Drug Treatment of Addictive Diseases

Release Date: November 1, 2011

Expiration Date: November 30, 2013


Jennifer A. Tilleman, PharmD, FASCP
Assistant Professor of Pharmacy Practice

Edward M. DeSimone II, RPh, PhD, FAPhA
Professor of Pharmacy Sciences

Elizabeth A. Kirby, PharmD Candidate
Creighton University School of Pharmacy and
Health Professions, Omaha, Nebraska


Dr. Tilleman, Dr. DeSimone, and Ms. Kirby have no actual or potential conflict of interest in relation to this activity.

Postgraduate Healthcare Education, LLC does not view the existence of relationships as an implication of bias or that the value of the material is decreased. The content of the activity was planned to be balanced, objective, and scientifically rigorous. Occasionally, authors express opinions that represent their own viewpoint. Conclusions drawn by participants should be derived from objective analysis of scientific data.


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Credits: 2.0 hours (0.20 ceu)
Type of Activity: Knowledge


This accredited activity is targeted to pharmacists. Estimated time to complete this activity is 120 minutes.

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Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients' conditions and possible contraindications or dangers in use, review of any applicable manufacturer's product information, and comparison with recommendations of other authorities.


To review the causes, neurobiological changes, and medication used in the treatment of substance-use and addictive disorders.


After completing this activity, the participant should be able to:

  1. Identify characteristics of addiction.
  2. Describe the goals of treatment and obstacles to efficacy.
  3. Identify pharmacologic treatments for substance-use and addictive disorders.
  4. Provide effective counseling to patients regarding medication used in the treatment of substance-use and addictive disorders.

An estimated 22.5 million individuals in the United States were diagnosed with substance abuse or dependence in 2009, according to the Substance Abuse and Mental Health Services Administration (SAMHSA). Of this number, an estimated 15.4 million were dependent on or abused alcohol alone, 3.9 million were dependent on or abused illicit drugs alone, and 3.2 million were dependent on or abused both alcohol and illicit drugs.1 The illicit drugs with the highest rate of abuse in 2009 were marijuana, pain relievers, and cocaine, at 4.3, 1.9, and 1.1 million, respectively. An increase was seen in pain reliever abuse or dependence from 1.5 million in 2002, with marijuana remaining constant and cocaine decreasing from 1.5 million.1 The estimated annual total cost in the U.S. related to substance abuse exceeds $600 billion. This includes productivity, health care, and crime-related costs associated with illicit drugs ($181 billion), tobacco ($193 billion), and alcohol ($235 billion). These estimates do not include the effects on individuals and families related to family dysfunction, employment loss, education, domestic violence, or child abuse.2 Currently, there are only five drugs approved for the treatment of alcohol and opiate dependence.

Addiction as a Disease

There is a growing body of support for the concept that addiction to drugs and alcohol is a disease.3 According to the disease model, an organ has a defect that produces signs and symptoms of a disease. For example, in stroke, a cerebral blood vessel (organ) has a defect (blood clot) that produces signs and symptoms (slurred speech, confusion, numbness or weakness in extremities). In alcoholism, the brain (organ) has a defect (neurobiological changes) that produces signs and symptoms (craving for alcohol, excessive drinking, fatty liver).

As research on addictive disorders continues to grow, numerous causes have been identified: heredity (genetics); a defect in the reward system of the brain (involving the neurotransmitter dopamine); a defect in the brain’s memory system (involving the neurotransmitter glutamate); and stress (involving corticotrophin-releasing factor [CRF]).3 These four causes are not necessarily independent but together contribute to the development of addiction. In addition, a number of coexisting psychiatric disorders (e.g., attention-deficit disorder and bipolar disorder) have also been associated with addiction. It is commonly accepted by addiction specialists that addiction to drugs and/or alcohol is not a matter of willpower.4 For purposes of this article, the use of the word drug in reference to drugs of abuse shall also include alcohol unless specifically noted otherwise.

