunoassay for the detection of amphetamines in oral fluid.

REFERENCES

1. Lee M-R, Yu S-C, Lin C-L and Yeh Y-Cia, Solid-phase extraction in Amphetamine and methamphetamine analysis of Urine, Journal of Analytical Toxicology, July/August 1997; 21: 278-282

2. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001; 783-788.

3. Hawks R L and Chiang C N, Urine Testing for Drugs of Abuse, NIDA Research Monograph, 1986; 73:

95-97

4. Cody J T, Detection of D, L-Amphetamine, D, L-Methamphetamine and illicit Amphetamine Analogs using Diagnostic Products Corporation's Amphetamine and Methamphetamine Radioimmunoassay, Journal of Analytical Toxicology, 1990; 14: 321-324

5. Albertson T.E., Derlet R.W. and Van Hoozen B.E. (1999) Methamphetamine and the expanding complications of amphetamines. West. J. Med. 170(4):214-219.

6. Huestis M.A. and Cone E.J. (2007) Methamphetamine disposition in oral fluid, plasma, and urine. Ann. N. Y. Acad. Sci. 1098:104-121.

7. Schepers R.J., Oyler J.M., Joseph R.E. Jr, Cone E.J., Moolchan E.T. and Huestis M.A. (2003) Methamphetamine and amphetamine pharmacokinetics in oral fluid and plasma after controlled oral methamphetamine administration to human volunteers. Clin. Chem. 49(1):121-132.

 

Barbiturate (BARB) Assay

Intended Use

The Evidence Barbiturate assay has been designed for use only on the Evidence analyzer for qualitative detection of barbiturates, in oral fluid using a cut-off of 20 ng/mL Phenobarbital.

Clinical Significance

Barbiturates are a class of around 12 compounds derivatised from barbituric acid. They are central nervous system (CNS) depressants and they can be used as sedatives, hypnotics, anaesthetics and anti-epileptic drugs (1). Barbiturates can be divided into three main groups according to their duration of action (2). The ultra-short-acting barbiturates are used clinically as anaesthetics, whilst the long-acting barbiturates have anti-convulsant properties (2). The short-acting compounds are typically used as hypnotics, particularly in patients already receiving barbiturates( 2). It is the short-acting barbiturates that are most favoured by drug abusers, due to their ability to reduce tension and produce a feeling of tranquility, without too much drowsiness (2). These include secobarbital, pentobarbital and amobarbital (2). The duration of action of short acting barbiturates is 3-6 hours (2).

Barbiturates have been subject to widespread abuse for their pleasurable intoxicating effects (3). For medical use barbiturates are generally administered orally, however, many drug users inject barbiturate in order to obtain a "rush" effect, disregarding the inherent risks of an overdose (3). An overdose of barbiturates leads to a dramatic fall in blood pressure and body temperature, depressed respiration and coma (1). Continued use of barbiturates can lead to the development of tolerance and withdrawal can be hazardous (1).

The short-acting barbiturates are extensively metabolized by the liver to more pharmacologically inactive hydroxylated compounds (1). Typical of short-acting barbiturates, secobarbital has a half-life of 19-34 hours, whereas long-acting barbiturate is much longer, e.g. phenobarbital has a half-life of about 24-140 hours (3). The free and total serum phenobarbital concentrations have been found to correlate closely with the concentrations in saliva (4, 5). Phenobarbital is the primary compound for detection by the Evidence Barbiturates assay.

Principle

The Evidence Barbiturate assay is a competitive chemiluminescent immunoassay for the detection of barbiturates in oral fluid.

REFERENCES

1. Widdop B. (2001) Chapter 37, Drugs of Abuse. In: Wild D. (ed), (2001) The Immunoassay Handbook, Second edition, Nature Publishing Group, London, Basingstoke, New York, 781-816.

