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  • 28 Mar 2018 9:16 AM | Anonymous

    Author: Amy Benson, PharmD, MHA
    MSHP Public Policy Committee Chair / Director of Pharmacy at Liberty Hospital


    The MSHP Public Policy Committee discussed the work the Hospital Advisory committee (HAC) has been completing with the Board of Pharmacy, Department of Health and Senior Services and Missouri Hospital Association (MHA).  Senate bill 501 required the removal of duplicative language from the DHSS regulations.  The HAC submitted its recommendations in December to remove several sections that are covered by CMS language and also provided additional language for expanded pharmacy technician roles.  The HAC continues to have conversations with the Board of Pharmacy to assist in moving this language through the regulation process.

    Another group is working with the Board of Pharmacy on revising the rules related to sterile compounding for pharmacies licensed under a Class H license.  A recommendation has been provided to the board to clarify the steps to take if/when compounding should cease based upon CFU counts exceeding USP 797 action levels.  The group will continue to work with the board to ensure public safety is improved while limiting the potential delays to patient care.

    Several bills have been introduced in both the House and Senate that apply to pharmacy practice in the state.

    SB 1068 – Establishes regulations for the duties of pharmacy technicians in a hospital setting.  The sponsor is Senator Sater and had the first read on 2/28/18.  (http://www.senate.mo.gov/18info/BTS_Web/Bill.aspx?SessionType=R&BillID=76743872)

    HB 1618 – Disposal of unused controlled substances.  The sponsor is Representative Barnes and is awaiting a 3rd reading.  https://house.mo.gov/bill.aspx?bill=HB1618&year=2018&code=R)

    SB 826 – Modifies provisions relating to pharmacy, including drug disposal, prescription limitations for controlled substance, and vaccine protocols.  The sponsor is Senator Sater and has passed.  http://www.senate.mo.gov/18info/BTS_Web/Bill.aspx?SessionType=R&BillID=70365560)

    HB 1870 – Allows certain medications in multidose containers used by a patient during a hospital stay to be sent with the patient at discharge.  The sponsor is Representative Barnes and has passed.  https://house.mo.gov/bill.aspx?bill=HB1870&year=2018&code=R)

    HB 1542 – Prohibits certain actions by pharmacy benefits managers.  Sponsor is Representative Morris and a public hearing has been completed.  https://house.mo.gov/bill.aspx?bill=HB1542&year=2018&code=R)


  • 22 Mar 2018 11:20 AM | Anonymous

    Welcome to Spring of 2018, known throughout the world as the season of drug shortages.  In this same spirit of shortages, I’ll keep my comments very brief in this issue.  In fact, I’d like to use this as an opportunity to ask questions.  We all know that recent drug and fluid shortages have made it extraordinarily difficult to provide optimal patient care in every situation.  In large part, our role as pharmacists is to get creative in these difficult times and to find unique solutions in the face of shortages.  The problem that we now see, however, is that as one drug is added to the shortage list there is an increased utilization of alternative agents which leads to that agent being added in turn.  It’s this problem that’s led me to sit in the corner, quietly rocking back and forth while mumbling incoherently as ketamine has now been added to this infernal list due to increased utilization stemming from the opioid shortage.  And I’m not even going to get started on the impact that the fluid shortages have had on our ability to practice.  What I want to do, however, is to tap into the collective brilliance of Missouri pharmacists to find out how you’re managing your practice in this challenging time.  So my questions to you are:

    Which shortage(s) have impacted your practice most profoundly?
    How have you changed your practice in light of shortage(s)?
    Are there any unique steps you or your institution have taken to mitigate the impact of shortages?
    What have you learned and what advice would you offer to others that could help navigate this problem?

    I would love to hear about the challenges you’ve faced, the lessons you’ve learned, and the successes you’ve realized and would really like to showcase what you’ve done to manage this growing problem.  Please don’t hesitate to email me at hamptonjp@umkc.edu to let me know!  Although we may not be able to directly solve the problem (unless one of you is getting ready to cut the ribbon on a new drug manufacturing facility), we can work together to share our knowledge and collectively try to minimize the impact of drug shortages.  When we work together there’s really no problem we can’t solve…except maybe finding the solution to creating an effective single stage to orbit, boost glide, sustained hypersonic platform (sorry, I have to release my inner aviation dork at least once per article).

    Thanks and stay strong!

    Jeremy P. Hampton, PharmD, BCPS
    President – Missouri Society of Health-System Pharmacists

    Clinical Associate Professor
    University of Missouri- Kansas City School of Pharmacy

    Clinical Specialist - Emergency Medicine
    Truman Medical Center

    ----

    As a side note, it feels like this is the worst that shortage problem has ever been.  I was very interested to learn, however, that from a numbers standpoint the problem of drug shortages has actually improved since 2009.  And here we thought we had it bad back in 2006…

    Source: University of Utah Drug Information Service
    Contact: Erin.Fox@hsc.utah.edu, @foxerinr for more information.

  • 22 Mar 2018 10:44 AM | Anonymous

    Authors:
    Sara Schenkelberg, PharmD: PGY-1 Walgreens Community Resident-Kansas City, MO
    Chad Cadwell, PharmD, AAHIVP: Walgreens Health System-Truman Medical Center-Kansas City, MO

    Program Number: 2018-03-01
    Approval Dates: 4/4/18-7/6/18
    Approved Contact Hours: One (1) CE(s) per LIVE session.
    Submit for CE: Click Here

    Objectives

    1. Review background and prevalence of Obsessive Compulsive Disorder
    2. Recognize obsession and compulsion behavior
    3. Understand diagnostic criteria set by DSM-V
    4. Identify place in therapy for CBT and SSRIs
    5. Identify place in therapy for alternative therapies


    Introduction
    Obsessive Compulsive Disorder, also known as OCD, is an anxiety disorder in which people have recurring, unwanted thoughts and behaviors that one feels the need to repeat repetitively. Many people have intrusive thoughts, and/or repetitive behaviors, but usually do not act on them. People with OCD have thoughts that are persistent, undesirable, and cause unwanted distress. Behaviors are visible or mental and interact with one’s daily activities and social interactions.

    Current estimates state this condition affects approximately 1 in 40 adults in the United States, affecting roughly 2.2 million adults or 1.0% of the adult population, and 1 in 100 children.22 It equally affects men, women, and children of all races and socioeconomic status.20,22 The average age of onset is 19, with 25% of cases occurring before age 14. OCD is not only common in the United States, but also worldwide. The World Health Organization ranks OCD as one of the top 20 causes of illness-related disability worldwide between ages 15-44.11 Despite OCD being a common mental illness, most only seek treatment after several years of suffering. Those who suffer from OCD tend to be secretive about their symptoms and suffer from shame and embarrassment, which can lead to a delay in treatment. Less than one-third of OCD sufferers receive appropriate pharmacotherapy and even less receive evidence-based psychotherapy.11

    Obsessions vs. Compulsions
    Obsessions are repeated, persistent, unwanted thoughts and urges that are intrusive and cause distress or anxiety. These thoughts are hard to ignore and typically intrude on daily thoughts. Obsessions often have themes to them, such as, fear of contamination, needing things orderly and symmetrical, aggressive or horrific thoughts about harming yourself or others.15,16

    Compulsions are repetitive behaviors that one feels driven to perform. These repetitive behaviors or mental acts are meant to prevent or reduce anxiety related to the obsessions. However, engaging in the compulsions brings no pleasure and may offer only a temporary relief from anxiety. As with obsessions, compulsions typically have themes. Examples of these themes include constantly washing and cleaning, checking, counting, following a strict routine, and demanding reassurance.15, 16

    Diagnosis
    Many people experience intrusive thoughts and exhibit repetitive behaviors. A diagnosis of OCD is made only if symptoms are time consuming (i.e. more than an hour per day), distressing and cause significant interference in functioning.14 Unlike physical diseases and illnesses, no specific laboratory tests are available to diagnose mental illness. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) acts as a manual for mental health professionals in giving an OCD diagnosis. Although not all experts agree on the definitions and criteria set forth in the DSM-5, it is considered the gold standard by most mental health professionals in the United States.2,3 In order to determine if a patient meets DSM-5 diagnostic criteria for OCD, the patient must experience the presence of recurrent, unwanted, and intrusive thoughts and/or repetitive behaviors or rituals intended to relieve the fear, anxiety, and/or distress associated with obsessions. Additionally, obsessions and compulsions must cause significant distress and impairment in social, academic, and/or family functioning. The exclusion clause is that the obsessions or compulsions are not best explained by another mental disorder (table 1).12 Further diagnostic criteria include the addition of a “with tics” specifier and specifier distinguishing one’s insight: “with good or fair insight,” “with poor insight,” or “with absent insight/delusional beliefs.”2,3

    In the early 1990s, investigators identified a subgroup of children who developed a sudden onset of OCD symptoms following an active infection with beta-hemolytic Streptococcus.21 This was later identified as PANDAS, an acronym for “pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections.” Newer research has shown that strep is not the only infection that can cause these sudden-onset symptoms. In a condition known as Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS), similar OCD symptoms are observed following a wide variety of infections, such as mycoplasma, mononucleosis, Lyme disease, influenza, and auto-inflammatory diseases.21,23 PANDAS/PANS is a rare condition that affects roughly 1 in 2,000 children.2,3 Both conditions should be managed with antibiotic treatment followed by standard OCD treatments for continued symptoms.