Etiology of Addiction

There are five levels of drug use: experimentation, recreational/social, habituation, abuse, and addiction (TABLE 1).5 In many cases, the path to addiction begins with either pleasure-seeking or a desire for relief of physical or psychological pain. A search often ensues for a substance or activity that provides relief from the pain or emotional emptiness. But when this substance is used, the relief is short-lived since the underlying reason for the drug use remains. Therefore, substance use must be repeated to gain relief again. This cycle involves a continuous ebb and flow between the various levels of use. Individuals move through these levels at differing rates, although some individuals never progress to addiction. During this process, the user may experience several phenomena (TABLE 2). The first of these is tolerance, a state in which increasingly larger doses of a substance must be taken in order to obtain the effects experienced with the original dose. Some examples of drugs that produce tolerance are opiates, amphetamines, and alcohol. The next is physical dependence, which can be described as a physiological adaptation to the chronic use of a substance with the precipitation of a withdrawal syndrome if the substance is abruptly stopped. As drug use continues over time, physiological or, more properly, neurochemical changes occur in the brain to accommodate this drug use. This means that when the user stops or just reduces the amount of a drug ingested, a substance-specific syndrome occurs that causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.6 This can range from simple headaches due to caffeine withdrawal to more than 20 different problems such as diarrhea, rhinitis, muscle cramps, and much more due to opiate withdrawal. The physically dependent person needs to continue to use the drug in order to prevent this withdrawal from occurring. The third change is psychological dependence, which can be described as emotional and mental preoccupation with a substance and a persistent craving for this substance by the user in order to reach a maximum level of functioning or feeling of well-being. The psychologically dependent person believes that he or she needs the drug in order to function normally.



Most drugs of abuse produce tolerance, almost all drugs of abuse can produce physical dependence (marijuana and hallucinogenic drugs such as LSD are a few of the exceptions), and all drugs of abuse can produce psychological dependence.

An intense neurologic craving that must be satisfied without regard to the costs involved starts to develop. This craving, along with tolerance and the need to prevent the effects associated with withdrawal, propels the abuser along a spiraling downward path into addiction. Deterioration of relationships, finances, employment, and health also begins to occur as use increases. Yet the abuse usually continues. This is the nature of addiction.


An individual’s predisposition to addiction may result from a genetic predisposition. Multiple genes affecting receptors, transcription factors, enzymes, and neuropeptides have been identified and implicated in drug and alcohol dependence. Predisposition to addiction is related to the number and types of genes that an individual possesses.7 For example, the dopamine D2 receptor gene A1 allele (DRD2A1), resulting in a reduced number of dopamine receptors, has been associated with alcoholism, cocaine addiction, and polydrug use. A CYP450 2D6 (CYP2D6) polymorphism has been associated with opiate addiction.5


Environmental influences, particularly stress, during the first 20 years of life, affect the development of brain circuitry, changing the brain’s reaction to outside influences. The experiences during the first 10 years of life are the most influential; however, the prefrontal cortex, where decision-making and impulse-control behaviors are controlled, is not fully developed until the early 20s. The neurochemical encoding of events, especially emotionally intense and repeated events (stress), creates strong memories that are easily recalled. These memories can also include the coping mechanisms or counterbehaviors that children learn to use to deal with emotional pain, stress, or abuse.8 Stress causes the release of CRF, which in turn reduces the number of dopamine (D2) receptors when stress becomes chronic.3 Because of this, the individual finds that there is reduced pleasure after using the addictive substance.9

Reward System

Use of psychoactive substances activates the brain’s reward circuitry through the release of dopamine, glutamate, gamma-aminobutyric acid (GABA), and other neurotransmitters. These circuitry systems are involved in reward and motivation, memory and learning, and inhibitory control over behavior. The increased release of dopamine and other neurotransmitters results in feelings of euphoria. Once thought to be the primary neurotransmitter involved in the process of “liking” a drug, dopamine has recently been identified as the neurotransmitter involved in “wanting” the drug.9 Continued exposure to psychoactive substances leads to a decreased production of endogenous dopamine and its receptors, requiring greater amounts of the substance to obtain the desired effect. Ironically, the user goes from “liking” the drug to ”wanting” the drug over time.

Memory System

When the reward system is activated and pleasure is experienced, the brain at its most primitive level recognizes this as an important event related to survival similar to eating and having sex. The effect is remembered and the individual is motivated to repeat the experience. Glutamate plays a role in memory encoding of the experience associated with this rewarding encounter.10 This is why drug “cues” such as smelling smoke, hearing the clink of ice cubes, seeing someone drink, or even talking about drug use can precipitate relapse even years after the last dose of a drug has been consumed.10 Dopamine and glutamate appear to work together as a memory-reward system.

