texas society of health-system pharmacists tshp … to you there have been some ... tshp is taking...

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Texas Society of Health-System Pharmacists

Volume 14 w Issue 2

Peptic Ulcer Disease

Child Obesity

2013 Annual Seminar

Mentorship

TSHP Journal

2TSHP Journal | V.14 I.2

TSHP JournalPublished by the

Texas Society of Health-System Pharmacists

3000 Joe DiMaggio #30-A Round Rock, Texas 78665-3994

Ph: (512) 906-0546 • Fax: (512) 852-8514Toll-free: (800) 242-8747 • www.tshp.org

ISSN: 2325-2804

2013 - 2014TSHP EdiTorial adviSory Board

Kathryn N. PidcockEditor

Stephen Davisassistant Editor

Board MembersTodd W. Canada; Becky K. Harvey; DeeDee Hu; Darrel Hughes; Cathy L. Koo; Lincy Lal; Jamie McCarrell; Rachel J. Musgrove, Student Member; Pamella S. Ochoa; Sara C. Ruppelt; Jennifer K. Seltzer; Eva Vindekilde; Matthew Wanat

TSHP STaffPaul F. DavisExecutive Director

Judy K. TurleyExecutive Assistant

Leah M. CodyDirector of Communications & Member Services

Rebecca A. EnglishMeetings & Membership Assistant

Mission StatementThe mission of TSHP is to enhance the growth, professional development, practice and public acknowledgement of our members’ ability to improve patient care.

PresidentEmory Martin

immediate Past PresidentBrian Cohen

President-ElectLarry Egle

TreasurerLinda Haines

SecretaryJabeen John

President-Elect designateShane Greene

Secretary-Elect designateSteven E. Knight austin area Ladan Panahi, President

Central Texas Megan A. McKee, President

Coastal BendHoward McClelland, President

East TexasBilly J. Sartor, Jr., President-Elect

El Paso areaDavid Romero, President

Gulf CoastBrian R. Fase, President-Elect

Heart of TexasJason Haislet, President

lubbock areaLatisha Tomlinson, President

Metroplex areaJack Iskander, President

PanhandleShawna E. King, President

rio Grande valleyIsidro Ramirez, President

West TexasMolly Minze, President

New Practitioner SectionLinda Haines, Chair

industry SectionMary Ann Whitacre, Chair

Pharmacy Management Section Rosanne A. Thurman, Chair

Technician SectionDeborah Sard, Chair

Student SectionRegina Roy, Chair

2013 - 2014 TSHP Board of dirECTorS

Texas Society ofHealth-System Pharmacists

The Texas Society of Health-System Pharmacists (TSHP) is the organization representing healthcare pharmacy practice in Texas. TSHP’s membership includes pharmacists, technicians and other healthcare

professionals whose goal is to optimize pharmacy practice for the public’s benefit. TSHP is an affiliate of the American Society of Health–System Pharmacists.

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Volume 14 | Issue 2Table of CoNTENTS

ColuMNSOutgoing President’s MessageFinal Message from Outgoing President Brian Cohen

President’s MessageFirst Message from President Emory Martin

Speaking of....Re-Inventing Local ChaptersDo you know what your local chapter is capable of?

45

fEaTurESPeptic Ulcer Disease: A ReviewTummy troubles...

Pulmonary Vein ThrombosisManagement following recent hemorrhagic stroke

Infection PreventionOptimizing Infection Prevention Practices with Medication Deliveries

Stress Ulcer ProphylaxisEvaluation of Prescriber Education on the Use of Stress Ulcer Prophylaxis in Non-ICU Patients

Child ObesityWhat’s the Pharmacist’s Role in Child Obesity

Lovaza vs. Fish OilEffectiveness of Lovaza Compared to OTC Fish Oil in Reducing Hypertriglyceridemia: A Retrospective Analysis

71520

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MEMBEr MaTTErS2013 Annual SeminarAustin, Texas - breaking more records than just the heat!

MentorshipThe Power of Mentorship - super charge your career

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30

27

37

18

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This year’s TSHP Annual Meeting was a resounding success, with record registration, attendance and involvement. As an organization, TSHP has grown in membership, innovation, financial stability and continues to look at what can provide more value to members, as well as opportunities for members to be more involved.

These are just a few examples of the many great things that happened this year within the profession and TSHP. None of this work could be accomplished without the many Council and Section members, Chairs, Board of Directors, Executive Committee and TSHP staff. I challenge each of you to reflect on what you can do to ensure the profession continues to expand care to our patients and take accountability for the outcomes of those patients. Thank you again for affording me the opportunity to serve you this past year.

When I began this year, I conveyed a message of expanding pharmacy services into new areas and for us all to take every opportunity to tell others what

the profession of pharmacy can do for patient care. I am happy to report to you there have been some accomplishments to achieve these high-reaching goals.

Many of our Texas pharmacists signed a petition that was sent to the White House to encourage pharmacists as healthcare providers. Additionally, the Texas Pharmacy Congress, consisting of the 3 primary pharmacy organizations, the state board, and the ACPE accredited colleges of pharmacy in Texas, began working on an inclusive vision for pharmacy practice in the State of Texas, encompassing patient care from the community to the institution and back.

Additionally, the TSHP Board of Directors selected its very first class of TSHP Fellows. This designation recognizes members who have made significant and sustained contributions to the Society and the profession. Under Chair Pam Price, the Council on Communication Affairs created a series of public relations videos called “I Am TSHP,” which you will be able to view on the TSHP website soon.