    Risk Factors
    There are no clearly established environmental risk factors for OCD. However, some patients describe the onset of symptoms after a biologically or emotionally stressful event.1 There have been components of genetic factors contributing to an increased risk for developing OCD. Twin and family studies have shown that people with first-degree relatives who have OCD are at a higher risk for developing OCD themselves. The risk is higher if the first-degree relative developed OCD as a child or a teen.22 Ongoing research continues to explore the connection between genetics and OCD, which may help improve OCD diagnosis and treatment.

    Treatment
    First-line treatments for OCD are cognitive-behavioral therapy (CBT) and selective serotonin reuptake inhibitors (SSRIs).2 The U.S. Food and Drug Administration approved clomipramine, fluoxetine, fluvoxamine, paroxetine, and sertraline for treatment of OCD in adults. Sertraline, fluoxetine, and fluvoxamine have also been approved for use in children six, seven, and eight years of age and above, respectively.5,6,7,12 Although meta-analyses of placebo-controlled trials suggest greater efficacy and superiority for clomipramine than for fluoxetine, fluvoxamine, paroxetine and sertraline, the results of head-to-head trials comparing clomipramine and SSRIs does not support clomipramine as a first line agent.14,16 SSRIs are considered first line because the agents have less side effects and are better tolerated than clomipramine (table 2).12 Unlike the SSRIs, clomipramine also blocks norepinephrine reuptake, muscarinic cholinergic receptors, H1 histamine receptors, and alpha1-adrenergic receptors. Thus, clomipramine is more likely to induce anticholinergic effects, weight gain, sedation, orthostatic hypotension, and cardiac arrhythmias.16 In choosing among the SSRIs, the prescriber should consider the safety and acceptability of particular side effects for the patient, including any applicable FDA warnings, potential drug interactions, past treatment response, and the presence of co-occurring general medical conditions.

    Cognitive Behavioral Therapy (CBT) alone is recommended for a patient who is not too depressed, anxious, or severely ill to cooperate with this treatment modality, or who prefers not to take medications. CBT is the only form of psychotherapy for OCD whose effectiveness is supported by controlled trials.16 Compared to traditional psychotherapy, in which sessions are spent merely discussing the client’s problems, CBT treatment for OCD is far more proactive.8 Yale-Brown Obsessive Compulsive Scale (Y-BOCS) is a common assessment tool therapists use to help the client create a detailed list of his or her symptoms.18 Y-BOCS is considered the gold standard assessment tool for OCD symptom severity. Y-BOCS is a 10-item, clinician-administered scale designed to rate symptom severity, not to establish a diagnosis.18

    This list of symptoms is then used as the primary tool in a form of CBT treatment called Exposure and Response Prevention (ERP). The CBT variant that relies primarily on behavioral techniques, such as Exposure and Response Prevention (ERP), has the strongest evidence base. In CBT consisting of ERP, patients are taught to confront feared situations and objects (i.e. exposure) and to refrain from performing rituals (i.e. response prevention). Literature and expert opinion suggest providing CBT at least once weekly for 13-20 weeks.16

    An SSRI alone is recommended for a patient who has previously responded well to a given drug, prefers treatment with an SSRI alone, or when CBT is not accessible. Starting with an SSRI alone may enhance cooperation with treatment by diminishing symptom severity.1,16 Combined treatment with SSRI and CBT is more effective than monotherapy for some patients, but is not always necessary. Combined treatment should be considered for patients who have had an unsatisfactory response to monotherapy, who have occurring psychiatric conditions for which SSRIs are effective, or have severe OCD. Most patients will not experience substantial improvement until 4-6 weeks after starting medication, and some who will ultimately respond will experience little improvement for as many as 10-12 weeks.1,16

    Changing Treatment
    Initial treatments rarely produce freedom from all OCD symptoms and there is typically opportunity for improvement.2 If the patient continues to have an inadequate response to treatment, there are second-line options to consider. Examples include augmenting an SSRI with an antipsychotic medication, switching to a different SSRI, or switching to venlafaxine. Venlafaxine, a serotonin-norepinephrine reuptake inhibitor with preferential serotonergic action, has been studied in comparison to paroxetine in a double blinded study and clomipramine in a single blinded study.1,16 The studies found no difference in the efficacy between venlafaxine and the comparator agents in acute control of OCD. Given the absence of evidence from placebo-controlled trials, venlafaxine is not the first-line treatment for OCD.2 Hence, the guidelines consider venlafaxine as a second-line monotherapy agent in the treatment of OCD. In 2006, the National Institute of Clinical and Health Excellence (NICE) guidelines for Obsessive Compulsive Disorder (OCD) recommended anti-psychotics as a class for SSRI treatment resistant OCD.2 The article aimed to systematically review a meta-analysis on the clinical effectiveness of atypical anti-psychotics augmenting an SSRI. Risperidone and aripiprazole can be used cautiously at a low dose as an augmentation agent in non-responders to SSRIs and CBT. However, these agents should be monitored at four weeks to determine efficacy.2

    If those options have been exhausted, consider less well supported strategies such as augmentation of SSRIs with clomipramine, buspirone, pindolol, or once-weekly morphine sulfate.2,12 Morphine sulfate should be avoided in patients with contraindications to opiate administration. Last resort therapies include monotherapy with dextroamphetamine, tramadol, monoamine oxidase inhibitors, ondansetron, transcranial magnetic stimulation, or deep brain stimulation.2,12 These options may be considered in selected circumstances.

    Relapse is common in OCD patients, so it’s important to continue some form of treatment. Patients should continue successful medication treatment for 1-2 years before considering a gradual taper by decrements of 10%-25% every 1-2 months while observing for symptom return or exacerbation.10

    Conclusion
    Obsessive Compulsive Disorder is an anxiety disorder that traps people in endless cycles of repetitive thoughts and behaviors. There has been research done that suggests genetics are a factor for developing OCD. However, more research needs to be conducted on the environmental reasons a person has OCD. Studies show OCD affects gender, race, and socioeconomic status equally. DSM-V is the current diagnostic tool used by clinicians. If a patient is diagnosed, there are treatment options with CBT and/or pharmacologic options. Choice of initial treatment modality is individualized and depends on factors such as the nature and severity of the patient’s symptoms, co-occurring psychiatric and medical conditions, availability of CBT, the patient’s past treatment history, current medications, and preferences.


    References:

    1. Abramowitz, J. Effectiveness of psychological and pharmacological treatments for obsessive-compulsive disorder: a quantitative review. Journal of Consult Clinical Psychology. 1997; 65(1): 44-52.

    2. American Psychiatric Association: Clinical Guidance on Obsessive Compulsive Disorder. Arlington, VA, American Psychiatric Association, 2013.

    3. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Arlington, VA, American Psychiatric Association, 2013.

    4. Bokor, G., Anderson, PD. Obsessive-Compulsive Disorder. Journal of Pharmacy Practice. 2014 April; 27 (2): 116-130.

    5. Clomipramine [package insert]. Hazelwood, MO: Mallinckrodt Inc.; Revised October 2012. Accessed 14 January 2018.

    6. Fluoxetine [package insert]. Indianapolis, IN: Eli Lilly and Company Inc.; 1987. Accessed 15 Jan 2018.

    7. Fluvoxamine [package insert]. Palo Alto, CA: Jazz Pharmaceuticals Inc.; 2008. Accessed 15 Jan 2018.

    8. Goodman, W, Lydiard, R. Recognition and Treatment of Obsessive-Compulsive Disorder. Journal of Clinical Psychiatry. 2007 December; 68 (12): e38.

    9. Keeley, M., Storch, E., Dhungana, P., et al. Pediatric Obsessive-Compulsive Disorder: A Guide to Assessment and Treatment. 2007 June; 28(6): 555-74.