Addiction is a chronic brain disease characterized by craving, loss of control, giving up previously pleasurable activities or relationships, spending a large amount of time in activities related to obtaining, using, and recovering from the substance, and compulsion to continue use regardless of negative consequences.11 The interaction of neurotransmitters, genes, environmental factors, especially stress, and the permanent neurochemical changes in the brain are responsible for making relapse a common part of recovery. Therefore, recovery from addiction is a continuous and lifelong process.


There are numerous obstacles to effective treatment of addiction. One of these is getting an individual into a treatment program. The 2009 National Survey on Drug Use and Health indicates reasons why individuals failed to enter treatment even though they recognized a need for help and made an effort to receive treatment. The most often reported reasons among those using illicit drugs or alcohol are related to lack of health coverage and not being ready to stop using at the time.1 Other obstacles are retention in in-patient treatment programs (28-180 days), adherence to treatment regimens including counseling and behavioral therapy, lack of a support system, and relapse.

The initial step in any addiction treatment program is realizing there is a need for help and taking action to obtain that help. The realization may come independently by the individual, or it may be the result of an intervention by family, friends, a coworker, an employer, a health care provider, or the legal system. Once help is sought, a treatment plan can be developed. There are numerous treatment methods for addiction, and a plan must be tailored to the needs of the individual. The treatment program must help the individual stop the addictive behavior, regain control over his or her life, and learn to cope with cravings and triggers to avoid relapse. To be effective, a treatment program should include some form of counseling, either individual or group, and behavioral therapy. The needs of the whole individual must be addressed, not just the use of the addictive substance or activity. Participation in a 12-step program can aid in recovery and in relapse prevention.

Treatment of Opiate Addiction

The term opiate refers to naturally occurring opium alkaloids (codeine and morphine) or their semisynthetic derivatives (e.g., heroin, hydrocodone, and oxycodone). The term opioid refers to synthetic agents that exert opium-like effects (e.g., meperidine and fentanyl). The term opiate will be used unless a specific clinical distinction is necessary.

Three medications have been approved for treatment of opiate addiction (TABLE 3). These are methadone, naltrexone, and buprenorphine. Methadone and buprenorphine can be used during the detoxification process and for maintenance treatment. Naltrexone, an opiate antagonist, is used in maintenance therapy to block the effects of opiates. The treatment of opiate addiction must be tailored to the specific needs of each patient with doses titrated to prevent withdrawal symptoms, craving, and relapse. Specific regulatory requirements exist for the dispensing and prescribing of methadone and buprenorphine for the treatment of opiate addiction (TABLE 4).



Methadone: Methadone, a mu-opiate receptor agonist, was approved by the FDA in 1947. It is a Schedule II narcotic approved for the treatment of severe pain, opiate agonist dependence, and opiate agonist withdrawal. Methadone has a slow onset of action of 30 to 60 minutes after oral dosing and a long duration of action with an elimination half-life of 8 to 59 hours. The advantages of methadone are that it can be administered orally, has once-a-day dosing, and has no euphoric effects when taken as prescribed as compared to other opiate agonists. Analgesia, respiratory depression, miosis (constriction of the pupils), reduced gastrointestinal motility, and physical dependence are still seen clinically. Tolerance to these effects generally occurs after several days of continuous treatment. Due to methadone’s extended duration of action, respiratory depressant effects may peak later and last longer than other effects. Methadone is metabolized primarily by CYP450 isoenzymes. Because of this, there are more than 100 drugs (CYP450 inducers and inhibitors) that produce a severe/ major drug interaction with methadone.32 Methadone is used as replacement therapy. Due to the cross-dependence between opiates, the physical dependence is transferred from the opiate of abuse to methadone.

Caution must be exercised during initiation of therapy regarding dose titration, conversion from one opiate to another, and concurrent use of central nervous system (CNS) depressants to avoid respiratory depression. A black box warning has been issued for methadone regarding cardiac effects, respiratory depression, and death. The cardiac effects include QT interval prolongation and torsades de pointes, a ventricular tachycardia that may lead to hemodynamic instability and potentially fatal ventricular fibrillation. Concurrent use of highdose methadone with other psychoactive drugs, especially cocaine, presents an increased mortality risk from torsades.12 The most frequent adverse effects seen with methadone include increased sweating, sleep disorders, nausea, and other withdrawal symptoms.13