With 2013 being a Texas Legislative year, our Council on Public Affairs & Advocacy, Political Action Committee and several TSHP members have been very active reviewing, writing, testifying and reaching out to State legislators about numerous bills involving the practice of pharmacy, making sure our legislators know what is important to our profession. Too many bills to mention, but a few included biosimilars, physician dispensing, pharmacy audits, compounding pharmacies and several policy changes with the Texas State Board of Pharmacy. One such accomplishment is Senate Bill 500, which adds a Pharmacy Technician as a member of the state board of pharmacy. This bill successfully made it through the legislative process and has been signed by the Governor.

TSHP is taking the lead organizing a Pharmacy Internship Task Force. This group will be discussing the tremendous burden on our student rotation sites and preceptors who are teaching the increasing number of pharmacy students across the state.

Outgoing President’s Message

From the Desk

Brian CohenTSHP President 2012-2013

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President’s Message

From the Desk

The Texas Medical Practice Act & Pharmacy Practice Acts include complementary sections regarding a physician’s delegation to a pharmacist. We often describe this as

“collaborative practice” or collaborative comprehensive medication management.”

In case you missed my colorful poster at our recent TSHP meeting, these Acts do NOT impose limits on how a hospital’s medical staff delegates “medication management” to hospital pharmacists, as long as certain criteria are met.

However, physician-pharmacist collaborative drug therapy management in the ambulatory care environment in Texas is limited to when: 1. the delegation follows a diagnosis, initial patient

assessment, and drug therapy order by the physician;2. the pharmacist practices in a hospital, hospital-based

clinic, or an academic health care institution.

Within delegated “drug therapy management”, the pharmacist typically practices within a traditional clinic setting (rather than retail pharmacy) and is authorized to perform the following: 1. collecting and reviewing patient drug use histories;2. ordering or performing routine drug therapy

related patient assessment procedures including temperature, pulse, and respiration;

3. ordering drug therapy related laboratory tests;4. implementing or modifying drug therapy,

including the authority to sign a prescription drug order for dangerous drugs.

The most common examples in Texas are pharmacist-led anticoagulation clinics, diabetes clinics, and lipid clinics. I am sure there are others.

Despite a decade of practice in this manner, the pharmacist acting as a “drug therapy management” provider is not recognized nor paid by CMS/Medicare.

• National pharmacist organizations continue to lobby for a change to CMS.

• If this is successful, other state and private payers may follow suit.

Texas Medicaid likewise has not recognized pharmacist provider status in this specific scenario of “delegated medication management”. Private insurers likewise have not.

Inpatient hospital pharmacists’ salaries are “in theory” typically covered by payment for a patient’s hospital stay. Health-care system pharmacists working in the ambulatory environment in comprehensive medication management practices are not so fortunate.

My current understanding is that reimbursement for ambulatory pharmacist providers services currently follows one of several paths. None of them are easy.1. Employer group (e.g., a city, county, or large company) pays 2. Reimbursement by private payer via a specially negotiated

mechanism outside of routine billing

Emory MartinTSHP President 2013-2014


3. Reimbursement by private payer via charge codes not covered by Medicare4. Reimbursement via charging a “facility fee” - provided the clinic is hospital-based (provider-based).5. “Incident-to billing” where a physician is compensated for pharmacists’ services, not the pharmacists themselves- provided care

is in a physician’s office, not in a hospital-based outpatient clinic6. Reimbursement via use of retail pharmacy MTM codes.

Although pharmacist medication management has been shown beneficial in a variety of disease states, until reimbursement methods are simplified, the practice cannot grow. It will remain primarily limited to academic teaching centers.

With the new emphasis on population health through accountable care organizations and the accompanying changes in how CMS paying for quality care, the need to bill as a provider may diminish somewhat, but part of the equation is simple recognition of the clinic pharmacist for a valuable job well done.

Please share with me your clinic-based pharmacist-led services. If you have experience - successes or failures – in seeking reimbursement for clinic-based pharmacist patient care services, please share them with me as we continue to highlight the need to address this issue.

What is CPE Monitor?ACPE and the National Association of Boards of Pharmacy (NABP) are developing a continuing pharmacy education (CPE) tracking service, CPE Monitor, that will authenticate and store data for completed CPE units received by phar-macists and pharmacy technicians from ACPE-accredited providers

What are the benefits of CPE Monitor?The service promises to save state board of pharmacy, CPE providers, pharmacists, and pharmacy technicians time and cost by streamlining the process of verifying that licensees and registrants meet CPE requirements and by providing a centralized repository for pharmacists’ and pharmacy technicians’ continuing education details.

This service will be particularly helpful to the growing number of pharmacists who are licensed in multiple states, and thus may need to meet the varied CPE requirements of different state boards of pharmacy.

How will CPE Monitor work?The CPE tracking system will create a direct link for sending CPE data from ACPE-accredited providers to ACPE and then to NABP, ensuring that all reported CPE units are officially verified by ACPE-accredited providers.

Pharmacists and pharmacy technicians may obtain a unique identification number from NABP to be used when reg-istering for a CPE activity from an ACPE-accredited provider. For a given Universal Activity Number, the provider will be offered a variety of mechanisms to upload each participant’s NABP e-profile ID number via the Provider Web Tool. After CPE units are processed by ACPE and NABP, pharmacists and pharmacy technicians will be able to login to a comprehensive electronic profile to access information about their completed CPE.