    10. Koran, Lorrin M., M.D.; Simpson, Blair H., M.D., Ph.D. Guideline Watch (March 2013): Practice Guideline for the Treatment of Patients with Obsessive-Compulsive Disorder. www.psychiatryonline.org. March 2013.

    11. Lexi-Comp, Inc. (Lexi-DrugsTM). Accessed 12 Jan 2018.

    12. Mcintrye, John S., M.D.; Charles, Sara C.; et al. Treating Obsessive-Compulsive Disorder: A Quick Reference Guide. American Psychiatric Association. July 2007.

    13. Paroxetine [package insert]. Research Triangle Park, NC: GlaxoSmithKline Inc.; December 2012. Accessed 15 Jan 2018.

    14. Reddy, J., Sundar, A., Narayanaswamy, J.; et al. Clinical practice guidelines for Obsessive-Compulsive Disorder. 2017. 59(5): 74-90.

    15. Seibell, Phillip J.; Hollander, Eric. Management of Obsessive-Compulsive Disorder. 2014; 6: 68.

    16. Sousa, MB, et al. A randomized clinical trial of cognitive-behavioral therapy and sertraline in the treatment of obsessive-compulsive disorder. Journal of Clinical Psychiatry. 2006; 67 (7): 1133.

    17. Stewart, Evelyn S. Obsessive Compulsive Disorder. Psychiatric Neurotherapeutics. 2016; 2: 23-50.

    18. Storch E., Larson M., Price L., et al. Development and psychometric evaluation of the Yale-Brown Obsessive-Compulsive Scale-Second Edition. Psychological Assess 2010a; 22(2): 223-232.

    19. Sertraline [package insert]. New York, New York: Pfizer Inc.; Revised January 2018. Accessed 14 January 2018.

    20. Swedo S., Leckman J., Rose N. From research subgroup to clinical syndrome: Modifying the PANDAS criteria to describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome). Pediatric Therapeutics 2012, 2:2.

    21. Swedo SE, Leonard HL, Garvey M.; et al. Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections: Clinical description of the first 50 cases. American Journal of Psychiatry 144:2, February 1998; pp 265-271.

    22. UpToDate Inc. Accessed 14 Jan 2018.

    23. What are PANS/PANDAS? American Psychiatric Association. September 7, 2017.

    Appendix

    Table 1. Symptoms of Other Psychiatric Disorders to be Differentiated From the Obsessions, Compulsions, and Rituals of Obsessive-Compulsive Disorder (OCD). 12


    Table 2. Dosing of Serotonin Reuptake Inhibitors (SSRIs) in Obsessive-Compulsive Disorder.12

    Click Here for a Self Assessment

  • 22 Mar 2018 10:34 AM | Anonymous

    Authors:
    Kim Ehrhard, PharmD Candidate 2019: UMKC School of Pharmacy
    Ben Miskle, PharmD Candidate 2018: UMKC School of Pharmacy
    Steve Stoner, PharmD, BCPP: UMKC School of Pharmacy

    It is estimated that there are about five million people currently taking antipsychotic medications and that number is continuing to rise as the use of antipsychotics has expanded beyond use for schizophrenia and are now used in bipolar disorder and major depression.1 Adherence is critically important with antipsychotic treatment and a consistent barrier to medication adherence has been some concern over long-term consequences of side effects. One of those concerns has been the potential for developing tardive dyskinesia (TD), which can be described as an involuntary, repetitive, purposeless movement, typically of the tongue, jaw, lips, face, trunk, or upper extremities.2 This side effect is thought to be caused by medications that work through dopamine receptor blockade, which include antipsychotic medications and gastrointestinal medications, such as metoclopramide.2,3 It is estimated that at least 1 in 10 patients exposed to antipsychotics has TD.1 A common assessment tool for TD is the 12-item Abnormal Involuntary Movement Scale (AIMS). Administration of this scale helps to identify the level of severity of the involuntary movements. An AIMS score of at least two, in two or more body regions, or a score of three to four, in at least one body region, in a patient with at least three months of cumulative antipsychotic drug exposure, equates to a probable diagnosis of TD.4 Until recently, if TD was not caught and addressed early it was thought to be irreversible. However, in 2017 the FDA approved two new medications indicated for the treatment of TD. These two medications, deutetrabenazine (Austedo™) and valbenazine (Ingrezza™) are similar in their primary mechanisms of action, but also possess distinct differences that should be considered.

    Mechanism of Action
    The exact mechanism of deutetrabenazine and valbenazine is unknown, though they likely exhibit their effects through reversible vesicular monoamine transporter 2 (VMAT2) inhibition.7,9 VMAT2 plays a key role in dopamine signaling as it is a transporter protein found in the presynaptic neurons of the CNS and helps package monoamines into synaptic vesicles for release within the synaptic cleft. TD is thought to be associated with prolonged exposure to dopamine receptor blocking agents and subsequent hyperactive dopamine signaling. This is thought to cause upregulation and hypersensitivity in postsynaptic dopamine D2 receptors in one of the areas of the brain that controls motor function.5,6 With deutetrabenazine and valbenazine selectively inhibiting the VMAT2 receptor, these medications are thought to provide reversible reductions of dopamine reuptake within the vesicle leading to a reduced number of monoamines available to bind hypersensitive postsynaptic dopamine D2 receptors.7,9

    Dosing/Drug Interactions
    Deutetrabenazine – The initial dose of deutetrabenazine is 6 mg twice daily for tardive dyskinesia. The dose may be increased weekly based on response and tolerability in increments of 6mg/day to a maximum of 48mg/day. With a total daily dose ≥12mg, administer in two divided doses and give with food. There are potential drug interactions to consider with deutetrabenazine. Deutetrabenazine is a substrate of CYP1A2, CYP2D6, and CYP3A4. In combination with strong CYP2D6 inhibitors like paroxetine, fluoxetine, bupropion, and quinidine, as well as poor CYP2D6 metabolizers, a maximum dose of 18mg/dose or 36mg/day should be utilized.8 Deutetrabenazine use should also be avoided with MAOIs.

    Valbenazine - The initial dose for valbenazine is 40 mg once daily. After one week, the dose should be increased to the recommended dose of 80mg once daily. Continuation of 40mg once daily may be considered for some patients. Valbenazine may be taken with or without food. There are important considerations to make when putting a patient on valbenazine including drug interactions. Valbenazine and its active metabolite are metabolized via CYP3A4 and CYP2D6. It is recommended that valbenazine be avoided in use with CYP3A4 inducers as concomitant may decrease the exposure of valbenazine and its active metabolite. Some examples of CYP3A4 inducers are rifampin, carbamazepine, and phenytoin. Dose reductions are also recommended during concomitant use with CYP2D6 and CYP3A4 inhibitors. Valbenazine should also not be used with any MAOIs.10

    There are some major warnings that come with each medication that need to be taken into account. Deutetrabenazine has the potential adverse effect of QT prolongation and should be adjusted with patients taking strong CYP2D6 inhibitors as well as those who are poor CYP2D6 metabolizers. Somnolence, diarrhea, fatigue, and xerostomia have shown to be the most prolific adverse effects associated with deutetrabenazine. One particular important side effect with deutetrabenazine is the black box warning for depression and suicidality in patients with Huntington’s Disease. Caution should be used in treating patients with a history of depression or prior suicide ideation. Deutetrabenazine is contraindicated in patients with untreated or inadequately treated depression.7-10

    With valbenazine, the major adverse effects include somnolence and QT prolongation. Due to somnolence, it is important that the patient avoids operating heavy machinery or activities that require them to be alert while taking this medication. Even though QT prolongation is a precaution to look at, the degree of QT prolongation is not clinically significant at concentrations expected with recommended dosing.10 Dose adjustments should be made in the situation of patients with congenital long QT syndrome, patients with arrhythmias, as well as patients on strong CYP3A4 or CYP2D6 inhibitors and poor CYP2D6 metabolizers.

