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110 Implementation of Personalized Medicine in a Community Psychiatry Practice
- Audrey Umbreit, Shirshendu Sinha, Emily Holm
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- Journal:
- CNS Spectrums / Volume 25 / Issue 2 / April 2020
- Published online by Cambridge University Press:
- 24 April 2020, p. 271
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Objective:
To describe the initial results of implementing pharmacogenomics testing in a community-based psychiatry practice and potential impacts on medication management.
Method:Retrospective chart review of prospectively maintained medical records of all adult patients with pharmacogenomics results from 9/01/2017 to 6/30/2019 under the care of psychiatrist and clinical pharmacist.
Results:A total of 51 patients met inclusion criteria. A total of 7 pharmacokinetic genes and, due to changes in the test report over time, a range of 6-10 pharmacodynamic genes relevant to psychotropic medications were evaluated per patient. Every patient had genetic variations, with an average of 6.1 per patient (range 3-9; SD= 1.5). Patients were taking an average of 3.6 (range 1-8; SD=1.7) psychiatric medications at the time of the genetic test, to treat an average of 5 psychiatric conditions (range 1-9; SD=2.2). An average of 1.2 (range 0-4; SD=1.0) gene-drug interactions were uncovered per patient. Following review by psychiatrist and pharmacist, medication adjustments resulted in patients remaining on an average of 3.6 psychiatric medications, but decreasing the average number of gene-drug interactions per patient to 0.8 (range 0-3, SD=0.8).
Discussion:The large number of genetic variations observed per patient is consistent with previous findings 1-2. The decrease in number of gene-drug interactions following testing demonstrates the practical utility of pharmacogenomics information to guide medication therapy. This study did not examine outcomes such as improvement in psychiatric condition or reduction in medication adverse effects; however, these endpoints have been evaluated in other trials 3-4.
Conclusions:Pharmacogenomics testing presents an opportunity for a personalized medicine approach in a community-based psychiatry practice.
98 Dronabinol-Induced Hypomania: A Case Report and Literature Review
- Shirshendu Sinha, Audrey Umbreit, Charles Sieberg
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- Journal:
- CNS Spectrums / Volume 24 / Issue 1 / February 2019
- Published online by Cambridge University Press:
- 12 March 2019, pp. 223-224
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Purpose
Present a case of dronabinol-induced hypomania.
BackgroundDronabinol is a synthetic derivative of cannabis that is commonly prescribed for chemotherapy-induced nausea and vomiting or cachexia due to HIV/AIDS. The safety in those with bipolar disorder warrants further investigation as previous studies suggest that the use of cannabis may be associated with exacerbation of manic symptoms. The risk of developing manic symptoms in patients with bipolar disorder who use dronabinol is largely unknown. Clinical Case: A 55-year-old Caucasian male, following with psychiatry since July of 2016 for substance use disorder (alcohol, cocaine and cannabis), bipolar I disorder, generalized anxiety, PTSD, and intermittent sleep disturbances, was prescribed dronabinol 2.5mg twice daily on 5/19/17 to treat wasting syndrome and significant weight loss due to underlying HIV. He has been abstinent from alcohol, tobacco, and illicit substances for more than a year. The patient’s relevant medication list includes: bupropion XL 150mg daily, quetiapine 300mg daily at bedtime, and trazodone 50–100mg at bedtime. At psychiatrist visit on 7/10/17, his bipolar disorder was noted to be stable. But, after his dose of dronabinol was increased on 7/21/17 to 5mg twice daily, the patient presented to psychiatrist on 8/1/2017 in a state of hypomania, with symptoms including: increased interest in sex, insomnia and increased animation. His judgment and impulse control were slightly impaired. Excluding the dronabinol dose increase, no other medication changes had taken place and the patient was not using alcohol or other substances. Quetiapine was discontinued and olanzapine 10mg at bedtime was started. Bupropion was discontinued, trazodone was tapered off, and dronabinol was discontinued. Upon follow up within a month, our patient’s hypomania symptoms resolved. He was also gaining weight with the olanzapine and reported improved sleep. He was continued on olanzapine 10mg at bedtime and continued off the trazodone, bupropion and dronabinol. He continues to remain abstinent from alcohol and illicit drugs.
DiscussionThe underlying mechanism of dronabinol-induced manic symptoms in those with bipolar disorder remains unclear but may involve dopamine. Sensitization of the dopaminergic system by THC is thought to be associated with the development of manic symptoms in those that use cannabis. THC is associated with increased dopaminergic cell firing, dopamine synthesis, and dopamine release when used acutely.
Other medications associated with causing manic symptoms include bupropion and trazodone, as relevant to our case. However, our patient was stable on these medications before the addition of dronabinol. Thus, it is reasonable to conclude that the dronabinol likely caused our patient’s hypomania symptoms.
ConclusionThis case emphasizes the need to evaluate mental health conditions before prescribing cannabis derivatives such as dronabinol.