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Background

Peptic Ulcer Disease (PUD) is an upper gastrointestinal (GI) affliction caused by a disruption of normal GI defense mechanisms. The two main causes of this disruption are Helicobacter pylori and non-steroidal anti-inflammatory drug (NSAID) usage. The GI tract is full of aggressive elements, such as acid and pepsin, to help digest food. These elements are managed by GI maintenance factors that protect the lining of the GI tract; these factors include mucus, bicarbonate, intrinsic epithelial cells, and good mucosal blood flow. The environment is conducive for the formation of a peptic ulcer when foreign agents, H. pylori or NSAIDs are introduced into the GI tract. The maintenance factors have to combat this new foreign agent as well as manage the aggressive elements. The aggressive elements begin to prevail and start to damage the lining of the GI tract resulting in the formation of a peptic ulcer. These peptic ulcers penetrate deeper than gastritis into the muscularis mucosa of the GI tract and can cause more damage, including GI bleeding, when the ulcer penetrates into an artery. The two main sections of the GI tract affected by peptic ulcers are the stomach and the duodenum, the first section of the small intestine that connects to the stomach.1 Stressful life situations, such as chronic diseases and ventilator use can also cause a disruption of these GI defense mechanisms and lead to the formation of a peptic ulcer; however, these ulcers are not as common as ulcers that result from H. pylori and NSAID usage.2 The purpose of this article is to review the pathophysiology of peptic ulcer disease and provide an update on treatment options, including information pertaining to older treatment options that may no longer be as effective due to antimicrobial resistance. With the increase of antimicrobial resistance, it is important to place emphasis on preventing ulcers before they occur and require treatment. H. pylori

Helicobacter pylori are helix-shaped, gram-negative bacterial organisms that are contracted by mouth and prefer to hide in gastric-type epithelial cells. Originally discovered in 1984 by Marshall and Warren, the bacteria led to new treatment options for stomach ulcers. Antibiotics previously were not the standard for PUD.3 Today, developed western countries have a lower rate of H. pylori infection most likely due to higher hygiene standards and wide-spread use of antibiotics.

AutHors

Lindy Haynes, PharmD, PGY-1 Pharmacy Resident,

HealthSpring Inc., A CIGNA Company

Omar Serna, PharmD, BCACP, Clinical Pharmacy Manager,

HealthSpring Inc., A CIGNA Company

Peptic Ulcer Disease: A Review


However, resistance to some of the most common antibiotics is now being seen with new strains of H. pylori. African-American and Hispanic individuals are more often infected, possibly due to socioeconomic factors. H. pylori infection is more prevalent in under developed countries due to contaminated water supplies and crowded living conditions. It is transmitted from person to person via the fecal-oral route.4 Once ingested, H. pylori produce urease which cleaves urea into ammonia and carbon dioxide forms an ammonia buffer surrounding the bacteria, allowing it to thrive in the acidic environment of the GI tract. Older studies showed that H. pylori accounts for 95% of all duodenum ulcers,5 but this is changing in more developed countries and now more recent studies show H. pylori accounting for 50-70% of duodenal ulcers.6

NSAID-Induced

While the prevalence of H. pylori is decreasing in developed countries, NSAID-induced peptic ulcer disease is on the rise. NSAIDs induce peptic ulcer disease via topical irritation and the inhibition of prostaglandin synthesis. Prostaglandins help regulate the GI maintenance factors by promoting good mucosal blood flow, healthy epithelial cells, and mucus and bicarbonate secretion. As prostaglandin synthesis is inhibited, maintenance factors start to diminish. This allows aggressive elements to flourish. Then the topical irritation in the GI tract begins to form a peptic ulcer because it is unable to heal properly.1 NSAID-induced peptic ulcers are diagnosed by ruling out the presence of H. pylori and noting recent NSAID usage in the patient’s medication history.

Risk Factors

Risk factors for H. pylori peptic ulcer disease include crowded living conditions, contaminated food or water, and low socioeconomic class.4 Risk factors for NSAID-induced peptic ulcer disease include age greater than 60 years, previous peptic ulcer or GI bleed, high-dose or multiple NSAID usage, concomitant use of medication that can irritate or increase bleeding in the GI tract, such as corticosteroids and anticoagulants, and smoking more than 10 cigarettes per day. Psychological stress, alcohol, and certain foods are also presumed to be risk factors for PUD. There has been no proven link between alcohol and other foods that cause dyspepsia and peptic ulcers, yet they should not be ruled out as a possible causative agent due to their irritating properties. Alcohol can cause mucosal damage and could help set the environment for a peptic ulcer to develop.7

Clinical Features

Signs and symptoms of peptic ulcer disease present the same for all peptic ulcers regardless of the original cause, H. pylori or NSAID-induced. Typical symptoms include episodic gnawing or burning epigastric pain. Epigastric pain tends

to occur 2-5 hours after a meal, on an empty stomach, or overnight. Some identifying features of peptic ulcer disease can depend on the location of the ulcer. Duodenal ulcer pain tends to be relieved by the consumption of food, whereas gastric ulcer pain tends to get worse with the consumption of food. However, symptoms may be unreliable, with 30% of patients not experiencing any abdominal pain. Therefore patients usually present to a physician because of an alarming sign of peptic ulcer disease rather than a symptom. Signs of a peptic ulcer include hematemesis, melena, anemia or heme-positive stools which indicates bleeding. Bleeding occurs when the peptic ulcer erodes into an artery. Vomiting would indicate an abdominal obstruction caused by the peptic ulcer. Persistent upper abdominal pain radiating to the back suggests that the ulcer has penetrated into an adjacent organ such as the pancreas or liver. Severe, spreading upper abdominal pain suggests the ulcer has perforated into the peritoneal cavity. A patient presenting with any signs of bleeding, obstruction, or specific abdominal pain should be referred for an immediate upper endoscopy.8