    Clinical Significance
    Deutetrabenazine – The ARM-TD study was a randomized, double-blind, placebo-controlled, parallel group study designed to assess the safety and efficacy of deutetrabenazine over the course of 12-weeks. This trial included patients who had been diagnosed with TD for ≥3 months before screening and an AIMS motor score ≥6 (using a modified AIMS scale) at both screening and baseline, verified by a blinded central rater, with the baseline AIMS score of 9.6. The primary efficacy endpoint was the change in AIMS dyskinesia total score from baseline to week 12 as assessed by two blinded central video raters. Patients were randomized to deutetrabenazine 6mg twice daily or matching placebo with alpha set at 0.05. Deutetrabenazine was titrated weekly by 6mg until adequate dyskinesia control was achieved, a significant adverse effect occurred, or the maximal allowable dose of 48mg/day was achieved. Deutetrabenazine was found to be superior to placebo with a reduction of 3.4 points in the AIMS score for deutetrabenazine (p=0.027).11

    Valbenazine - The KINECT 3 study was a randomized, double-blind, placebo-controlled trial designed to assess the safety and efficacy of valbenazine. This trial included patients with moderate to severe tardive dyskinesia as determined by clinical observation and an underlying diagnosis of schizophrenia, schizoaffective disorder, or a mood disorder, with a baseline AIMS score of 10. The primary efficacy endpoint was the mean change from baseline in the AIMS dyskinesia total score at the end of Week 6 when patients were given fixed doses of valbenazine 40 mg, valbenazine 80 mg, or placebo with alpha set at 0.05.


    The valbenazine 80 mg group was found to be statistically significant with a 3.2 point reduction in the total AIMS score compared to placebo (P<0.001).12 These results are also found to be clinically significant as a change of 3 in the AIMS score can significantly improve a patient’s quality of life.13 It is important to note that longer trials are necessary to understand the long-term effects of deutetrabenazine and valbenazine in patients with tardive dyskinesia, as well as trials comparing the efficacy of deutetrabenazine in comparison with valbenazine for treatment of TD.

    Role in Therapy
    Both deutetrabenazine and valbenazine have been shown to be effective in treating TD, a once thought incurable side-effect of antipsychotic therapy. For patients whose TD is not improved by a reduced dosage of antipsychotic medication or a change in antipsychotic therapy, the VMAT2 inhibitors provide a potential treatment option for TD.


    References:

    1. Cloud LJ, Zutshi D, Factor SA. Tardive dyskinesia: therapeutic options for an increasingly common disorder. Neurotherapeutics. 2014;11(1):166-176

    2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013:712

    3. Kenney C, Hunter C, Davidson A, et al. Metoclopramide, an increasingly recognized cause of tardive dyskinesia. J Clin Pharmacol. 2008;48(3):379-384.

    4. Guy W. ECDEU Assessment Manual for Psychopharmacology. Washington DC: US Department of Health, Education and Welfare; 1976. pp. 534–7.

    5. Stahl SM. Essential Psychopharmacology Online. Based on: Stahl SM. Stahl’s Essential Psychopharmacology. 4th ed. Cambridge, UK: Cambridge University Press; 2013. http://stahlonline.cambridge.org/essential_4th_chapter.jsf?page=chapter5_introduction.htm&name=Chapter%205&title=Conventional%20antipsychotics#c02598-5-1. Accessed January 2nd, 2018

    6. Sayers AC, Bürki HR, Ruch W, et al. Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias: effects of clozapine, haloperidol, loxapine and chlorpromazine. Psychopharmacologia. 1975;41(2):97-104.

    7. Deutetrabenazine. Lexi-Drugs Online. Hudson (OH): Lexi-Comp, Inc. 1978-2015 [cited 2018 Jan 4]. Available from: https://online.lexi.com/lco/action/doc/retrieve/docid/patch_f/6454757

    8. Austedo (deutetrabenazine)[package insert]. Teva Pharmaceuticals USA, Inc., North Wales, PA;2017.

    9. Valbenazine. Lexi-Drugs Online. Hudson (OH): Lexi-Comp, Inc. 1978-2015 [cited 2018 Jan 4]. Available from: https://online.lexi.com/lco/action/doc/retrieve/docid/patch_f/6463109

    10. Ingrezza (valbenazine)[package insert]. Neurocrine Biosciences, Inc,, San Diego, CA;2017.

    11. Fernandez H, Factor S, Hauser R, et al. Randomized Controlled Trial of Deutetrabenazine for Tardive Dyskinesia. Am J Neurol. 2017;88:2003-2010.

    12. Hauser R, Factor S, Marder S, et al. KINECT 3: A Phase 3 Randomized, Double-Blind, Placebo-Controlled Trial of Valbenazine for Tardive Dyskinesia. Am J Psychiatry. 2017;174:476-484.

    13. Stacy M, Kurlan R, Burke J, Siegert S, Liang G, O’Brien C. An MCID for AIMS Dyskinesia Total Score Change in Subjects with Tardive Dyskinesia. Mov Disord. 2017; 32 (suppl 2).

  • 22 Mar 2018 10:33 AM | Anonymous

    Authors:
    Thi Dang, PharmD Candidate 2019: UMKC School of Pharmacy
    Leigh Anne Nelson, PharmD, BCPP: UMKC School of Pharmacy

    Alcohol Use Disorder (AUD) is a pattern of alcohol use that includes compulsive alcohol use, loss of control over alcohol intake, and having withdrawal symptoms when decreasing or ceasing alcohol intake. Alcohol effects on physical, psychological, and mental health can lead to many diseases and injury-related health conditions. In the United States, AUD is most common between ages 18 through 29 and overall, the rate of AUD is increasing. The Amercian Psychiatric Association (APA) developed a new practice guideline in 2018, which provides recommendations regarding appropriate use of medications for treatment of AUD, assessment to reduce the psychological and public health consequences from problematic alcohol use and guidelines to enhance the effectiveness of treatment. APA recommends appropriate pharmacotherapy to patients with AUD, including naltrexone, acamprosate, disulfiram, topiramate, and gabapentin. Additionally, the guideline cautions against use of certain medications, such as antidepressants and benzodiazepines.

    Naltrexone is offered to patients with moderate to severe AUD or opioid use disorder to reduce alcohol consumption and help decrease cravings. The recommended starting dose of oral naltrexone is 50 mg daily and maximum is 100 mg daily. Common adverse events from oral naltrexone include abdominal pain, nausea, diarrhea, vomiting and dizziness. Overall, it is well tolerated. For long acting naltrexone, patients may consider naltrexone intramuscular (IM) injection. The recommended dose is 380 mg IM every 4 weeks. Associated side effects of intramuscular naltrexone include pain or induration at the injection site and increased potential for bleeding in patients who take anticoagulants. Because naltrexone reduces the efficacy of opioids for analgesia and elevates hepatic enzymes, APA recommends against using naltrexone as a treatment for AUD if patients also use opioids or anticipate the need for opioids in the near future. Naltrexone should also be avoided in patients with acute hepatitis or liver failure.

    Acamprosate is recommended to treat patients with moderate to severe AUD and helps to reduce alcohol consumption. The recommended starting dose is 666mg three times daily. A common side effect is diarrhea. Overall, it is well tolerated. Acamprosate is excreted through kidneys, hence, serum creatine should be measured at baseline. Acamprosate is not recommended for patients who have severe renal impairment or when CrCl is less than 30 mL/min. In patients with mild to moderate renal impairment with CrCl between 30-50 mL/min, the acamprosate dose should be reduced. The main barrier of using acamprosate is the medication needs to be dosed three times a day.

    Disulfiram is offered to patients with moderate to severe AUD, who are intolerant to naltrexone and acamprosate. It is not the first line of treatment. Disulfiram is appropriate only for patients who seek abstinence and are actively using alcohol or products containing alcohol. The usual recommended dose of disulfiram is 250 mg daily and common side effects include liver toxicity, tachycardia and QTC prolongation. Disulfiram is associated with several drug interactions that may limit its use and is not recommended in patients with seizure disorders. Ritonavir and other antiretroviral medications increase disulfiram levels through CYP450 3A4 and metronidazole can cause psychosis and confusion when combined with disulfiram. To help avoid possible drug interactions with disulfiram, patients should let healthcare providers or emergency personnel know that they are taking disulfiram.

    Topiramate is recommended for patients with moderate to severe AUD, who are intolerant to naltrexone and acamprosate. The recommended starting dose is 200-300 mg daily. Common adverse events include weight loss, sedation, cognitive dysfunction and dizziness. Before starting topiramate as an initial treatment for AUD, it is appropriate to assess the patient’s cognitive status and renal function. In patients with renal impairment, the topiramate dose should be reduced.

    Gabapentin helps to reduce the alcohol consumption and increases the rate of abstinence in patients with AUD. The recommened starting dose is between 900 to 1800 mg/day and associates with common adverse events include fatigue, insomina, and headache. In patients with renal impairment, the dose of gabapentin should be adjusted.

    APA recommends against use of specific medications, including antidepressants and benzodiazepines. Antidepressant medications should not be used for treating AUD unless the patient has comorbid conditions, such as depression or anxiety disorder. Before starting pharmacotherapy for patients with AUD, the initial evaluation should include the assessment for comorbid psychiatric disorders. Benzodiazepines are not the primary treatment of AUD, except for alcohol detoxification or the treatment of alcohol withdrawal. Because of the risk for sedation, behavioral impairment, respiratory depression, benzodiazepines or other sedative-hypnotic agents should be limited.