2. Simpson D., Braithwaite R.A., Jarvie D.R., Stewart M.J., Walker S., Watson I.W. and Widdop B. (1997) Screening for drugs of abuse (II): cannabinoids, lysergic acid diethylamide, buprenorphine, methadone, barbiturates, benzodiazepines and other drugs. Ann Clin Biochem, 34(5):460-510.

3. Kwong T.C., Chamberlain R.T., Frederick D.L., Kapur B. and SunshineI. (1988) Critical Issues in Urinalysis of Abused Substances: Report of the Substance-Abuse Testing Committee. Clin. Chem. 34(3):605-632.

4. Shen D. (1989) [Saliva phenobarbital concentration in epileptics] Zhonghua Shen Jing Jing Shen Ke Za Zhi. 22(6):369-370, 382.

5. Tokugawa K., Ueda K., Fujito H. and Kurokawa, T. (1986) Correlation between the saliva and free serum concentration of phenobarbital in epileptic children. Eur. J. Pediatr. 145(5):401-402

 

Benzodiazepine (BENZ1 & BENZ2) Assay

Intended Use

The Evidence Benzodiazepine test has been designed for use on the Evidence analyzer for qualitative detection of benzodiazepine compounds, drugs with sedative and hypnotic effects, in oral fluid using a cut-off concentration of 1 ng/mL

Clinical Significance

The benzodiazepines are a group of over 20 structurally related central nervous system depressant drugs, each group varying considerably in their potency and clinical effects. The benzodiazepines are the most widely prescribed sedative/hypnotic drugs due to their wide range of uses (1,2,6). They are prescribed to treat anxiety, stress and insomnia. They are also used both as pre-medication and for induction of general anaesthesia. Most specific uses include the management of alcohol withdrawal, control of epileptic fits and relief of muscle spasms (3).

Benzodiazepines were first developed as hypnotic sedatives in the late 1960s and replaced the more problematic barbiturates, then associated with numerous overdoses (4). Benzodiazepines have the potential to elicit dependence and be abused, both in high doses and in low, therapeutic doses (5). They are taken because of their mood-altering properties and are known as 'downers' due to their ability to lessen the effects of opiate withdrawal and after-effects of ecstasy, amphetamine and LSD. However, chronic abuse leads to blurred vision, confusion, slow reflexes, slurred speech and hypotension(2). In spite of this, benzodiazepines are relatively safe drugs and have almost completely replaced the more toxic barbiturates.

Overdose and death are usually the result of the combination of benzodiazepine with other drugs or alcohol rather than taken alone (2,6).

Benzodiazepines are extensively metabolized by the liver by processes of N-dealkylation and hydroxylation followed by glucuronidation and only trace amounts of the parent compound are excreted. The most common metabolites are oxazepam and nordiazepam (2,5). Benzodiazepines are classified according to elimination half-life. Long-acting, intermediate and short-acting, and ultra-short acting benzoziazepines show half-lives exceeding 24 hours, between 5 and 24 hours, and less than 5 hours, respectively (7).

Evidence performs two benzodiazepine assays based on oxazepam and lorazepam, in the form of two discrete test regions (DTR) on the Drugs of Abuse (DoA) biochip. By performing both tests simultaneously the main benzodiazepines and their metabolites can be detected, giving a more accurate indication of recent drug use. Both results should be considered when identifying benzodiazepine preliminary positive samples.

Principle

The Evidence Benzodiazepine Class Assays are competitive chemiluminescent immunoassays for the detection of benzodiazepines in oral fluid.

REFERENCES

1. Beselt RC, Urine Drug Screening by Immunoassay: Interpretation of Results. In: Beselt RC, Advances in Analytical Toxicology, vol 1, chapter 5, 97-102.

2. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001; 790-793

3. Wolff K, Garretty D and Hay AWM, Micro-extraction of commonly abused benzodiazepines for urinary screening by liquid chromatography, Ann Clin Biochem, 1997; 34: 61-67

4. Garetty D J, Wolff K, Hay AWM and Raistrick D, Benzodiazepine misuse by drug addicts, 1997; 34: 68-73

5. Beck O, Lafolie P, Hjemdahl P, Borg S. Odelius G and Wirbing P, Detection of Benzodiazepine Intake in Therapeutic Doses by Immunoanalysis of Urine: Two Techniques Evaluated and Modified for Improved Performance, Clinical Chemistry, 1992; 38(2): 271-275

6. Simpson D, Braithwaite RA, Jarvie DR, Stward MJ, Walker S, Watson IW and Widdop B, Screening for drugs of abuse: II. Cannabinoids, lysergic acid diethylamide, buprenorphine, methadone, barbiturates, benzodiazepines and other drugs, Annals of Clinical Biochemistry, 1998; 34(5): 483-492

7. Greenblatt DJ, Shader RI, Divoll M, Harmatz JS. Benzodiazepines: a summary of pharmacokinetic properties. Br. J. Clin. Pharmacol. 1981; 11 Suppl 1:11S-16S.

 

Cocaine Metabolite (BZG) Assay

Intended Use

The Evidence Cocaine metabolite assay is intended for use on the Evidence analyzer for qualitative detection of cocaine in the form of the cocaine metabolite, benzoylecgonine, in oral fluid at a cut-off concentration of 20 ng/mL.

Clinical Significance

Cocaine is a potent psychoactive substance, also known as 'coke' and 'snow' and it is extracted from the leaves of the South American shrub Erythroxylon coca (1, 2). The Coca leaves are traditionally chewed or sucked resulting in a slow absorption of the drug and hence a slow onset of action. Cocaine hydrochloride is a fine powder that may be insufflated (snorted), producing quick absorption and onset of effects. Intravenous use leads to a quick and powerful but brief effect. 'Crack' is a freebase form of cocaine which when smoked produces an immediate 'high', with a more intense euphoria and so has become the choice for many users (1, 3, 4). Cocaine causes severe psychological dependence. The abuse of cocaine dramatically increased in the middle and late 1980s and it continues to receive much attention by federal and local law enforcement (4).

Cocaine is administered in small doses. It stimulates the central nervous system (CNS) and the resulting effects include; increased alertness, euphoria, sense of confidence and physical strength that may encourage risk-taking behaviour (2, 3). It can also have local anaesthetic properties and cause an increased blood pressure, heart rate and body temperature. The euphoric effects show rapid onset, however within an hour they wear off leaving anxiety, fatigue and depression (3). Chronic abuse and overdose of cocaine can cause acute cocaine intoxication, which can lead to profound CNS stimulation, resulting in seizures and cardiac arrest (3, 4). Cocaine is also used in combination with other recreational drugs such as heroin, which contributes to many cocaine-associated deaths (5).

In the body, cocaine is rapidly converted to metabolites by enzymatic and chemical processes. The two major metabolites of cocaine are benzoylecgonine (BZG) and ecgonine methyl ester( 5).

Principle

The Evidence Cocaine Metabolite assay is a competitive chemiluminescent immunoassay for the detection of Benzoylecgonine in oral fluid.

REFERENCES

1. Beselt RC, Urine Drug Screening by Immunoassay: Interpretation of Results. In: Beselt RC, Advances in Analytical Toxicology, vol 1, chapter 5, 112-116

2. Analytical Toxicology, vol 1, chapter 5, 81-123.

3. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001; 796-799.

4. Substance-Abuse Testing Committee, Critical issues in urinalysis of abused substances: report of the substance-abuse testing committee, Clin Chem, 1988; 34:605-32

5. Glass L R, Ingalls S T, Schilling C L and Hoppel C L, Atypical Urinary Opiate Excretion Pattern, Journal of Analytical Toxicology, October 1997; 21:509-514.