Diagnosis and Testing for H. pylori

Non-invasive There are several different tests that can detect the presence of H. pylori. These tests include both invasive and noninvasive testing. A comparison chart for these tests can be found in Table 1.8 The first noninvasive testing option is serum testing to detect the presence of H. pylori antibodies in the blood through an enzyme-linked immunosorbent assay (ELISA). The serum test is not affected by medications, which can result in false negatives among the other noninvasive tests. It should be used only for initial detection of H. pylori versus eradication testing due to its lower sensitivity and specificity compared to other noninvasive tests.8 Another noninvasive test for H. pylori is the urea breath test. This option is the least invasive for patients and studies have shown it to be equally effective as invasive testing when performed properly. This test is more expensive compared to some of the other noninvasive tests. 8,9 The urea breath test works by detecting C-urea, which is created by H. pylori and exhaled as carbon dioxide. It is important to note that certain medications can cause a false negative result to occur. Antibiotics and bismuth should be held four weeks before conducting a urea breath test and anti-secretory medications such as proton pump inhibitors (PPIs) and H2 blockers should be held for two weeks to prevent a false negative result. The urea breath test is good for initial detection and eradication testing.10 The stool antigen test also detects H. pylori and it is noninvasive, though less convenient than the urea breath test. The stool antigen test identifies the H. pylori bacterial antigen in a stool sample. However the same false negative results with the urea breath test applies to the stool antigen test and medications should be held before testing. The stool antigen test is less convenient but highly accurate allowing

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it to be the most cost-effective method for initial testing and eradication testing of H. pylori.10,11

Table 1- Comparison of Diagnostic Testing for H. pylori8

TEST SENSITIVITYSPECIFICITY PROS CONS

Non-Invasive TestsSerologic ELISA 85% │79% • Quick and readily avail-

able in most institutions• Not affected by medications

• Not as sensitive or spe-cific for H. pylori

• Can only be used for ini-tial detection

• Requires blood sampleUrea Breath Test 95-100% │ 91-98% • Most convenient test for pa-

tient and practitioner • Good for initial detection

and eradication testing

• Medication use can cause false negative

• More expensive

Stool Antigen Test 91-98% │94-99% • Most cost-effective method• Good for initial detection

and eradication testing• Highly accurate

• Medication use can cause false negative

• Less convenient than UBT

Invasive TestsHistology >95% │ 100% • High specificity • Expensive

• Inconvenient, unpleasant• Bleeding risk• Results in 2-3 days

Culture 70-80% │ 100% • High specificity • Expensive• Inconvenient, unpleasant• Bleeding risk• H. pylori stability

Rapid Urease Test 93-97% │ 100% • High specificity• More cost effective than

other invasive tests• Rapid results

• Expensive• Inconvenient, unpleasant• Bleeding risk• Medication use can

cause false negative

InvasivePeptic ulcers are sometimes found during an endoscopy and a biopsy can be obtained. This biopsy can be used to determine the presence of H. pylori. An endoscopy procedure is expensive, unpleasant, and carries an increased risk of bleeding and perforation. Therefore noninvasive tests should be used as first-line testing. However, once the biopsy has been taken it can be tested for the presence of H. pylori through several different tests. One test that may be performed is histology. Histological testing physically looks for the presence of short, curved, or spiral bacillus on the epithelial surface or in the mucous layer. The average time for test results is two to three days making this test less attractive as a first line invasive diagnostic test. A second way to test the biopsy is by taking a culture. H. pylori can be identified by gram stain and biochemical tests. Culture testing tends

to be performed only in research centers dedicated to H. pylori infection because the bacteria are very unstable once taken out of the gastric environment. Culture testing is 100% specific for H. pylori but sensitivity is often lower. Culture testing can be useful in determining sensitivity and resistance to antimicrobial therapy; therefore, these tests are often performed in areas of high antibiotic resistance. Another test that can be performed to detect the presence of H. pylori from the biopsy is the Rapid Urease Test. This test yields more rapid results, is much cheaper, and is approximately as sensitive and specific when compared to culture and histological testing. However patients taking proton pump inhibitors can yield false-negative results.12

Treatment of H. pylori PUD

There were traditionally two standard medication regimens


to treat H. pylori PUD, a basic triple drug therapy regimen and an alternative quadruple regimen. However, with increasing resistance to antimicrobial therapy, more strategic therapy needed to be developed. The traditional triple-drug therapy consists of treatment with a PPI, amoxicillin, and clarithromycin for 7-14 days. Table 2 shows the appropriate dosing of various PPIs used to help eradicate H. pylori. Prevpac® is available for those having trouble adhering to the triple-drug medication regimens. Prevpac® organizes the triple-drug therapy into a convenient package making it easier to remember to take the medications correctly. Prevpac® contains a PPI (lansoprazole), amoxicillin, and clarithromycin. Recent studies show that a 7-day course of therapy is equally as effective as a 14-day course of therapy and could lead to less bacterial resistance.14 Many countries have started to see an increased incidence of resistance to clarithromycin and recent studies in these areas show a regimen consisting of PPI, amoxicillin, and metronidazole to be more effective at eradicating H. pylori.15 Patients with a contraindication to the triple-drug therapy can utilize the quadruple-drug therapy consisting of bismuth subsalicylate, metronidazole, tetracycline, and a PPI for 14 days. This is a more complicated medication regimen and can promote non-adherence through its complexity and increased treatment length leading to increased drug resistance. Patients should be counseled on the dangers of bacterial resistance due to non-compliance. Tetracycline has been recently discontinued by its manufacturer, though it is still available in combination products for H. pylori

