Pharmacotherapy: The Journal of Human Pharmacology and Drug TherapyVolume 37, Issue 10 p. e112-e117 CorrigendumFree Access ACCP Virtual Poster Symposium This article corrects the following: ACCP Virtual Poster Symposium Volume 37Issue 6Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy pages: e38-e70 First Published online: June 22, 2017 First published: 18 October 2017 https://doi.org/10.1002/phar.2028AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat In ACCP Virtual Poster Symposium,1 the Case Report Abstracts were excluded from the originally published article. Here are the missing Abstracts: Case Reports ADR/Drug Interactions 213. Withdrawal Effects from Domperidone Requiring Prolonged Tapering Schedule. Pouran Manzouri, Pharm.D. and Matt Mink, BSP ACPR CSPI CGP; Poison and Drug Information Service (PADIS), Alberta Health Services, Calgary, AB, Canada Introduction: Domperidone is a dopamine blocker with both gastrokinetic and antiemetic activity. When used off-label in many countries to improve breast milk supply, cases of withdrawal syndrome have been reported on discontinuance. We present a case of domperidone withdrawal requiring prolonged tapering schedule. Case: A 32-year-old female was started on domperidone 20 mg QID for stimulation of milk production after giving birth. After 9 months, she stopped breastfeeding and domperidone was discontinued. Two weeks later, she presented to her physician with symptoms of insomnia, anxiety, nausea, headaches and palpitations. The physician restarted domperidone at a dose of 20 mg TID with a dose tapering schedule of 10 mg weekly. A week later, the patient called a medication advice service complaining of increased insomnia with dose tapering attempts. A slower tapering rate of 5 mg per week was recommended. She attempted numerous times to discontinue domperidone, but each time her symptoms returned. She further decreased her tapering rate down to 2.5 mg every 2 weeks before successfully discontinuing domperidone 10 months later. Discussion: Domperidone withdrawal effects similar to our patient's symptoms have been reported in the literature. The Naranjo Adverse Drug Reaction Probability Scale (score = 6) was used to determine a probable causative link to the domperidone. Higher doses of domperidone may have contributed to the withdrawal symptoms by inducing tolerance. Tapering by 10 mg per week as cited in the literature, did not help our patient, and a longer tapering period was implemented. Whether this approach should be applied to similar cases is unclear. Conclusion: Domperidone use as a galactogogue is not without risk. Clinicians and nursing mothers should be aware of potential adverse effects including withdrawal symptoms, which may last several months. Higher risks for withdrawal may be observed in patients using doses greater than 30 mg per day for longer durations. 214. Lansoprazole-induced Thrombocytopenia: A Case Report. Mohamed Saad, Pharm.D., BCPS and Hassan Mitwally, Pharm.D., BCPS; Pharmacy Department, Al-Wakra Hospital, Hamad Medical Corporation, Qatar Introduction: Proton pump inhibitors (PPI) may rarely cause thrombocytopenia. To our knowledge, only one case of lansoprazole-induced thrombocytopenia has been reported previously. Case: A 50-year-old Asian male with history of diabetes mellitus type II, hypertension and coronary artery disease was admitted for ureteroscopy under general anesthesia. During anesthesia induction, he developed cardiac arrest. After return of spontaneous circulation, he was shifted to the intensive care unit where his home medications (aspirin and clopidogrel) were resumed and lansoprazole and subcutaneous heparin were initiated for stress ulcer prophylaxis and venous thromboembolism prophylaxis, respectively. His platelets dropped gradually from 315×103/mm3 on admission to nadir of 57×103/mm3 on day five. After excluding disseminated intravascular coagulopathy and heparin-induced thrombocytopenia; lansoprazole was changed to ranitidine. Platelets recovered over next few days. Later during his hospital stay, he developed thrombocytosis then ranitidine was changed back to lansoprazole (re-challenge was not intended). His platelets dropped again from 669×103/mm3 to 315×103/mm3 on day 5 of re-initiation. After stopping lansoprazole, there was rebound increase in platelets to 567×103/mm3. Thorough review of his medical record showed that lansoprazole was prescribed for 7 days 30 months before this admission, platelets weren't checked at that time and he has been using pantoprazole for the last few weeks before admission. Discussion: This patient had probable lansoprazole-induced thrombocytopenia [Naranjo score = 8]. Although thrombocytopenia didn't occur in the second time, his platelet count decreased by more than 50% which confirms the causal relationship. PPI-induced thrombocytopenia was previously reported with omeprazole, lansoprazole and pantoprazole. Interestingly; this patient's platelets were stable on pantoprazole, indicating that this adverse drug reaction (ADR) is an individual agent effect rather than a class effect. Conclusion: Lansoprazole may cause thrombocytopenia which is unlikely to be a class effect. Clinicians should be vigilant to this ADR when other common causes of thrombocytopenia are excluded. 