Methadone has been shown effective when patients are retained in a treatment program. An estimated 67% will decrease illicit use of opiates, 61% will decrease HIV risk behaviors, and 58% will decrease their drugand nondrug-related criminal behavior.14 Methadone is used during detoxification to control withdrawal symptoms. The dose should be titrated to the patient’s response without causing sedation. With methadone’s extended half-life, steady state may not be achieved for at least 5 days. During maintenance treatment, continued dosage titration is required to reduce craving, block euphoric effects from any other opiates, and achieve tolerance to methadone’s sedating effects. This indicates a need for customization of therapy to the individual patient and continued monitoring. Some individuals will require long-term therapy, while others may discontinue treatment. Gradual tapering is required upon discontinuation of methadone, and the patient should be appropriately counseled regarding the possibility of relapse.

Buprenorphine (Subutex): Buprenorphine is a mixed opiate agonist-antagonist. It is a Schedule III narcotic, which can only be prescribed under the conditions set forth in the Drug Addiction Treatment Act of 2000.15 The FDA has approved the injectable and transdermal formulations for the treatment of moderate or severe pain, while the sublingual formulation is approved for the treatment of opiate agonist withdrawal and treatment. In combination with naloxone, buprenorphine sublingual tablets and sublingual films are approved for the treatment of opiate dependence. Buprenorphine with naloxone (Suboxone) is available as 2-mg/0.5-mg sublingual film and sublingual tablets. Naloxone is an opiate-receptor antagonist and has no clinical effect when taken orally. However, if buprenorphine/naloxone is administered intravenously or intramuscularly, opiate withdrawal is precipitated. As a partial agonist, buprenorphine has a pharmacologic ceiling effect resulting in reduced risk of overdose, abuse, and toxicity. The most common adverse effects related to buprenorphine include headache, pain, insomnia, withdrawal symptoms, sweating, anxiety, nausea, depression, rhinitis, and constipation.16,17 The effects are expected to occur during treatment. Elevated liver function tests have occurred during clinical trials but appear to be unrelated to buprenorphine dosing except in patients with hepatitis at baseline.16,17 Additional adverse effects related to sublingual film were oral hypoesthesia, glossodynia, and oral mucosal erythema.18

Buprenorphine is metabolized by the CYP450 3A4 system. Inducers of this system (e.g., phenytoin and St. John’s wort) could lead to reduced levels of buprenorphine, yielding possible withdrawal symptoms. Due to the ceiling effect of buprenorphine, inhibitors of CYP450 3A4 (e.g., fluconazole and clarithromycin) should present limited clinical effects unless CNS depressants are taken along with parenteral administration of buprenorphine.16 Both buprenorphine and buprenorphine/naloxone have been shown to be effective in reducing opiate use. During a 4-week clinical trial, 38.5% of buprenorphine-treated patients had opiate-negative urine tests compared to 5.8% in the placebo group.17 Opiate craving was also reduced in buprenorphinetreated patients when compared to placebo.17

Buprenorphine alone is recommended during the initiation of opiate-dependence treatment to reduce withdrawal symptoms. The initial dose is given at least 4 hours following the last use of opiates or at the early signs of opiate withdrawal. The dose is titrated over 2 days, and maintenance therapy is then initiated. If buprenorphine is given too closely to the last dose of an opiate agonist or if too little or too much is administered, withdrawal may be precipitated. The timing of initiation of buprenorphine is, therefore, crucial. Buprenorphine/ naloxone is recommended for maintenance therapy with the dose titrated based on patient response. The goal is reduced craving, suppression of withdrawal symptoms, and retention in the treatment program.

Patients being switched between sublingual film and tablets should be monitored for overmedication or withdrawal due to differences in relative bioavailability.18 Withdrawal symptoms occur with discontinuation of buprenorphine therapy. A gradual tapering with close physician monitoring and counseling is recommended. If relapse appears probable, therapy should be continued. A medication guide is required with each dispensing of Suboxone sublingual film to comply with risk evaluation and mitigation strategies (REMS). The manufacturer of Suboxone sublingual film does not recommend cutting the films because there are no cutting marks on the packaging, stability of cut film cannot be assured, and the child-resistant packaging is ineffective once cut. The manufacturer does recognize that owing to cost or other factors, patients may need to cut the films. In this case, pharmacists must counsel patients about the problems associated with cutting the film, especially the loss of the child-resistant packaging and the necessity of ensuring that children do not have access to the product. If children place the film in their mouth, emergency medical treatment should be sought immediately.19

Naltrexone (ReVia, Vivitrol): Naltrexone is a competitive opiate receptor antagonist that eliminates the euphoric effects of opiates and appears to reduce craving. Endogenous opiates and their effect on the opiate reward pathway are thought to have a role in alcoholism. The FDA has approved naltrexone, both orally and intramuscularly, for the treatment of opiate dependence and alcoholism.