eradication. These combination products include Helidac® and Pylera®. A strategic way to try and overcome bacterial resistance is by using a method of treatment called sequential therapy. This therapy is designed to start the patient on a PPI and amoxicillin, which H. pylori rarely develops resistance, for five days to kill the majority of the bacterial load. Then follow with a five-day course of PPI, clarithromycin, and tetracycline to finish eradicating the bacteria. This therapy option is rather complicated for patients to follow and could result

in non-adherence or taking the wrong medication at the wrong time. In treatment failure patients, a salvage therapy consisting of levofloxacin, amoxicillin, and a PPI may be used to successfully eradicate the bacteria. This treatment option is also not favored because with continued use, H. pylori can become resistant to levofloxacin. A recent Italian study suggests that rifabutin might be effective in treating H. pylori resistant to levofloxacin, clarithromycin, metronidazole, and tetracycline.16 Table 3 shows the comparisons between the different treatment regimens. In addition, studies have looked at using probiotics to treat H. pylori

infection but these studies show that probiotics alone will not be effective in ridding H. pylori. Probiotics are beneficial for reducing side effects of the medication therapy and preventing an H. pylori infection by maintaining good bacteria in the gut. The good bacteria compete for space and nutrients and help prevent H. pylori from flourishing in the GI tract.17 There are also investigational agents including a vaccine for H. pylori that are in the process of being developed.18

Table 2- Proton Pump Inhibitor Recommended Dosing for H. pylori Eradication Therapy19

Proton Pump Inhibitor Dose Dosage Forms Estimated Pricing (drugstore.com)

Esomeprazole 40 mg QD DR capsules; granules; IV $6.33/capsuleLansoprazole 30 mg BID OTC; DR capsule and

tablet; powder$3.33/capsule

Dexlansoprazole 60 mg QD DR capsule $5.62/capsulePantoprazole 40 mg QD DR capsule; granules; IV $5.87/capsuleRabeprazole 20 mg BID DR capsule $8.33/capsuleOmeprazole 20 mg BID OTC; DR capsule; pow-

der; granules $1.11/capsule

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Table 3- Therapy Options for Eradication of H. pylori14-16

Therapy Options (Duration of Therapy)

Medications Estimated Pricing Using Omeprazole as PPI (drugstore.com)

Triple-drug First-Line Therapy PPI Amoxicillin 1000mg BIDClarithromycin 500mg BID

7-day course: $98.5614-day course: $197.12

Triple-drug First-Line Therapy Prevpac®• Lansoprazole 30mg BID• Amoxicillin 1000mg BID• Clarithromycin 500mg BID

14-day course: $427.99

Triple-drug Alternate Therapy (penicil-lin allergy)

PPIMetronidazole 500mg BIDClarithromycin 500mg BID


Triple-drug Clarithromycin Resistance Therapy

PPIAmoxicillin 1000mg BIDMetronidazole 500mg BID


Quadruple-drug Second-Line Therapy PPIHelidac® • Bismuth Subsalicylate 525mg QID• Metronidazole 250mg QID• Tetracycline 500mg QID


Quadruple-drug Second-Line Therapy PPIPylera™• Bismuth Subsalicylate 420mg QID• Metronidazole 375mg QID• Tetracycline 375mg QID

10-day course:$787.99

Sequential Therapy First 5 days PPI + Amoxicillin 1000mg BIDLast 5 days PPI Clarithromycin 500mg BID Tetracycline 500mg QID

10-day course: $85.50 (based on tetracycline availability)

Salvage Therapy

PPIAmoxicillin 1000mg BIDLevofloxacin 500mg QD


Treatment and Prevention of NSAID-induced PUD

TreatmentPatients presenting with suspected NSAID-induced PUD should first be tested for the presence of H. pylori and treated with antimicrobial therapy if warranted. First-line treatment is to remove the offending agent. However, health care providers often find this difficult because many patients have an underlying disease that mandates NSAID therapy. The treatment of choice for NSAID-induced PUD is a PPI for 8 weeks. PPI therapy showed an increased rate

of healing compared to H2-receptor antagonists and is the preferred first-line therapy. PPIs have an improved side effect profile compared to misoprostol, which can also be used to heal ulcers. Healing rates improved when the NSAID was discontinued but healing still occurred in patients that had to continue the NSAID during PPI therapy. It is important to note that taking enteric coated aspirin did not increase healing rates among patients and several ulcers did not heal at all until the enteric coated aspirin was discontinued.7 Table 4 shows the various agents used in the treatment and maintenance of NSAID-induced peptic ulcer disease. While


PPI therapy is preferred as first-line therapy we must keep in mind it may not be applicable to all patients. Thus either

of the other agents may be viable options.