215. Hyponatremia Associated with Long-Acting Injectable Paliperidone Use: A Case Report. Alex Isaacs, Pharm.D.1, Carol Ott, Pharm.D.1 and Shannon Eaves, Pharm.D.2; (1) Department of Pharmacy Practice, Purdue University College of Pharmacy/Eskenazi Health, Indianapolis, IN (2) Department of Pharmacy Services, Eskenazi Health, Indianapolis, IN Introduction: Paliperidone is an atypical antipsychotic with adverse reactions including injection site reactions, sedation, and extrapyramidal disorder. Hyponatremia due to atypical antipsychotics is rare, but we report a case of hyponatremia due to long-acting injectable (LAI) paliperidone. Case: A 62-year-old male with schizophrenia was admitted for psychosis and administered a one-time dose of LAI paliperidone 234 mg IM. A medication history revealed only LAI paliperidone. On hospital day eight, the serum sodium was 111 mEq/L with a repeat of 110 mEq/L. Serum osmolality, urine osmolality, and urine sodium ruled out psychogenic polydipsia. Paliperidone was the only medication the patient had received in the past three months, suggesting this as a cause of hyponatremia due to the syndrome of inappropriate diuretic hormone (SIADH). Hyponatremia was managed with parenteral normal saline, but while hyponatremic, a witnessed seizure occurred which was acutely managed. Four weeks later, paliperidone 234 mg IM was administered and the patient was discharged only on LAI paliperidone. Two weeks later, the patient was readmitted with encephalopathy. Repeat laboratory testing revealed hyponatremia due to SIADH. With a Naranjo score of 7, paliperidone was discontinued as the probable cause of SIADH. Six weeks after the last dose of paliperidone, the serum sodium was within normal limits for the first time in three months. Discussion: SIADH has been documented with atypical antipsychotics. A previous case report documented SIADH with LAI paliperidone two days after the initial dose. However, the current case showed delayed onset occurring one year after initiation. Additionally, the strength of this case report is the recurrent episodes of hyponatremia due to SIADH occurring due to the continuation of LAI paliperidone. Conclusion: Long-acting injectable paliperidone can induce hyponatremia and providers must be aware of and monitor for the possibility of this adverse effect. 216. Enzalutamide-Warfarin Interaction Necessitating Warfarin Dosage Adjustment: A Case Report. Jenna L. Parrett, Pharm.D., MPA, BCPS1, Anne B. Reaves, Pharm.D., BCACP2, Timothy Self, Pharm.D.3 and Ryan E. Owens, Pharm.D., BCPS4; (1) Blount Memorial Hospital, Maryville, TN (2) Methodist University Hospital, Memphis, TN (3) College of Pharmacy, The University of Tennessee Heath Science Center, Memphis, TN (4) Department of Pharmacy: Clinical and Administrative Sciences, University of Oklahoma College of Pharmacy, Oklahoma City, OK Introduction: Enzalutamide has been implicated as a moderate CYP2C9 and CYP2C19 inducer. Therefore, it is recommend to avoid narrow therapeutic index drugs that are substrates of these enzymes, such as warfarin. Other than conducting additional INR monitoring, virtually no clinical guidance is provided regarding the management of this interaction if used concomitantly. Case: A 77-year-old Caucasian male with a past medical history of deep vein thrombosis presented to clinic for warfarin management post-hospital discharge with an INR of 1.4, receiving warfarin 56 mg weekly. The patient had previously been stable on a weekly warfarin dose of 45 mg but it was noted he had recently started enzalutamide. The patient was increased to warfarin 63 mg weekly and maintained an INR of 2.1. Enzalutamide was temporarily discontinued and the patient's warfarin dose was decreased to 32 mg per week, resulting in two therapeutic INRs. Enzalutamide was later restarted and warfarin was increased to 63 mg weekly which resulted in an INR of 3.2. Discussion: A single-dose pharmacokinetics study first described this interaction, indicating significant reductions in plasma concentrations of both S-warfarin and R-warfarin by enzalutamide. Despite these findings, one previous case report described no interaction in a patient taking enzalutamide and warfarin concomitantly for 1 year, contributed in part to a possible CYP2C9 polymorphism. Although our patient's course was not without confounding circumstances that could have also effected the INR, including a hospital admission, the changes in INR after starting and stopping enzalutamide can be adequately