 

Methadone (MDONE) Assay

Intended Use

The Evidence methadone test has been designed for use only on the Evidence analyzer for qualitative detection of methadone, a narcotic pain-relieving drug, in oral fluid using a cut-off concentration of 5 ng/mL.

Clinical Significance

Methadone is a synthetic opioid analgesic, structurally related to Propoxyphene, and used clinically to decrease pain. Methadone was first synthesized as a substitute for morphine in Germany during the Second World War and has similar analgesic properties (1, 2).

Methadone is used in opioid withdrawal programs to replace the dependence of heroin, an illegal and short acting drug. Methadone being longer acting is taken to decrease the drug craving and the aim of the program is to help drug abusers to develop a lifestyle free of street drugs (4).

It is available in tablet and linctus form or as a solution for intramuscular injection. Methadone is prescribed on a wide scale and so there is danger of the drug finding its way into the street market of drug abusers (2, 5).

The side affects associated with methadone use can include physiological dependence, sedation, respiratory depression, respiratory failure and hypoxia. In cases of overdose this can cause coma, seizures, hypotension, and death (2-4).

Methadone is rapidly absorbed from the gastrointestinal tract and undergoes extensive metabolism in the liver. It is metabolized by mono- and di- N-demethylation to unstable metabolites that cyclise to give 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) and 2-ethyl-5-methyl-3,3-diphenylpyrroline (EMDP) (1, 2, 6). These metabolites are excreted in the urine and bile. The half-life of (R,S)-methadone is 15-60 hours, and 10-40 hours for (R)-methadone (7). It has been reported that oral fluid testing is as accurate as urinalysis in detecting the presence or absence of methadone (8). Levels of methadone in saliva have been found to be higher than in plasma with the salivary concentration well correlated to the methadone dose over a dosage range (9).

Unchanged methadone is the primary compound for detection by theEvidenceMethadone assay.

Principle

The Evidence Methadone assay is a competitive chemiluminescent immunoassay for the detection of methadone in oral fluid.

REFERENCES

1. Simpson D., Braithwaite R.A., Jarvie D.R., Stewart M.J., Walker S., Watson I.W. and Widdop B. (1997) Screening for drugs of abuse (II): Cannabinoids, lysergic acid diethylamide, buprenorphine, methadone, barbiturates, benzodiazepines and other drugs. Ann. Clin. Biochem. 34(5):460-510.

2. Widdop B. Drugs of Abuse. In: Wild D. (ed). The immunoassay handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001; 781-816.

3. Kwong T.C., Chamberlain R.T., Frederick D.L., Kapur B. and SunshineI. (1988) Critical issues in urinalysis of abused substances: Report of the Substance-Abuse Testing Committee. Clin. Chem. 34(3):605-632.

4. Anderson I.B. and Kearney T.E. (2000) Use of methadone. West. J. Med. 172(1):43-46.

5. Ling W. and Wesson D.R. (1990) Drugs of abuse - opiates. West. J. Med. 152(5):565-572.

6. Pohland A. and Boaz H.E., Sullivan H.R. (1971) Synthesis and identification of metabolites resulting from the biotransformation of DL-methadone in man and in the rat. J. Med. Chem. 14(3):194-197.

7. Couper F.J. and Logan B.K. Drugs and Human Performance Fact Sheets, Report from the National Highway Traffic Safety Administration, WashingtonDC. April 2004, page 55.

8. Bennett G.A., Davies E. and Thomas P. (2003) Is oral fluid analysis as accurate as urinalysis in detecting drug use in a treatment setting? Drug Alcohol Depend. 72(3):265-269.

9. Wolff K., Hay A. and Raistrick D. (1991) Methadone in saliva. Clin. Chem. 37(7):1297-1298.

 

Opiates (OPIAT) Assay

Intended Use

The Evidence Opiates test has been designed for use only on the Evidence analyzer for qualitative detection of opiates in oral fluid, using a cut-off concentration of 40 ng/mL. Qualitative results obtained can be utilized in the diagnosis and treatment of opiate use or overdose.