    To improve the quality of care and treatment outcomes for patients with AUD, APA developed this updated practice guideline to provide information on the comparative effectiveness of naltrexone, acamprosate, topiramate, gabapentin, and disulfiram. Additionally, the practice guideline includes recommendations and sugesstions related to the psychiatric evaluation of patients with AUD.


    Reference:

    American Psychiatric Association (2018, January 19). The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. Retrieved Feburary 19, 2018, from https://psychiatryonline.org/doi/pdf/10.1176/appi.books.9781615371969


  • 22 Mar 2018 10:27 AM | Anonymous

    Author: Nicole Burns, PharmD; PGY-1 Pharmacy Resident: Christian Hospital

    Adherence is just one of many potential barriers that may prevent patients from reaping the benefits of their prescribed therapies. Fortunately, there are a number of tools available to assist them with the task of remembering to take their medication. Many patients utilize applications on their smart phone as well as alarms, calendars, pill boxes, and various other reminders. Although non-adherence is common across all areas of medicine, patients with  Abilify MyCite®, aripiprazole with an Ingestible Event Marker (IEM), was approved by the Food and Drug Administration in November of 2017. This is the first approved medication in the United States with a digital ingestion tracking system. If your first thought was that this technology could potentially bring a schizophrenic patient’s delusion to life, you aren’t alone. It is rather ironic that the first roll-out of an ingestible medication tracking system is in a medication used for patients with psychiatric disorders.

    The Abilify MyCite® system is composed of three main components: an oral tablet with a built-in IEM, a patch, and a smart phone application. The Abilify MyCite® Patch should be applied to the left side of the body just above the lower edge of the rib cage. After ingestion, the IEM in the Abilify MyCite® tablet will become activated upon interaction with gastric fluid and will then send a signal to the patch that the medication has been taken. Patients must also download the MyCite® application to their phone and have Bluetooth enabled in order for the data to be recorded. Of note, it may take up to two hours for the system to detect ingestion although most ingestions are detected within 30 minutes.

    Patients may take this medication with or without food. The MyCite® Patch should remain on the individual during activities such as showering, swimming, and exercising. The MyCite® Patch should be replaced at least one weekly. Otherwise, the phone application will conveniently prompt patients to change their patch when needed.

    This technology serves additional purposes other than tracking ingestion. Abilify MyCite® also has the capability to measure a patient’s physical activity via step counting and detect sleep duration and disruptions by recording changes in posture. This information may be incredibly helpful to healthcare providers, as sleep disturbances and abrupt changes in amount of physical activity may serve as markers of a worsening psychological condition that could require immediate intervention.

    During a small four-week observational pilot study in 12 patients with bipolar and 16 patients with schizophrenia, feasibility and patient acceptance of the digital ingestion tracking technology was evaluated. Patients included in the pilot were required to be on a stable regimen of oral mood stabilizers or antipsychotics for at least 14 days with no anticipation of changes being made during the study.

    Candidates were excluded if they scored a three or higher on the suspiciousness/paranoia section of the Brief Psychiatric Rating Scale (BPRS). This tool is utilized to assess the severity of a patient’s psychiatric symptoms with a score from 1-7, with 1 being not present, 3 being mild, and 7 being extremely severe. Patients were also excluded if they had diagnoses or symptoms of substance use disorder, unstable medical illnesses, implanted electrical devices, or were pregnant.

    In this particular patient population, Abilify MyCite® did not lead to worsened psychosis. In fact, 70% of the patients in this pilot found the concept of the digital tracker easy to understand. A total of 89% thought the digital tracker could be useful to them and 78% wanted reminders sent to them if they forgot to take their medication.

    The most common adverse effect in this study was skin irritation at the patch site (occurred in 18% of participants). One patient was withdrawn from the study due to worsening paranoia and development of a BPRS score of >3. The patient was known to have a prior history of paranoia, but did not express any concerns related to the ingestible tracker or study staff. It was determined that the exacerbation was unrelated to the patient’s participation in the study.

    Although the first medication to be marketed with this digital tracking technology was tested in a clinically stable patient population with psychiatric ailments, the clinical utility of the tracking device itself is limitless. There are many ongoing studies pertaining to application of this technology to medications for cardiovascular diseases, Hepatitis C, and tuberculosis with promising preliminary results in hundreds of patients. Additionally, future generations of patients will be excellent candidates for digital tracking of medication adherence for a wide variety of medical conditions, as more advanced technology is already largely present and welcomed in their daily lives.

    References:

    1. Abilify MyCite® (aripiprazole tablets with sensor) [package insert]. Otsuka America Pharmaceutical Inc., Rockville, MD; 2017. https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/207202lbl.pdf. Accessed February 15, 2018.

    2. Rosenbaum L. Swallowing a spy- The potential uses of digital adherence tracking. N Engl J Med. 2018;378(2):101-103.

    3. Kane JM, Perlis RH, DiCarlo LA, Au-Yeung K, Duong J, and Petrides G. First experience with a wireless system incorporating physiologic assessments and direct confirmation of digital tablet ingestions in ambulatory patients with schizophrenia or bipolar disorder. J Clin Psychiatry. 2013;74(6):e533-540.

    4. Proteus Digital Health, Inc. Proteus Digital Health website. https://www.proteus.com. Accessed February 20, 2018.


  • 22 Mar 2018 10:23 AM | Anonymous

    Authors:
    Hoda Alhlou, PharmD Candidate 2018: UMKC School of PharmacySteve Stoner, PharmD, BCPP: UMKC School of Pharmacy

    A new innovative technology has been introduced the in the area of mental health with Abilify MyCite®. The technology is a combination of both drug and medical device used to help track and monitor medication adherence in patients with psychiatric conditions for which aripiprazole is an appropriate treatment option. These conditions may include schizophrenia, major depressive disorder, and bipolar disorder. A unique property of this technology is that it will provide the option to alert caregivers and healthcare providers when the patient administers a dose. In order to be a participant in this new drug monitoring system, patients are required to provide their consent and to provide others involved in their care with the monitoring information. The MYCITE® application can also track patient’s self-reported mood and rest. There are four elements to the Abilify MyCite® System, which include:

    1. Aripiprazole tablet with an Ingestible Event Marker (IEM)® sensor inside
    2. MYCITE® transdermal patch
    3. MYCITE® Application (available only on smartphones)
    4. Web-based portal available for caregivers and healthcare providers

    Dosages are available in 2mg, 5mg, 10mg, 15mg, 20mg, and 30mg with the recommended starting dose recommended to be 10-15mg daily with titration to a maximum dose of 30mg daily. The application of the transdermal patch should be accurate and instructions are available on the MYCITE® application. As with most transdermal applications, the patch should not be taken off while showering, swimming or exercising and can be changed weekly or sooner, if necessary.


    Reference:

    Abilify Mycite®. [package insert]. Otsuka Pharmaceutical Co, Tokyo, Japan; 2017.



    A Detailed Overview of Abilify MyCite: Utilization of Adherence Trackers in Patients with Psychiatric Disorders

    Author: Nicole Burns, PharmD; PGY-1 Pharmacy Resident: Christian Hospital

    Adherence is just one of many potential barriers that may prevent patients from reaping the benefits of their prescribed therapies. Fortunately, there are a number of tools available to assist them with the task of remembering to take their medication. Many patients utilize applications on their smart phone as well as alarms, calendars, pill boxes, and various other reminders. Although non-adherence is common across all areas of medicine, patients with Abilify MyCite®, aripiprazole with an Ingestible Event Marker (IEM), was approved by the Food and Drug Administration in November of 2017. This is the first approved medication in the United States with a digital ingestion tracking system. If your first thought was that this technology could potentially bring a schizophrenic patient’s delusion to life, you aren’t alone. It is rather ironic that the first roll-out of an ingestible medication tracking system is in a medication used for patients with psychiatric disorders.

    The Abilify MyCite® system is composed of three main components: an oral tablet with a built-in IEM, a patch, and a smart phone application. The Abilify MyCite® Patch should be applied to the left side of the body just above the lower edge of the rib cage. After ingestion, the IEM in the Abilify MyCite® tablet will become activated upon interaction with gastric fluid and will then send a signal to the patch that the medication has been taken. Patients must also download the MyCite® application to their phone and have Bluetooth enabled in order for the data to be recorded. Of note, it may take up to two hours for the system to detect ingestion although most ingestions are detected within 30 minutes.