correlated. Additionally, no other interacting medications, dietary vitamin K changes, or interacting disease states were noted during his clinical course. Conclusion: Despite enzalutamide package labeling, avoiding warfarin is not always feasible in clinical practice. Our case highlights this interaction's clinical significance and provides insight on appropriate management, with approximately 30–50% adjustment in warfarin dose needed to maintain a therapeutic INR. 217. Sulfamethoxazole/Trimethoprim Use Resulting in Liver Transplantation Case Report. Taylor Hendrix, Pharm.D. candidate1, Danielle Padgett, Pharm.D.2 and Shanise Patterson, Pharm.D.3; (1) College of Pharmacy, University of Tennessee Health Science Center, Memphis, TN (2) Methodist University Hospital, Memphis, TN (3) Methodist South Hospital, Memphis, TN Introduction: SMX-TMP is commonly prescribed for the treatment of UTIs and SSTIs, however there is little evidence regarding identification of patients at risk of severe adverse reactions. Acute fulminant liver failure is a rare adverse effect of SMX-TMP, however the frequency has not been defined. This case highlights the detrimental effects of SMX-TMP requiring liver transplantation. Case: A 23-year-old African American female with a history of hypertension and morbid obesity presented with weakness and fatigue for one week. The patient was prescribed a three-day course of SMX-TMP and on day two of therapy started to experience RUQ pain, vomiting, and rash. On day three of therapy the patient presented with scleral icterus and positive monospot test. Her AST and ALT were >2000 U/L and total bilirubin was 16.1 mg/dL. Ten days after the beginning of SMX-TMP therapy, the patient was in acute hepatic failure with a total bilirubin of 25.16 mg/dL, INR of 4.2, and SCr of 2.5 mg/dL. Patient tested negative for glucose-6-phosphate deficiency(G6PD), EBV IgM was negative, EBV IgG was positive. Hepatitis A, B, C, HIV, and HSV were negative. Acetaminophen was not detectable. The patient was listed in UNOS as status Ia for orthotopic liver transplant (OLT) with a MELD score of 40 thirteen days after beginning SMX-TMP therapy, and received a deceased donor liver transplant one day later. She was discharged six days post successful transplant. Discussion: Patient had no known risk factors for adverse effects related to SMX-TMP, including renal or hepatic disease, G6PD deficiency, or documented folate deficiency. Conclusion: We present the first known case of hepatic failure requiring OLT presumed secondary to a three-day course of SMX-TMP with negative G6PD and positive monospot test with negative EBV IgM. Critical Care 218. Case Report of Guanfacine to Transition from Dexmedetomidine in a Patient with Labile Blood Pressure. Abigail Burka, Pharm.D.1 and John Barwise, MD2; (1) Pharmacy Practice, Lipscomb University, Nashville, TN (2) Veterans Affairs Tennessee Valley Healthcare System Introduction: ICU delirium is associated with increased morbidity and length of stay. Dexmedetomidine, an α2A receptor agonist, may shorten the duration of delirium; however high costs often preclude prolonged use. To our knowledge there are no previous reports of using the highly selective α2A receptor agonist, guanfacine, to transition from IV dexmedetomidine in a delirious patient. Case: A 77-year-old male veteran with past medical history of alcohol abuse, depression and post-traumatic stress disorder was hospitalized following lobectomy. On POD#1, he developed ICU delirium which was treated with dexmedetomidine. As a transition to oral therapy, guanfacine 1 mg BID was initiated the following day and subsequently titrated to 2 mg BID. The patient remained CAM-ICU negative while on guanfacine monotherapy for 5 days, after which it was discontinued. On POD #10, the patient's respiratory status declined and he underwent tracheostomy to support mechanical ventilation. He became delirious and dexmedetomidine was reinitiated before transitioning to guanfacine 2 mg BID the following day. While on guanfacine monotherapy, the patient became CAM-ICU negative and was discharged to a nursing facility on POD #31. Overall, the patient was CAM-ICU positive 17.2% of his stay, but was CAM-ICU positive only 5.1% of the time he was treated with guanfacine monotherapy (p=0.0015). His blood pressure was labile throughout his ICU stay, however guanfacine was not associated with an increase in proportion of days with hypotension (1 vs 0.73, p=0.1422) or hypertension (0.4 vs 0.63, p=0.2665). Discussion: Although similar use of clonidine has been described for delirium, guanfacine's selectivity for the α2A receptor coupled with lack of activity at the I1-IBS receptor favors future investigation into guanfacine as an economic oral alternative to dexmedetomidine. Conclusion: This case suggests that guanfacine may be a viable oral delirium treatment for a patient with labile blood pressure. 