Clinical Significance

Morphine and codeine are opiates. They are narcotic analgesic drugs, obtained from the opium poppy. Morphine is one of the most popular analgesics for the control of severe pain. Heroin and hydrocodone are semi-synthetic derivatives of morphine and codeine but are more correctly classified as opioids. These drugs are potent central nervous system depressants with effects including; the relief from pain, a dream-like euphoric state, narcosis and apathy (1, 2).

Illicit opiate use remains a major problem. Continued use can lead to tolerance and physical dependence. Heroin is the most commonly abused derivative and it is 2-3 times more potent than morphine. With added acetyl groups it has better penetration across the blood-brain barrier than morphine. Addicts can take heroin either by intravenous injection, nasal insufflation ('snorting') or orally (2, 3).

Opiate poisoning can result in individuals suffering respiratory depression, pinpoint pupils and often deep coma. Overdose by intravenous injection can result in death within a few minutes(2). Results from a study monitoring opiate use in substance-abuse treatment patients indicated that oral fluid testing was highly sensitive for detecting opiate usage (5). The Evidence Opiates assay is directed towards morphine.

Principle

The Evidence Opiates assay is a competitive chemiluminescent immunoassay for the detection of opiates in oral fluid.

REFERENCES

1. Beselt RC, Urine Drug Screening by Immunoassay: Interpretation of Results. In: Beselt RC, Advances in Analytical Toxicology, vol 1, chapter 5, 112-116

2. Analytical Toxicology, vol 1, chapter 5, 81-123.

3. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001; 796-799.

4. Substance-Abuse Testing Committee, Critical issues in urinalysis of abused substances: report of the substance-abuse testing committee, Clin Chem, 1988; 34:605-32

5. Dams R., Choo R.E., Lambert W.E., Jones H. and Huestis M.A. (2007) Oral fluid as an alternative matrix to monitor opiate and cocaine use in substance-abuse treatment patients. Drug Alcohol Depend. 87(2-3):258-267.

 

Phencyclidine (PCP) Assay

Intended Use

The Evidence Phencyclidine test has been designed for use only on the Evidence analyzer for qualitative detection of phencyclidine in oral fluid, using a cut-off concentration of 10 ng/mL.

Clinical Significance

Phencyclidine, 1-phenylcyclohexylpiperidine, is also known as PCP and "Angel dust" (1). The drug was developed in the 1950s as an intravenous anaesthetic (2). Although legitimately used in veterinary medicine as a tranquiliser (3), it has never been approved for human use (2) because of its post-operative hallucinations, agitation and mental disturbances. A combination of its euphoric and hallucinogenic properties, together with an ease of synthesis from readily available chemicals has resulted in PCP of varying purity being obtainable illicitly. The many effects of PCP are variable, unpredictable, and depending on the amount used include euphoria, relaxation, stimulation, sensations of weightlessness and increased strength, visual and auditory distortions, anxiety, panic, bizarre illusions and amnesia. In addition paranoia is seen which can provoke violent behaviour (4). Chronic abuse of PCP can lead to memory loss, depression, and a psychosis that recurs on exposure to the drug (3). Deaths have also been reported after use, however, these may be due to associated irrational behaviour, rather than to the toxic effects of the drug (2, 4).

PCP is used by smoking with tobacco or marijuana, nasal insufflation ('snorting'), intravenous injection and oral ingestion (3, 5). The effect of PCP may vary with dose, the user's settings and previous experiences with PCP (3).

The Evidence Phencyclidine Assay, tests for the parent molecule, 1-phenylcyclohexylpiperidine. Few substances cross-react with PCP in immunoassays (6).

Principle

The Evidence Phencyclidine Assay is a competitive chemiluminescent immunoassay for the detection of phencyclidine in oral fluid.