Table 4 – Treatment of NSAID Induced Ulcer20,21

Generic Name Duodenal or Gas-tric Ulcer Heal-ing (mg/dose)

Maintenance of Ul-cer Healing(mg/dose)

Estimated Pricing(drugstore.com)

Proton Pump InhibitorsOmeprazole 20–40mg daily 20–40mg daily $1.11/capsuleLansoprazole 15–30 daily 15–30mg daily $3.33/capsuleRabeprazole 20mg daily 20mg daily $8.33/capsulePantoprazole 40mg daily 40mg daily $5.87/capsuleEsomeprazole 20mg–40mg daily 20mg–40mg daily $6.33/capsuleDexlansoprazole 30mg–60mg daily 30mg daily $5.62/capsule

H2-receptor antagonistsCimetidine 300mg four times daily

400mg twice daily800mg at bedtime

400mg–800mg at bedtime $0.60/tablet

Famotidine 20mg twice daily40mg at bedtime


Nizatidine 150mg twice daily300mg at bedtime


Ranitidine 150mg twice daily300mg at bedtime


Promote mucosal defenseSucralfate 1 g 4 times daily

2 g twice daily1–2 g twice daily1 g 4 times daily

$1.80/tablet

ProstaglandinMisoprostol 200mcg 4 times daily 200mcg 2-3 times daily $0.95/tablet

PreventionOften NSAID-induced ulcers can be prevented by prescribing prophylactic therapy in high risk patients. Patients at high risk for developing PUD include those with a prior history of GI event (ulcer or hemorrhage), age greater than 60 years, high dose of NSAIDs, and concurrent use of corticosteroids or anticoagulants. While sucralfate has been shown to help in the prevention of peptic ulcers it not widely used due to its multiple doses per day, large tablet size, and the need to separate from meals and medications. In addition, constipation is the most common side effect reported, which may be troublesome especially in the elderly. Prophylactic therapy with misoprostol or a PPI has been shown to be effective in preventing NSAID-induced PUD. Studies showed H2-receptor antagonists were not effective in preventing gastric ulcers, the most common type of ulcer caused by NSAIDs. H2-receptor antagonists were only effective at preventing duodenal ulcers and should not be used as prophylactic therapy for NSAID-induced PUD. Misoprostol is a prostaglandin that prevents PUD by replacing the natural

GI protective prostaglandins that are disrupted by NSAID usage. Studies have shown misoprostol to be effective as prophylactic therapy however it has an increased risk of side effects compared to PPIs. Some side effects include severe abdominal pain and diarrhea.7,13

Discussion

Peptic ulcer disease can result from several disruptive factors that offset the natural GI defense mechanisms. This disruption can cause natural aggressive factors to precipitate the formation of peptic ulcers in the GI tract. There are several risk factors associated with the development of PUD including bad hygiene, age, and medication usage. These risk factors can be used to help prevent PUD as prevention becomes more important with increasing antimicrobial resistance. Treatment goals include addressing the underlying cause of PUD, addressing discomfort associated with the ulcer, healing the ulcer, preventing reoccurrence and complications associated with PUD. The cause of PUD determines the

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treatment strategy. Treatment for NSAID-induced PUD starts by removing the offending agent from the patient’s medication regimen and reducing risk factors associated with developing PUD, followed by treatment with a PPI for 8-12 weeks. PUD caused by H. pylori must be first diagnosed and then treated with a drug regimen consisting of a PPI and antimicrobial therapy followed by eradication testing a month after discontinuing the medications to determine the complete eradication of H. pylori. Options for eradication testing include the urea breath test and the stool antigen test. There are several therapy options for treating PUD and factors, such as patient contra-indications to medications and areas with a high incidence of antimicrobial resistance, should be taken into consideration when determining which therapy to choose. It is usually best to start a patient on the traditional triple-drug therapy option because this is the simplest medication regimen and the highest incidence for compliance due to low adverse effects and simplicity. If a patient has a penicillin allergy they should be started on the alternative triple-drug therapy that replaces amoxicillin with metronidazole. If the patient has tried the traditional triple-drug therapy and failed, the quadruple-drug therapy would be appropriate to use but runs the risk of non-compliance due to complexity of the regimen. In certain areas of the world where resistance to H. pylori is high, the triple-drug therapy for resistance to clarithromycin should be considered. This regimen uses metronidazole and amoxicillin instead of clarithromycin. Another strategic therapy option would be to consider sequential therapy but this regimen is more confusing for the patient and can result in non-compliance more often than the simplified regimens. For treatment failure options, replacement antibiotics exist such as levofloxacin or rifabutin but H. pylori will continue to develop resistance to these antibiotics so they should be used strategically.

Based on the literature, the authors conclude that traditional triple-drug therapy containing a PPI, amoxicillin, and clarithromycin is the most efficacious and cost-effective treatment in areas susceptible to clarithromycin and should be used as first line therapy. In patients with a penicillin allergy, amoxicillin should be replaced by metronidazole. In areas of high clarithromycin resistance, metronidazole should replace clarithromycin. Sequential therapy is also cost effective and can be used as first line therapy in patients known to be treatment compliant with a more difficult dosing regimen. Quadruple therapy is the most expensive regimen, due to the tetracycline drug shortage, and should be reserved for patients that fail first line therapy. Salvage therapy should be reserved for patients who fail first and second line treatment regimens. Table 3 shows a more attractive cost associated with salvage therapy but it is important that broader antibiotics, such as levofloxacin, are reserved as treatment failure regimens to prevent antimicrobial resistance in the future. Treatment regimens

containing pre-packaged medications such as Helidac® and Pylera® are going to be more expensive because these packs are available in brand name only. These regimens should be considered primarily when patients have difficulty complying with the traditional medication regimens.