The most common adverse events related to oral naltrexone are nausea, headache, dizziness, fatigue, vomiting, anxiety, and nervousness.20 Diarrhea and headache, along with expected opiate withdrawal symptoms, were seen in patients being treated for opiate dependence.21 In addition to these reactions, patients treated with naltrexone injection also experienced site-related reactions including pain, induration, infection, and allergic reactions.22 A black box warning related to hepatotoxicity exists for naltrexone and is related to doses higher than those recommended. Naltrexone should not be used in patients with acute hepatitis or liver failure.

Although oral naltrexone can reduce opiate use in patients, retention in a treatment program is seen as an obstacle to positive results.23 A review article found that opiate-dependent patients treated with injectable formulations of naltrexone may use fewer opiates than those treated with placebo or oral naltrexone.22 Naltrexone will precipitate withdrawal in an individual who has taken shortacting opiates in the last 7 days or long-acting opiates in the last 10 days.24 Patients must therefore be opiate free for 7 to 10 days prior to initiation of naltrexone therapy. The response to initial dosing should be monitored carefully for any signs of withdrawal. Relapse following treatment with naltrexone presents an increased risk of overdose and death due to reduced tolerance or increased sensitivity to opiates. A medication guide is required with each dispensing of naltrexone injection to comply with REMS. Injectable naltrexone is supplied as a kit, along with specific instructions and all supplies necessary for administration.

Medication-Assisted Treatment for Alcoholism

Three medications have been approved for maintenance of abstinence in the treatment of alcoholism (TABLE 5). These are disulfiram, acamprosate, and naltrexone. Treatment of alcoholism may require long-term medication use to maintain a patient in recovery. Medication use in combination with counseling and support mechanisms, including 12-step programs, can provide tools necessary to prevent relapse.


Disulfiram (Antabuse): Disulfiram, approved by the FDA in 1951 for the treatment of alcoholism, is an inhibitor of aldehyde dehydrogenase. Ethanol is metabolized first by alcohol dehydrogenase to acetaldehyde, which is then metabolized by aldehyde dehydrogenase to acetic acid. When disulfiram inhibits aldehyde dehydrogenase, acetaldehyde accumulates in the serum. This increase in serum concentration of acetaldehyde produces uncomfortable reactions, which may include throbbing headache, nausea, severe vomiting, dyspnea, tachycardia, hypotension, blurred vision, vertigo, and confusion.

Due to the nature of the adverse effects of disulfiram, maintenance of blinding during a clinical trial is difficult. Reviews of disulfiram outcome studies have recognized this difficulty and indicate mixed efficacy from clinical trials.25 In a recent review, six of 10 studies indicated that disulfiram had a significantly better effect on abstinence than placebo, other, or no treatment. The other four studies found no other treatment with a significantly better effect on abstinence than disulfiram. In nine of these 10 studies, voluntary cognitive therapy, psychotherapy, or counseling was provided to the patients.25

A black box warning exists for disulfiram indicating that a patient should not ingest disulfiram when intoxicated or without the patient’s full knowledge. It further states that the physician should provide instruction to the patient’s relatives. A safety literature review in 1999 concluded that rare fatal hepatitis (1:30,000 patientyears), neuropsychiatric problems (1:15,000 patient-years), and skin complications have been reported in disulfiramtreated patients. Tiredness, headache, and sleepiness were reported as less serious adverse effects.26 Prior to treatment with disulfiram, patients must have abstained from the consumption of alcohol for at least 12 hours. Patients should not ingest alcohol for at least 2 weeks after the last dose of disulfiram.