    Patients may take this medication with or without food. The MyCite® Patch should remain on the individual during activities such as showering, swimming, and exercising. The MyCite® Patch should be replaced at least one weekly. Otherwise, the phone application will conveniently prompt patients to change their patch when needed.

    This technology serves additional purposes other than tracking ingestion. Abilify MyCite® also has the capability to measure a patient’s physical activity via step counting and detect sleep duration and disruptions by recording changes in posture. This information may be incredibly helpful to healthcare providers, as sleep disturbances and abrupt changes in amount of physical activity may serve as markers of a worsening psychological condition that could require immediate intervention.

    During a small four-week observational pilot study in 12 patients with bipolar and 16 patients with schizophrenia, feasibility and patient acceptance of the digital ingestion tracking technology was evaluated. Patients included in the pilot were required to be on a stable regimen of oral mood stabilizers or antipsychotics for at least 14 days with no anticipation of changes being made during the study.

    Candidates were excluded if they scored a three or higher on the suspiciousness/paranoia section of the Brief Psychiatric Rating Scale (BPRS). This tool is utilized to assess the severity of a patient’s psychiatric symptoms with a score from 1-7, with 1 being not present, 3 being mild, and 7 being extremely severe. Patients were also excluded if they had diagnoses or symptoms of substance use disorder, unstable medical illnesses, implanted electrical devices, or were pregnant.

    In this particular patient population, Abilify MyCite® did not lead to worsened psychosis. In fact, 70% of the patients in this pilot found the concept of the digital tracker easy to understand. A total of 89% thought the digital tracker could be useful to them and 78% wanted reminders sent to them if they forgot to take their medication.

    The most common adverse effect in this study was skin irritation at the patch site (occurred in 18% of participants). One patient was withdrawn from the study due to worsening paranoia and development of a BPRS score of >3. The patient was known to have a prior history of paranoia, but did not express any concerns related to the ingestible tracker or study staff. It was determined that the exacerbation was unrelated to the patient’s participation in the study.

    Although the first medication to be marketed with this digital tracking technology was tested in a clinically stable patient population with psychiatric ailments, the clinical utility of the tracking device itself is limitless. There are many ongoing studies pertaining to application of this technology to medications for cardiovascular diseases, Hepatitis C, and tuberculosis with promising preliminary results in hundreds of patients. Additionally, future generations of patients will be excellent candidates for digital tracking of medication adherence for a wide variety of medical conditions, as more advanced technology is already largely present and welcomed in their daily lives.

    References:

    1. Abilify MyCite® (aripiprazole tablets with sensor) [package insert]. Otsuka America Pharmaceutical Inc., Rockville, MD; 2017. https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/207202lbl.pdf. Accessed February 15, 2018.

    2. Rosenbaum L. Swallowing a spy- The potential uses of digital adherence tracking. N Engl J Med. 2018;378(2):101-103.

    3. Kane JM, Perlis RH, DiCarlo LA, Au-Yeung K, Duong J, and Petrides G. First experience with a wireless system incorporating physiologic assessments and direct confirmation of digital tablet ingestions in ambulatory patients with schizophrenia or bipolar disorder. J Clin Psychiatry. 2013;74(6):e533-540.

    4. Proteus Digital Health, Inc. Proteus Digital Health website. https://www.proteus.com. Accessed February 20, 2018.


  • 22 Mar 2018 10:15 AM | Anonymous

    Authors:
    Afreen Syeda Ziauddin, Pharm.D. Candidate 2019: St. Louis College of Pharmacy
    Laura Challen, Pharm.D., MBA, BCPS, BCACP: St. Louis College of Pharmacy

    The prevalence of autism has skyrocketed over the last decade. In the 1980’s, one in 2000 children was diagnosed with autism. According to the CDC, that demographic has significantly increased to one in 68 children being diagnosed with autism in the United States.1 With autism on the rise, the cost of caring for autistic patients in the United States has increased to 236 billion dollars per year.2 The increased cost of caring for autistic patients is mainly attributed to the lifetime care that is associated with autism. This can be alleviated with early diagnosis and intervention.2 With the rise of this patient population, it has been speculated what role pharmacists play in the treatment of patients on the autistic spectrum. Pharmacists are well positioned to be a valuable resource in caring for and serving the autistic patient population in both a clinical and community setting.

    Autism spectrum disorder (ASD) is a rising neurodevelopmental disorder. While patients are usually diagnosed early, there are many aspects to being on the spectrum. Patients who are diagnosed with ASD usually display the social and cognitive defects associated with autism by the age of 3.3 ASD includes “core” symptoms, such as repetitive behaviors, language impairment, and lack of socialization.4 Milder forms of ASD include Asperger’s syndrome and pervasive developmental disorder (PDD). In the past, studies were performed to assess the effectiveness of certain pharmacological therapies in the treatment of core symptoms. The use of naltrexone, selective serotonin reuptake inhibitors, atypical antipsychotics, antidepressants, cholinergic agents, and oxytocin were studied in order to see their effectiveness in treating core symptoms.5 Unfortunately, these studies were deemed inconclusive, and as a result, there is currently no definitive treatment for the core symptoms of autism.5 Current pharmacological therapy is aimed at treating other aspects of autism such as: irritability, aggression, self-injury, hyperreactivity, and inattention.6 Agents, such as Risperdal® (risperidone) and Abilify® (aripiprazole), have been used in the treatment of aggression and mood, respectively.7 Despite the milestones made in treating certain symptoms of autism, the current needs of the autistic patient population and their families include the prevalence of adverse drug reactions (ADR’s), drug related problems (DRP’s) and medication adherence.7

    Newer research has further reinforced the need for psychiatry specialized pharmacists. In 2014, a randomized, prospective, open label study was published by the pharmacy faculty of Chiang Mai University in Chiang Mai, Thailand. They assessed the importance of psychiatry trained pharmacists in treating autistic patients.7 The inclusion criteria of this study required participants to be between the ages of 2 to 12 years old, meet the DSM IV criteria for autism, and demonstrate at least one disruptive behavior such as irritability, aggression, self-injury, or temper tantrums. The exclusion criteria for this study included a history of head trauma or stroke, abnormal ECG results, or comorbid psychiatric disorders. Over the course of eight weeks, patients were randomized in a 1:1 ratio to either a psychiatry specialized pharmacist (PS) or a non-specialized pharmacist in assessing their currently pharmacotherapy regimen.7 The primary outcome of this study was assessing the number of patients who demonstrated at least one drug related problem (DRP). The secondary outcome assessed the mean aberrant behavior checklist (ABC-Irritability) and number of DRP’s in each group.7 The aberrant behavior checklist measures the presence of behaviors usually prevalent in autistic patients such as irritability, aggression, self-injury, and tantrums. An increase in this score directly correlates with the presence of these behaviors, while a decrease in this score indicates less prevalence of these behaviors. As a result of this study, it was found that the prevalence of DRP’s decreased by 52% in the intervention group vs. 16% in the control group. The ABC-Irritability score decreased from 26.7 + 7.2 to 9.8 + 5.6 in the interventional group vs. 24.0 + 5.7 to 17.7 + 7.9 in the control group. Potential limitations of this study include a disproportionate amount of patients taking risperidone in the control group and having a higher percentage of male patients. Despite limitations, the data suggests that PS pharmacists are a valuable resource in serving autistic patients.7 The collaboration of PS pharmacists with the healthcare team can further increase patient outcomes by potentially catching more medication errors, develop medication protocols, and even promoting positive perceptions about medications leading to increased medication adherence.7

    In addition to the increasing need for PS pharmacists, community pharmacists play an equally important role. Autism not only affects patients, but also their families. Community pharmacists are well positioned to interact with patients’ families and guide caretakers. They play an increasing role in assessing the treatment of non-core symptoms of autism such as insomnia, mood, anxiety, hyperreactivity, and attention deficit disorders.4 Within the community pharmacy setting, pharmacists can also play a vital role in recommending alternative dosage forms, such as compounded products, for autistic patients. Dosage forms such as suppositories, solutions, suspensions, and tablets can be made to meet the individual needs of patients with ASD.8

    The growing demographic of autistic patients has warranted the need for pharmacists to be aware and trained in serving this patient population. By doing so, pharmacists will be better positioned to work with patients, their families, and other healthcare providers in promoting optimal patient care.


    References:

    1. Autism Speaks. New government survey pegs autism prevalence at 1 in 45. www.autismspeaks.org/science/science-news/new-government-survey-pegs-autism-prevalence-1-45. Accessed February 19, 2018.