Conclusion

In conclusion peptic ulcer disease affects many people across the world and can be effectively cured if treated properly. H. pylori infection can be eradicated if antimicrobial therapy is used strategically to delay bacterial resistance. H. pylori is becoming more resistant to traditional antimicrobial therapy so it is important to counsel infected patients about the importance of taking their medication regimen correctly so we will continue to have effective antimicrobial therapy in the future. NSAID usage should be monitored closely especially in patients with high risk factors and preventative steps should be taken to prevent PUD. PUD can be properly managed and prevented if patients are educated concerning the risks and the importance of taking their medication regimen to properly heal the ulcer and prevent complications.

References:1. Chan FK, Leung WK. Peptic -ulcer Disease. Lancet. 2002;

360:933-41.

2. Yang YX, Lewis JD. Prevention and treatment of stress ulcers in critically ill patients. Seminars in Gastrointestinal Disease. 2003; 14(1):11-19

3. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1984; 1:1311-15.

4. Francesco VD, Ierardi E, Hassan C, et al. Helicobacter pylori therapy: Present and Future. World J Gasrointest Pharmacol Ther. 2012; 3(4):68-73.

5. Borody TJ, George LL, Brandl S, et al. Helicobacter pylori-negative duodenal ulcer. Am J Gastroenterol. 1991; 86(9):1154.

6. Ciociola AA, McSorley DJ, Turner K, et al. Helicobacter pylori infection rates in duodenal ulcer patients in the United States may be lower than previously estimated. Am J Gastroenterol. 1999; 94(7):1834.

7. Lanza FL.A Guideline for the Treatment and Prevention of NSAID-Induced Ulcers. Am J Gastroenterol. 1998; 93:2037-46.

8. Ramakrishnan K, Salinas R. Peptic Ulcer Disease. Am Fam Physician. 2007; 76:1005-12.

9. Kazami S, Tavakkoli H, Habizadeh MR, et al. Diagnostic values of Helicobacter pylori diagnostic tests: stool antigen test, urea breath test, rapid urease test, serology and histology. J Res Med Sci. 2011; 16(9):1097-1104.


10. Atherton JC, Spiller RC. The urea breath test for Helicobacter pylori. Gut. 1994; 35:723-725.

11. Gisbert JP, Pajares JM. Stool antigen test for the diagnosis of Helicobacter pylori infection: a systematic review. Helicobacter. 2004; 9:347-368.

12. Ricci C, Holton J, Vaira D. Diagnosis of Helicobacter pylori: Invasive and non-invasive tests. Best Practice and Research Clinical Gastroenterology. 2006; 21(6):299-313.

13. Lanas A, Polo-Tomas M, Roncales P, et al. Prescription of and Adherence to Non-Steroidal Anti-Inflammatory Drugs and Gastroprotective Agents in At-Risk Gastrointestinal Patients. Am J Gastroenterol. 2012; 107:707-714.

14. Sokwala A, Shah MV, Devani S, et al. Helicobacter pylori eradication: A randomized comparative trial of 7-day verses 14-day therapy. S Afr Med J. 2012; 102(6):368-371.

15. Nishizawa T, Suzuki H, Suzuki M, et al. Proton pump inhibitor-amoxicillin-clarithromycin verses proton pump inhibitor-amoxicillin-metronidazole as first-line Helicobacter pylori eradication therapy. J Clin Biochem Nutr. 2012; 51(2):114-116.

16. Gisbert JP, Castro-Fernandez M, Perez-Aisa A, et al. Helicobacter pylori: usefulness of an empirical fourth-line rifabutin-based regimen. Exp Rev Gastroenterol Hepatol. 2012; 6(4):437-439.

17. Lesbros-Pantoflickova D, Corthesy-Theulaz I, Blum AL. Helicobacter pylori and Probiotics. J Nutr. 2007; 137:812S-818S.

18. Yang WC, Chen L, Li HB, et al. Identification of two novel immunodominant UreB CD4+ T cell epitopes in Helicobacter pylori infected subjects. Vaccine. 2012; 31:1204-1209.

19. Lexi-Comp Website. http://online.lexi.com/lco/action/home. Accessed Sept. 10, 2012

20. Malfertheiner P, Chan FKL, McColl KEL. Peptic ulcer disease. Lancet. 2009: 374:1449–1461.

21. Raskin JB, White RH, Jackson JE, et al. Misoprostol dosage in the prevention of nonsteroidal anti-inflammatory drug-induced gastric and duodenal ulcers: a comparison of three regimens. Ann Intern Med. 1995; 123:344-350.

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ABSTRACTP u r p o s e : A ca s e of pulmonary vein thrombosis (PVT) in a patient who had a recent basal ganglial hemorrhagic stroke one month prior to admission is reported.

Summary: An 81-year-old female with a recent history of basal ganglial hemorrhagic st roke presented with tachycardia and dyspnea. Computed tomography (C T) angiogram of the

chest revealed a left inferior and superior pulmonary vein thrombus. Laboratory studies were negative for coagulopathy workup. The decision to initiate anticoagulation therapy was complicated by the patient’s recent history of hemorrhagic stroke and fragile status. The patient tolerated intravenous (i.v.) unfractionated heparin infusion and oral warfarin without any bleeding complications upon discharge. A subsequent CT of the head showed continual resolution of the hemorrhage despite anticoagulating the patient for one week.

Conclusion: An 81-year-old female with PVT and a recent history of basal ganglial hemorrhagic stroke tolerated anticoagulation therapy with unfractionated heparin i.v. infusion and warfarin without any bleeding during the hospital

stay. The benefit of anticoagulation for PVT outweighed the risk of bleeding in this patient.