219E. Neuroleptic Malignant Syndrome Secondary to Low Dose Quetiapine. Amie Algrim, Pharm.D.1 and G. Morgan Jones, Pharm.D., BCPS, BCCCP2; (1) Department of Pharmacy, Methodist University Hospital, Memphis, TN (2) Department of Pharmacy, Methodist University Hospital, Memphis, TN Emergency Medicine 220. Capsaicin Topical in Emergency Department Treatment of Cannibinoid Hyperemesis Syndrome. Rachael Duncan, Pharm.D. and Michelle Maguire, Pharm.D.; Department of Pharmacy, Swedish Medical Center, Englewood, CO Introduction: Marijuana is now reported as the most commonly used illicit drug in the United States. The rising rate of marijuana consumption has led to the classification of a new clinical condition, cannabinoid hyperemesis syndrome (CHS). Emergency physicians across the country are struggling to manage this new condition, finding most antiemetic treatments to be ineffective. A novel treatment approach that has shown some success is the use of capsaicin topical. Case: A 32 year old female presented to the emergency department with nausea, vomiting, and diffuse abdominal pain for 1–2 days. She reported being a daily marijuana user and endorsed taking frequent, hot showers to alleviate her symptoms. Once in the emergency room she was given multiple medications, including metoclopramide 10 mg IV, two doses of ondansetron 4 mg IV, hydromorphone 0.5 mg IV, ketorolac 30 mg IV, lorazepam 1 mg IV with no improvement in her symptoms. She was later treated with an application of capsaicin 0.025% cream to her abdomen with an improvement in nausea and vomiting, and was discharged home. Discussion: Capsaicin, the active component of chili peppers, is a new option emerging for the treatment of CHS. The TRPV1 receptor is found in the peripheral nervous system and has been found to be activated only by scalding heat greater than 109 degrees Fahrenheit and capsaicin. Capsaicin can also be used as a diagnostic tool. Conclusion: With the rise in cannabis legalization and use, the incidence of CHS is likely to increase exponentially. CHS should be considered in patients presenting with diffuse abdominal pain and severe nausea and vomiting with a significant history of marijuana use. The tell-tale sign of CHS is the resolution of symptoms while bathing in hot water. In patients presenting with the above signs and symptoms, topical capsaicin 0.025% should be considered. Endocrinology 221. Dramatic Lowering of HbA1C Upon Elimination of a Dietary Supplement: A Case Report. Emily Wiederanders, Pharm.D.1 and Lauren Odum, Pharm.D.2; (1) SSM Health (2) SSM Health St. Clare, Fenton, MO Introduction: Human growth hormone increases insulin resistance via increased glucose production and decreased peripheral glucose uptake. One dietary supplement, SeroVital®, claims to increase human growth hormone by 682%. This is the first case report to our knowledge linking the removal of this supplement to a profound reduction in HbA1C. Case: A 63-year-old Caucasian female was referred by her family medicine provider to the pharmacist for management of diabetes. Labs revealed an HbA1C of 13.7% and correlating glucose of 322 mg/dL. Upon review of her medications, she was taking metformin 1000 mg twice daily for the last week; this lowered home fasting glucose readings to about 250 mg/dL. It was also discovered that she was taking SeroVital®. The pharmacist recommended that she stop this supplement and a phone call one week later demonstrated an average 50 mg/dL decrease in morning fasting glucose readings. She reported no change in diet at this time. Glimepiride 1 mg daily was added. Two weeks later, the patient reported fasting glucose readings 90–130 mg/dL and a decrease in sugary beverage intake. After three months, the HbA1C was repeated and decreased to 6.4%, which was a 53% reduction from baseline. Discussion: Although case reports of this particular supplement worsening glucose levels are not found in the literature, human growth hormone has a known side effect of hyperglycemia. A limitation to this case is an unquantifiable report of dietary changes. However, she had no significant weight change and reported no dietary changes immediately after the supplement was stopped. Metformin typically has a maximum HbA1C lowering capacity of 1.5% and glimepiride of 2%; therefore, it is unlikely that these changes alone brought the patient to goal. Conclusion: The dramatic HbA1C lowering with minimal additional medication emphasizes the importance of analyzing all medications, including supplements, to improve chronic disease management. Hematology/Anticoagulation 222E. Treatment Failure of Apixaban in a Patient with Metastatic Pancreatic Cancer. Nicole East, Pharm.D., BCPP, Jesse Sullivan, Pharm.D., BCPS, BCCCP and Jaclyn Winnicki, Pharm.D. Candidate; School of Pharmacy and Health Sciences, Fairleigh Dickinson University, Florham Park, NJ 223. A Case of Intra-arterial Thrombolysis