Q&A: Clinical Challenges in Substance Use Disorders
Q&A: Clinical Challenges in Substance Use Disorders
Dr. Domingo is Assistant Professor at Baylor College of Medicine in Houston. Dr. Kosten is JH Waggoner Chair and Professor of Psychiatry, Neuroscience, Pharmacology, Immunology & Pathology and Co-Director, Dan Duncan Institute for Clinical and Translational Research at The Menninger Department of Psychiatry & Behavioral Sciences, Baylor College of Medicine.
Editor’s Note: We are pleased to present this brief summary based on the presentation, “Solving Clinical Challenges in Substance Use Disorders,” which took place on Monday, September 18 at the 2017 Psychiatric Congress. This was a cases/questions session that offered answers to a range of questions about diagnosis, treatment options, and management of adverse effects.
Q: I have a lot of patients who smoke cannabis. Many say they use cannabis for what seems to be purely therapeutic reasons (eg, pain). Is it diagnostically important to differentiate substance use disorders attributable to an attempt to “self-treat” from other forms of substance use disorders?
A: As a treatment provider, the most prudent approach to addressing this issue is application of the DSM-5 diagnostic criteria for assessing substance use disorders (SUD). If a patient meets 4 or more of those criteria, they have objectively met requirements consistent with a diagnosis of a moderate SUD that could benefit from treatment. At the point of this determination, while the patient’s cannabis use as a form of “self-treatment” or a mitigation of some other disorder may provide value-added information, clinical treatment remains within prescribed guidelines. When considering mitigation of other pathological conditions like chronic pain, it is important to be aware of the cannabis source and the data supporting or refuting the mitigation.
Commercial sources such as state-sold cannabis products (eg, transdermal cannabis for pain) differ markedly from research cannabis or FDA-approved products. The efficacy, dose, routes of administration, or adverse effects of commonly used and commercially available cannabis products in the US are unknown.
Legal access to low THC/high-cannabidiol products for other “legal uses” in various states include PTSD, cancer, epilepsy, cachexia, glaucoma, HIV/AIDS, traumatic brain injury, Tourette syndrome, addiction, anxiety, depression, sleep disorders, and degenerative neurological conditions (eg, Alzheimer disease, amyotrophic lateral sclerosis, Huntington disease, Parkinson disease, vascular dementia). However, most all of these uses, although legally prescribed, are not supported by clinical trials data.
The few clinically demonstrated uses are pain, nausea, and vomiting, multiple sclerosis related spasticity, appetite stimulation in cachexia, and glaucoma. For all these conditions, the effects of cannabinoids are modest, and other FDA-approved treatments are more effective. Some uses such as for glaucoma are even harmful. Smoking cannabis significantly lowers intraocular pressure, but does not prevent nerve damage, while other glaucoma agents do prevent the nerve damage. Another particular controversy is using cannabidiol as an anticonvulsant in children refractory to other therapies. This effect was first noted in the 1940s, but no controlled clinical trials have tested it as an anticonvulsant.
Q: How do you decide in a patient with opiate addiction when to use an opiate antagonistic therapy (eg, naltrexone), when to use opiate partial agonist therapy (eg, buprenorphine), and when to use opiate agonist therapy (eg, methadone)?
A: A pharmacological maintenance regimen is widely accepted as the optimal strategy toward recovery from opioid use disorder (OUD). Compared with detoxification alone, these maintenance regimens are associated with much higher rates of treatment retention, reduction in illicit opiate use, decreased craving, and generally improved social functioning.
Current OUD pharmacotherapies for relapse prevention are methadone, naltrexone, and buprenorphine. Their mechanisms of action (MOA) differ in that methadone as a full µ-opioid receptor agonist, involves cross-tolerance at high doses, while naltrexone blocks the µ-opioid receptor and simply blocks euphoria. Buprenorphine has an interesting intermediate MOA as a partial opioid agonist that can provide cross-tolerance and withdrawal relief at low doses, while blocking euphoria at high doses like naltrexone.
In choosing among these medications for OUD here are some considerations. Methadone has a built-in structure of the program for better or for worse, but some patients will be well served by its structure. Methadone itself has a greater risk of diversion and overdose risk than buprenorphine, so “take-homes” of methadone are more restrictive. Naltrexone is difficult to start on because of the need for detoxification, but it is easy to stop without any withdrawal, which can make adherence difficult. Buprenorphine has two appealing attributes in that it is easy to start without requiring detoxification, but difficult to discontinue because of its agonist activity.
Overall, in choosing agonist versus antagonist therapy a key question is “What does the patient and family want?” The initial choice is a collaborative process among patient, family, employer, and sometimes other outside criminal justice negotiations.
The majority of patients with OUD prefer buprenorphine over the other 2 pharmacotherapies, and it has much to recommend it. Buprenorphine has reduced overdose potential and abuse liability and less severe withdrawal than methadone when stopped. It is comparable to methadone in treatment retention and reduced heroin abuse, and it can be given in the physician’s office leading to increased availability and reduced stigma.
While sublingual buprenorphine needs to be take daily, long-acting implanted buprenorphine can last several months. Compared with placebo it is significantly better in retention at 6 months (64% vs 26%) (n = 114 vs 54) and in attaining an illicit opioid-free state (64% vs “too many dropouts”). It is also comparable to 8-mg sublingual buprenorphine with 6 month retention (64% vs 64%; n = 114 vs 119) and rates of opioid-free urines (31% vs 33%).
The adverse effects of the implant include implant site pain, itching, and redness, as well as body symptoms of headache, depression, constipation, nausea, vomiting, and back pain. Further limitations are that it is equivalent to only 8-mg sublingual buprenorphine, when the average sublingual dose is 12 to 16 mg, and implanting and removal can be difficult for the average physician.
The major problem with buprenorphine is the insufficient number of physicians prescribing it for the 2.5 million treatment-seeking OUD patients. While most prescribers can be allowed up to 100 patients per prescriber and this number was recently increased to 275 patients, most prescribers provide for less than 10 OUD patients.