    2. Autism Speaks. Lifetime Costs of Autism Average $1.4 Million to $2.4 Million. https://www.autismspeaks.org/science/science-news/lifetime-costs-autism-average-millions. Accessed February 19, 2018.

    3. Terrie, Y. Understanding Autism: The Role of the Pharmacist in the Management of Autism. Pharmacy Times. 2007;12:53-62.

    4. Autism Speaks. Symptoms of Autism. https://www.autismspeaks.org/what-autism/symptoms. Accessed February 19, 2018.

    5. Bowers K, Lin P, Erickson C. Pharmacogenomic Medicine in Autism: Challenges and Opportunities. Pediatr Drugs. 2015;17:115-124.

    6. Farmer C, Thurm A, Grant P. Pharmacotherapy for the Core Symptoms in Autistic Disorder: Current Status of Research. Drugs. 2013;73:303-314.

    7. Wongpakaran R, Suansanae T, Tan-khum T, et al. Impact of providing specialty pharmacist intervention on reducing drug-related problems among children with autism spectrum disorder related to disruptive behavioural symptoms: A prospective randomized open-label study. J Clin Pharm Ther. 2017;42:329-335.

    8. Community Pharmacy. Autism. http://communitypharmacymd.com/autism/. Accessed February 20, 2018.


  • 22 Mar 2018 9:56 AM | Anonymous

    Authors:
    Tera Raymond, PharmD; PGY-1 Pharmacy Resident: Kansas City VA Medical Center
    Keith Anderson, PharmD, BCPP: Kansas City VA Medical Center
    Rachel Walker, PharmD, BCPP: Kansas City VA Medical Center

    Parkinson’s disease, a chronic and progressive neurologic disorder, afflicts nearly 10 million people worldwide.1 The characteristic motor symptoms of Parkinson’s disease, including bradykinesia, muscular rigidity, resting tremor, and postural instability, are thought to be caused by a loss of dopamine producing cells, along with decreased dopamine concentrations within the brain.2 Many of the common therapies available for Parkinson’s disease work to alleviate these motor symptoms through either dopamine agonism or blockade of dopamine metabolism in the brain. Despite medication strategies being available to manage bothersome motor symptoms, no therapies exist for the prevention or cure of Parkinson’s disease. While medication therapies are available for managing the burden that may arise with progressive motor symptoms, even fewer treatment options are available for non-motor symptoms, which are often reported by patients and caregivers as more troublesome and distressing.2

    Non-motor symptoms, such as depression, dementia, and sleep disturbances are associated with a decreased quality of life and increased lifestyle strain to patients and their caregivers than the more well-known motor symptoms.3 Psychosis is the most frequently reported non-motor symptom, and is often the most debilitating, affecting more than 50% of patients with Parkinson’s disease.4,5 The clinical presentation may vary, but is generally characterized by features such as visual and presence hallucinations and less commonly delusions and illusions.6 Previously, there had been no standard diagnostic criteria for Parkinson’s disease psychosis. However, in 2007 a new set of criteria was proposed by the National Institutes of Neurological Disorders and Stroke-National Institute of Mental Health (NINDS-NIMH).7 This new criteria defines Parkinson’s disease psychosis as the presence of illusions, hallucinations, delusions, or a false sense of presence that is recurrent or continuous for one month after the onset of Parkinson’s disease, and cannot be attributed to another cause.7

    The underlying pathophysiology of Parkinson’s disease psychosis is associated with three main neurotransmitter systems: dopaminergic, cholinergic, and serotonergic.3 The primary hypothesis for psychosis previously revolved around the overstimulation of dopamine receptors in the brain, and subsequently involved dose reduction of dopaminergic medications as initial therapy for psychosis.3 However, several observations have shown no difference in resolution of psychotic symptoms with dopaminergic medication adjustments.3 Additional neurotransmitter pathways have become entwined in the mechanism, specifically an imbalance of anticholinergic and dopaminergic systems in the striatum and a loss of serotonergic neurons and dysregulation in the brain.3 In addition, other factors of Parkinson’s disease outside of neurotransmitters may also play a part in the development of psychosis, including advanced Parkinson’s disease, patient age, and cognitive decline.3 Despite a proposed mechanism for the development of psychosis and the neurotransmitters thought to play a part in developing symptoms, the therapies available for treatment are sparse.

    Historically, antipsychotic medications have been the primary treatment modality studied in regards to managing Parkinson’s disease psychosis.  Prior to initiating or adjusting medication therapy for symptom management, any potential underlying causes for acute psychosis should be addressed, such as including acute infections or ingestion of stimulants.8 Medication adjustments and tailoring of therapies to remove any non-essential medications that may exacerbate or worsen psychosis symptoms, such as anticholinergic medications or benzodiazepines, is a key first step.9 This may also require a step-wise approach to remove dopaminergic medications, while still maintaining motor function.7 At this step in therapy, patients and caregivers may have to consider initiation of additional medications if psychosis symptoms are not effectively managed with adjustments of dopaminergic medications.7

    Currently, the medications commonly utilized in Parkinson’s disease psychosis include quetiapine and clozapine. However, more recently, pimavanserin has been studied as a novel therapy for this unique niche of patients.3 While these antipsychotics are the mainstay of therapy, it is important to note that the second generation antipsychotics still carry a black box warning in patients with dementia in regards to concern for causing sudden death.9 First generation antipsychotics are often not utilized in this population due to lack of data supporting improvement of psychosis symptoms, and the tendency to cause worsening of motor symptoms.10 Second generation antipsychotics, including olanzapine, aripiprazole, and risperidone have also been studied. The data is limited supporting the use of these medications to improve psychosis symptoms and have not shown statistical significance for symptom relief but instead have shown a worsening of motor symptoms.3 In patients with both psychosis and dementia, cholinesterase inhibitors have also been studied. Although data from these trials show improvement in cognitive function, there was no significant changes in psychotic symptoms.3

    Clozapine is the most heavily-studied therapy for Parkinson’s disease psychosis, with evidence to support its use in minimizing psychosis symptoms, including hallucinations, due to its unique mechanism of action involving all three neurotransmitters affected in psychosis.3,7 Although recommended in guidelines and showing promise in clinical trials, clozapine requires extensive monitoring and frequent laboratory draws due to the risk of agranulocytosis.3,11 At the lower doses utilized in Parkinson’s disease, clozapine has not been shown to cause long-term metabolic problems as seen with higher doses.  However, other side effects, such as hypotension and sedation, are still commonly encountered.9 While effective for symptom control and with little to no worsening of motor symptoms, the intense monitoring makes it a less favorable choice for initial management.9 Despite the data that supports clozapine’s use in therapy, quetiapine is often utilized as first-line therapy.  Quetiapine is similar to clozapine in structure and mechanism, but with less frequent required monitoring.9 Although quetiapine has been studied in the treatment of Parkinson’s disease psychosis, evidence is lacking regarding its efficacy in managing psychosis symptoms, specifically hallucinations.3 Regardless of the data, use of quetiapine is still recommended by the American Academy of Neurology guidelines and has not been shown to worsen motor symptoms.11

    Pimavanserin, a novel therapy, has recently received FDA approval for hallucinations and delusions associated with Parkinson’s disease psychosis.12 Pimavanserin acts via a combination of selective serotonin antagonism and inverse agonism, and demonstrated beneficial results in clinical trials by reducing non-motor symptoms associated with psychosis, including minimization of hallucinations and delusions.12 When compared to placebo, pimavanserin did not show an effect on worsening motor function, and was the first medication to show a beneficial effect in reducing caregiver burden.12,4 The most common adverse reactions noted in clinical trials were nausea, constipation, peripheral edema, and confusion. Post-marketing monitoring has also noted adverse effects including somnolence, rash, and reactions similar to angioedema.12 Pimavanserin is classified as an atypical antipsychotic and still carries a warning for increased mortality in elderly patients with dementia and risk for increased QT prolongation, similar to warnings and precautions with other antipsychotics.12

    Pimavanserin shows potential as a novel agent for management of non-motor symptoms associated with Parkinson’s disease psychosis.  However, more data and clinical trials are needed comparing pimavanserin versus current treatments to determine its appropriate place in therapy. In addition, the guidelines for non-motor symptoms in Parkinson’s disease by the American Academy of Neurology have not been updated since 2006.  Consequently, quetiapine and clozapine are still recommended as first-line agents.11 Despite the lack of support within guidelines at this time, pimavanserin shows promise for use in patients suffering from hallucinations and delusions caused from Parkinson’s disease. With less rigorous monitoring and clinical data supporting its effect on psychosis, pimavanserin may soon find a place in the guidelines as recommended therapy for Parkinson’s disease patients.