with Alteplase in a Patient with Hypothenar Hammer Syndrome but without Underlying Aneurysm. Harshal Shukla, Pharm.D. and Vicken Yaghdjian, Pharm.D.; Department of Pharmacy, Montefiore Medical Center, Bronx, NY, NY Introduction: Hypothenar hammer syndrome is a cause of symptomatic ischemia of the hand secondary to the formation of aneurysm or thrombosis of the ulnar artery in the setting of an incomplete palmar arch. Acute occlusive thrombus or embolus of the hand represents a complex problem that often may require immediate surgical intervention. Case: A 57-year-old former truck driver presented with worsening pain and subsequent development of significant cyanosis with early gangrenous changes of the left second and third fingertips. He had significant callous of the hypothenar eminence and reported that not only was his left hand his “driving” hand but he also used a cane in his left hand to ambulate. Initial angiogram revealed only ulnar artery occlusion at the wrist with reconstitution just distal to the hypothenar eminence. The catheter-directed thrombolytic regimen consisted of Alteplase 1 milligram (mg) per hour (total 24 mg over 24 hours) and Heparin was infused through the sheath sidearm at a rate of 500 units per hour. Repeat angiography was conducted after about 20 hours of infusion. This revealed a widely patent ulnar artery and resolution of the thrombus with antegrade filling of the deep palm arch. The digital vessels were seen now to continue from the arch to the digits. Discussion: Overall, favorable outcomes have been shown when thrombolysis is performed in the acute setting with angiographic or clinical improvement nearly 80 percent of the time. Nearly half of the reported cases have no complications but the remaining series report a pooled complication rate of about 18 percent. Conclusion: Catheter-directed thrombolytic therapy in situations of acute occlusive thrombus of the hand may provide a therapeutic option for patients with suspected hypothenar hammer syndrome. However, thrombolytic therapy carries risk of significant hemorrhagic complications. Before initiating therapy, careful judgment about the possibility for bleeding risk is required. Infectious Diseases 225. First Case of Pre-XDR TB in the Pacific Region. Angelina Eustaquio, Pharm.D.1, Racquel Sperrazzo, Pharm.D.1, Jason Boyd, Pharm.D.1 and Janna Manglona, MD2; (1) Pharmacy Department, Guam Memorial Hospital Authority, Tamuning, Guam (2) Department of Public Health and Human Services, Mangilao, Guam Introduction: Successful treatment of TB (tuberculosis) and prophylaxis for LTBI (latent tuberculosis infection) prevents progression to MDR-TB (multidrug-resistant TB) and XDR-TB (extensively drug-resistant TB). Risk factors for poor outcomes include treatment delay and prior failed regimens. In the US in 2010–2013, of the 413 cases of MDR-TB, 49 had pre-XDR, and 12 had XDR-TB. This case represents the first reported pre-XDR-TB in the Pacific region. Case: 36-year-old Micronesian female, married with 4 children, presented to the ED in March and April 2015 with complaints of fever and cough, was treated for respiratory symptoms and discharged. Five weeks later, she was admitted with worsening symptoms, multilobar infiltrates, had PPPD (positive PPD), and started on first-line TB meds. It was then discovered patient had contact with MDR-TB relative in 2009, PPPD, deferred LTBI treatment due to pregnancy, and lost to follow-up. Regimen was changed with CDC guidance, and prioritized contacts were offered prophylaxis. Central line infection, thrombosis, and drug side effects prompted multiple drug holds and restarts. With developing resistance, potential for close contact transmission, and worsening disease, patient was isolated to an intermediate care facility (ICF) for DOT (directly observed treatment) of bedaquiline, amikacin, cycloserine, moxifloxacin, ethambutol, linezolid, clofazimine, and vitamin B6. One week later, resistance to moxifloxacin was confirmed and discontinued. Discussion: This is the first reported pre-XDR-TB case and first use of bedaquiline/clofazimine combination in the Pacific. The ICF removed barriers to successful treatment of pre-XDR by limiting contacts and providing close drug monitoring after lost to follow-up, advancing disease, drug side effects and prior failed regimens. Conclusion: Treating contacts of MDR-TB patients should remain a public health priority to prevent further transmission. Clinical success relies on communication and collaboration between health institutions and organizations for drug access, surveillance data, clinical support, and willingness to prioritize public health issues. We apologize for this error. Reference 1ACCP virtual poster symposium. Pharmacotherapy 2017; 37: e38– 70. Volume37, Issue10October 2017Pages e112-e117 ReferencesRelatedInformation

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