Disulfiram is used as an aversive agent in the treatment of alcoholism. Patients must be fully informed of the effects that will occur with the ingestion of alcohol or alcohol-containing preparations while taking disulfiram. The use of metronidazole is contraindicated during disulfiram therapy and for at least 2 weeks following the last dose. The development of acute psychoses and confusion, resulting from CNS toxicities, may occur due to combined disulfiram-metronidazole inhibition of aldehyde dehydrogenase. It is recommended that disulfiram be used with caution in patients with hepatic cirrhosis or insufficiency. For patients who have discontinued successful treatment with disulfiram, restarting the medication along with behavioral therapy may be appropriate when stressful or high-risk relapse situations are anticipated. This will help the patient cope with these events and prevent relapse.27

Acamprosate (Campral): Acamprosate, approved by the FDA in 2004 for the treatment of alcoholism, appears to have a centrally mediated effect of lowering neuronal excitability. With chronic alcohol consumption, upregulation of glutamatergic system neurotransmitters occurs to counter the sedative effects of the GABAnergic system. When alcohol consumption ceases, an imbalance occurs resulting in anxiety, sleeplessness, and hyperexcitability. Acamprosate reduces neuronal glutamatergic hyperactivity, helping to restore balance and assisting the patient to remain abstinent. A reanalysis of three pivotal European trials indicated that patients treated with acamprosate were 3.0 times more likely to remain completely abstinent at 13 weeks and 1.8 times more likely to be completely abstinent at 52 weeks when compared to those treated with placebo.28

Acamprosate is not metabolized hepatically and is excreted unchanged by the kidneys. It is safe for patients with severe liver disease, but does require dosing adjustment in patients with moderate renal impairment and should not be used in those with severe impairment. Acamprosate appears to have a good safety profile, with diarrhea being the most common adverse reaction reported during treatment.29 Therapy with acamprosate is generally started 5 days after cessation of alcohol consumption.27 With a half-life of 20 to 33 hours, full effectiveness of acamprosate might not be seen for at least 5 days. Therapy should be continued if a patient relapses. Acamprosate has been used in combination with oral naltrexone, but this is not an FDA-approved combination therapy. Acamprosate does not affect opiate receptors and may be appropriate therapy for patients who are undergoing opiate-dependence treatment.27 No withdrawal symptoms occur upon discontinuation of acamprosate, and tapering is not required.27

Naltrexone (ReVia, Vivitrol): As stated above, naltrexone also contains an FDA-approved indication for use in the treatment of alcoholism. Hospitalization related to both alcohol relapse and psychiatric conditions have been seen in patients treated for alcoholism.20 Additional side effects and limitations of use were previously discussed and listed in TABLE 3.

A comparative review of oral and injectable naltrexone for the treatment of alcohol dependence revealed inconsistent results related to the reduction of relapse.30 After 3 months of treatment, oral naltrexone reflected significantly lower relapse rates than placebo. The injectable formulation did not indicate a significant reduction in relapse at 3 months, but reflected a 17% to 25% reduction in heavy drinking days during 6 months of treatment.30 Another analysis of patients who were abstinent from alcohol use for at least 4 days prior to clinical-trial entry revealed a 32% total abstinence rate for patients treated with 380 mg of injectable naltrexone compared to an 11% rate for placebo patients after 24 weeks of treatment.31 Treatment with naltrexone is generally initiated 3 to 7 days after last ingestion of alcohol to reduce the occurrence of side effects, especially nausea.27 Patients should be advised to continue naltrexone therapy in the event of alcohol relapse to limit the severity of the relapse.27 Treatment for alcoholism is recommended for at least 3 months and may require up to 1 year for effective therapy.


As the most accessible health care providers, pharmacists are in a unique position to identify individuals in need of treatment for addiction, whether patients, coworkers, or employees. Pharmacists must learn to recognize the signs of addiction, but must also recognize the differences in the various levels of psychoactive substance use. Reviewing a patient’s profile for signs of potential habituation and abuse, then encouraging treatment and counseling, may halt the cycle of addiction. It is important to maintain a complete medication profile since patients often receive methadone from an outpatient treatment program. This should help decrease the potential risk of dangerous drug–drug interactions. Pharmacists should also be vigilant regarding the potential abuse of opiate agonists used in the treatment of opiate dependence, such as methadone and buprenorphine. This includes monitoring for illegitimate prescriptions for these substances. It is important to know how to contact local resources that are available for addiction treatment. Pharmacists are expected to provide their patients with honest information about medications for treatment of addiction and the adverse events that can be expected. Inquiring about a patient’s recovery efforts and providing emotional support can help to maintain a patient in the treatment program and may lead to higher success rates. Without intervention and treatment, addiction to drugs and alcohol is a chronic, progressive, relapsing, and potentially fatal disease.5


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