    References:

    1. Connolly BS, Lang AE. Pharmacological treatment of Parkinson disease: a review. JAMA. 2014 Apr 23-30;311(16):1670-83. doi: 10.1001/jama.2014.3654.

    2. Combs BL, Cox AG. Update on the treatment of Parkinson's disease psychosis: role of pimavanserin. Neuropsychiatr Dis Treat. 2017 Mar 8;13:737-744. doi: 10.2147/NDT.S108948. eCollection 2017.

    3. Goldman JG1, Vaughan CL, Goetz CG. An update expert opinion on management and research strategies in Parkinson's disease psychosis. Expert Opin Pharmacother. 2011 Sep;12(13):2009-24. doi: 10.1517/14656566.2011.587122. Epub 2011 Jun 2.

    4. Cummings J, Isaacson S, Mills R, et al. Pimavanserin for patients with Parkinson's disease psychosis: a randomised, placebo-controlled phase 3 trial. Lancet. 2014 Feb 8;383(9916):533-40. doi: 10.1016/S0140-6736(13)62106-6. Epub 2013 Nov 1.

    5. Taddei RN, Cankaya S, Dhaliwal S, et al. Management of Psychosis in Parkinson's Disease: Emphasizing Clinical Subtypes and Pathophysiological Mechanisms of the Condition. Parkinsons Dis. 2017;2017:3256542. doi: 10.1155/2017/3256542. Epub 2017 Sep 12.

    6. Friedman JH. Parkinson disease psychosis: Update. Behav Neurol. 2013 Jan 1;27(4):469-77. doi: 10.3233/BEN-129016.

    7. Wilby KJ, Johnson EG, Johnson HE, Ensom MHH. Evidence-Based Review of Pharmacotherapy Used for Parkinson's Disease Psychosis. Ann Pharmacother. 2017 Aug;51(8):682-695. doi: 10.1177/1060028017703992. Epub 2017 Apr 6.

    8. Frei K, Truong DD. Hallucinations and the spectrum of psychosis in Parkinson's disease. J Neurol Sci. 2017 Mar 15;374:56-62. doi: 10.1016/j.jns.2017.01.014. Epub 2017 Jan 5.

    9. Chang A, Fox SH. Psychosis in parkinson’s disease: epidemiology, pathophysiology, and management. Drugs. 2016 Jul;76(11):1093-118. doi: 10.1007/s40265-016-0600-5.

    10. Weintraub D, Chen P, Ignacio RV, et al. Patterns and trends in antipsychotic prescribing for Parkinson disease psychosis. Arch Neurol. 2011 Jul;68(7):899-904. doi:10.1001/archneurol.2011.139.

    11. Miyasaki JM, Shannon K, Voon V, et al. Practice parameter: evaluation and treatment of depression, psychosis, and dementia in Parkinson disease (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006 Apr 11;66(7):996-1002.

    12. Neuplazid [package insert]. San Diego, CA: ACADIA Pharmaceuticals Inc.; 2017.



  • 22 Mar 2018 9:45 AM | Anonymous

    Authors:
    Lara Kerwin, PharmD and Roxane Took, PharmD
    Millennial Assistant Professors of Pharmacy Practice at the St. Louis College of Pharmacy

    The “411” on Millennials 

    ...as People:
    Students of the “Millennial Generation” are born between the years of 1980-2000. This group also goes by the name of “Gen Y,” “Nexters,” and the “Me, Me, Me Generation.”1-3 Historic events that have occurred during and impacted the way they view the world include September 11th, 2001; legalization of gay marriage, and the election of the first African American president of the United States of America. Millennials have grown up in the age of technology. They have a reputation for being lazy, entitled narcissists who “live with their parents but will save us all!”1

    ...as Learners:
    Millennial students are goal-oriented multi-taskers. They want context and to understand purpose behind the task at hand.3,4,14 They care more about collaborative, active learning in groups than studying. These learners may be needy for feedback and anticipate immediate responses from their instructors. Millennials appreciate scheduling flexibility as well as customization of learning experiences to their goals and interests.3-5 Having a strong predisposition toward praise for any work and that they do contributes to the generalization that Millennials have poor work ethic, lack critical thinking skills, and have a superficial awareness of self.6

    Precepting Millennials with Intention Several effective approaches to training Millennial learners in the experiential setting have been described:

    • ASHP’s Four Roles of a Preceptor7,13: Instructing, Coaching, Modeling, and Facilitating in sequence over the course of a rotation experience facilitates Millennial learners in building clinical confidence and competence in a stepwise fashion. These four roles played by you, the preceptor, also create many opportunities to offer feedback, which helps Millennials thrive. 
    • Bloom’s Taxonomy integrating into Kitchner & King’s Reflective Judgment Model8:
    1. When a student begins a rotation “module” or starts a rotation year, they respond well to boundaries and clearly-communicated high expectations that seem individualized; this is best facilitated through a preceptor who is personally invested in the student’s development and serves as a role model.
    2. As students feel comfortable with basic clinical knowledge or patient care skills, it is appropriate to challenge their “black and white” understanding of knowledge to explore and reflect upon clinical “gray areas.” This removes the safety blanket of recall-based, study guide-driven rote memorization from what is acceptable and forces the student to consider alternatives and draw new conclusions.
    3. Now that the Millennial is reflecting, encourage learning from mistakes through constant hypothesizing and testing. They may be hesitant to engage in this phase due to fear of failure or disappointing you, the preceptor. However, it is in this stage that they refine problem-solving skills and participate in “real” learning.
    • Creative Inter-Change Model9: Authentic Interactions allow for the preceptor and Millennial student to begin the learning experience from a place of open communication of expectations and goals. Appreciative Understanding allows both parties to learn about and from one another. Through Creative Integrating, the Millennial receives praise for “what’s going well” and constructive feedback for improvement opportunities, again building their confidence and competence. When they are showing consistent proficiency toward learning objectives and outcomes, Millennial learners are ready to Expand Capacity and handle additional responsibility, which should be encouraged by the preceptor.

    Table 1. Anticipated Challenges and Proposed Solutions for Precepting Millennials10-12,14


    References:

    1. Stein J. Millennials: the me, me, me generation. Time. May 2013. http://time.com/247/millennials-the-me-me-me-generation/.

    2. Gardner SF. Preparing for the nexters. Am J Pharm Educ. 2006;70(4):Article 87.

    3. Boysen PG, Daste L, Northern T. Multigenerational challenges and the future of graduate medical education. Ochsner J. 2016;16(1):101-107.

    4. Dilullo C, Mcgee P, Kriebel RM. Demystifying the millennial student: a reassessment in measures of character and engagement in professional education. Anat Sci Educ. 2011;4(July/August):214-226. doi:10.1002/ase.240.

    5. Preceptor Newsletter. http://news.pharmacy.vcu.edu/wp-content/uploads/sites/3395/2014/01/Newsletter_Vol_10_Issue_1_Winter_Spr_2014.pdf. Published 2014.

    6. Fjortoft N. The selfie generation and pharmacy education. Am J Pharm Educ. 2017;81(4):Article 61.

    7. Weitzel KW, Walters EA, Taylor J. Teaching clinical problem solving: a preceptor’s guide. Am J Heal Pharm. 2012;69(18):1588-1599. doi:10.2146/ajhp110521.

    8. Sylvia L, Barr J. What matters in a student-centered approach? In: Pharmacy Education: What Matters in Learning and Teaching. Sundbury: Jones & Bartlett Learning; 2011:25-56.

    9. Case Di Leonardi B, Gulanick M. Precepting and diversity: focus on cultural and generational differences. In: Precepting Graduate Students in the Clinical Setting. Chicago; 2008:83-99.

    10. Nevin CR, Westfall AO, Rodriguez JM, et al. Gamification as a tool for enhancing graduate medical education. Postgrad Med J. 2014;90:685-693. doi:10.1136/postgradmedj-2013-132486.

    11. Desy JR, Mph DAR, Wolanskyj AP. Milestones and millennials: a perfect pairing--competency-based medical education and the learning preferences of generation Y. Mayo Clin Proc. 2017;92(2):243-250. doi:10.1016/j.mayocp.2016.10.026.

    12. Meister J, Willyerd K. Mentoring Millennials. Harv Bus Rev. 2010;(May).

    13. Cuellar L, Ginsburg D. Preceptor’s Handbook for Pharmacists. 3rd ed. Bethesda: American Society of Health-System Pharmacists; 2016.

    14. Roberts DH, Newman LR, Schwartzstein RM. Twelve tips for facilitating millennials’ learning. Med Teach. 2012;34:274-278. doi:10.3109/0142159X.2011.613498.


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