REFERENCES

1. Couper F.J. and Logan B.K. Drugs and Human Performance Fact Sheets, Report from the National Highway Traffic Safety Administration, WashingtonDC. April 2004, page 79.

2. National Institute of Drug Abuse, NIDA InfoFacts: PCP (Phencyclidine).

3. Widdop B. Drugs of Abuse. In: Wild D. (ed). The immunoassay handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001; 781-816.

4. Kwong T.C., Chamberlain R.T., Frederick D.L., Kapur B. and SunshineI. (1988) Critical Issues in Urinalysis of Abused Substances: Report of the Substance-Abuse Testing Committee. Clin. Chem. 34(3):605-632.

5. McCarron M.M., Walberg C.B., Soares J.R., Gross S.J. and Baselt R.C. (1984) Detection of phencyclidine usage by radioimmunoassay of saliva. J. Anal. Toxicol. 8(5):197-201.

6. Walberg CB, Gupta RC, Quantification of phencyclidine in urine by enzyme immunoassay, J Anal Toxicol, 1982; 6: 97-9.

 

Cannabinoids (THC) Assay

Intended Use

The Evidence Cannabinoids test has been designed for use only on the Evidence analyzer for qualitative detection cannabinoids in oral fluid, using a cut-off of 4 ng/mL.

CLINICAL SIGNIFICANCE

The Cannabinoids are a group of more than 60 C-21 compounds found in the plant, Cannabis sativa (1). The active ingredient in Cannabinoids is (-)D(9)-tetrahydrocannabinol (THC). THC produces effects of euphoria, sedation and an altered time sense (2, 3). Cannabinoids can be used in the treatment of various medical conditions, including glaucoma, asthma, multiple sclerosis and as an anti-emetic in patients undergoing cancer chemotherapy (3, 6).

Marijuana is one of the most commonly used illegal substances in the United States and in many countries around the world (5). As a 'street' drug it is sold primarily as hashish (the plant resin) or marijuana (flowering tops of the female plant). Pure THC is almost never available on the 'black market' (1, 3). The primary route of illicit consumption of cannabis is by smoking in cigarettes or pipes. It can also be ingested in cakes and confectionery and hashish oil (the most potent form) can be taken intravenously. An overdose of THC can cause hallucinations, coma and death (2,)(3).

The illicit use of marijuana as a recreational drug has led to the wide development of methods to detect if an individual has been using the drug (5). The time after marijuana use during which a positive test may result depends on the route of administration, potency of THC, frequency of use and sample matrix type (1). Unlike urine testing, oral fluid detection times start almost immediately after drug exposure - especially after smoking (4, 7).

For oral fluid analysis, the primary target is the parent D9-THC compound.

PRINCIPLE

The Evidence Cannabinoid Assay is a competitive chemiluminescent immunoassay for the detection of cannabinoids in oral fluid.

REFERENCES

1. Substance-Abuse Testing Committee. Critical issues in Urinalysis of abused substances: report on the substance-abuse testing committee. Clin Chem, 1988; 34: 605-32.

2. Schuckit MA, Drug and Alcohol Abuse; A clinical guide to Diagnosis and Treatment, fifth edition, Kluwer Academic/Plenum Publishers, 2000; 11-12.

3. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001; 793-796.

4. Verstraete AG, Detection times of drugs in blood, urine and oral fluid. Ther. Drug Monit. Apr 2004: 26.

5. Huestis M A, Mitchell J M and Cone E J, Detection Times of Marijuana Metabolites in Urine by Immunoassay and GC-MS, October 1995; 19: 443-449.

6. Huffman J W, Zhang X, Wu M, Joyner H H and Pennington W T, Synthesis of (±) - 11-Nor-9-carboxy-D9-tetrahydrocannabinol: New Synthetic Approaches to Cannabinoids, J. Org. Chem. (1991), 56; 1481-1489.7.

7. Drummer OH, Drug testing in oral fluids. Clin. Biochem. Rev. Aug 2007:27.