IntroductionAnticoagulation therapy in patients with recent intracranial hemorrhage presents a therapeutic dilemma; the benefit of anticoagulation for a condition needs to outweigh the risk of bleeding. Pulmonary vein thrombosis (PVT) is a rare but potentially life-threatening condition that can lead to ischemic stroke, myocardial infarction and limb ischemia through peripheral embolization.1-4 The treatments of PVT include anticoagulation, thrombectomy, lobectomy or pulmonary resection.2,5 We report a case of PVT treated with anticoagulation in a patient who had a recent basal ganglial hemorrhagic stroke.

Case ReportAn 81 year-old Caucasian woman (height 165 cm, weight 75 kg, ideal body weight 57 kg) was brought to the emergency department (ED) from a skilled nursing facility for tachycardia secondary to breathing treatment with albuterol/ipratropium 2.5 mg-0.5 mg/3 mL for dyspnea. Her past medical history included a basal ganglial hemorrhagic stroke with intraventricular extension, secondary to uncontrolled hypertension, diagnosed one month prior to admission and resultant left sided hemiplegia; hypertension; paroxysmal atrial fibrillation, with a CHADS2 Score of 2 (which is calculated by adding 1 point each for congestive heart failure, hypertension, age 75 years older or diabetes and 2 points for a history of stroke and transient ischemic attack)1,

2; dyslipidemia; chronic obstructive pulmonary disease; type 2 diabetes mellitus; gastroesophageal reflux disease; neurogenic bladder; open-angle glaucoma; chronic anemia and chronic back pain. She denied tobacco, alcohol or illicit

Management of pulmonary vein thrombosis following recent hemorrhagic stroke:

A case report

AutHors

Edward Vaughn II, PharmD

Arlis Hamann, PharmD

Cathy Koo, PharmD, BCPS, Assistant Professor

Texas A&M Health Science Center Rangel College of Pharmacy, Kingsville, TX

Special Thanks: Nahid J. Rianon, M.D. and

Jeremy Garcia, Pharmacist Intern


drug use, but reported a prior history of tobacco use 15 years ago. Her medications prior to admission included metoprolol tartrate 50 mg orally (p.o.) twice daily, prednisone 10 mg p.o. daily, pantoprazole 40 mg p.o. daily, simvastatin 20 mg p.o. at bedtime, latanoprost 0.005% 1 drop to both eyes at bedtime, albuterol/ipratropium (2.5 mg-0.5 mg/3 mL) nebulizer every 4 hours as needed for dyspnea and hydrocodone/acetaminophen 7.5/325 mg p.o. every 6 hours as needed for pain. She was not on warfarin prior to the hemorrhagic stroke or in the skilled nursing facility. The patient reported an allergy to codeine and sulfa drugs with unknown reaction.

The patient’s initial blood pressure was 138/81 mmHg and the heart rate was 120 beats per minute in the ED. The patient’s baseline laboratory studies are listed in Table 1. In the ED, the initial electrocardiogram showed sinus tachycardia, which later evolved into atrial fibrillation with rapid ventricular rate. Metoprolol tartrate 50 mg p.o. every six hours was initiated. On hospital day two, the patient’s blood pressure was 124/78 mmHg and the heart rate was 102 beats per minute. The metoprolol therapy was titrated for appropriate rate control during the hospital stay. A transthoracic echocardiogram (TTE) reported a left ventricular ejection fraction of 60 - 65% with impaired left ventricular relaxation, and mild mitral valve regurgitation. A computed tomography (CT) angiogram of the chest was performed in the ED, which did not identify any arterial pulmonary emboli but revealed a left inferior and superior pulmonary vein thrombus. No transesophageal echocardiogram (TEE) was performed because the TTE and CT angiogram of the chest were performed as part of the workup for dyspnea. Once PVT was found on CT chest, there was no need to perform a TEE. A CT of the head reported a decrease in the size of the basal ganglial hemorrhage and interval resolution of the intraventricular hemorrhage compared to the CT of head at admission. Laboratory tests revealed International Normalized Ratio (INR) of 0.99, normal protein C and protein S levels and a negative result of Factor V Leiden mutation. Creatinine clearance was 40 ml/min calculated using the Cockcroft-Gault equation. One dose of enoxaparin 80 mg was given subcutaneously (s.c.) in the ED.

Table 1. Baseline Laboratory StudiesLaboratory Study (Reference Range) Baseline ValueSodium (134-145 mEq/L) 132Potassium (3.5-5.1 mEq/L) 5.1Chloride (95-109 mEq/L) 95Carbon dioxide (24-32 mEq/L) 30Creatinine (0.5-1.4 mg/dL) 0.5Blood urea nitrogen (7-22 mg/dL) 25

Glucose (70-99 mg/dL) 290Calcium (8.5-10.5 mg/dL) 9.3

Laboratory Study (Reference Range) Baseline ValueWhite blood cell (3.7-10.4 X 103/cm3) 11.2Hemoglobin (12.0-16.0 g/dL) 12.7Hematocrit (36.0-48.0%) 37.6Platelet (133-450 103/cm3) 245Prothrombin time (12.0-14.7 seconds)

13.3

International normalized ratio (0.85-1.17)

0.99

Activated partial thromboplastin time (22.9-35.8 seconds)

23.0

Protein C NormalProtein S NormalFactor V Leiden Mutation Negative

The medical team deemed that the patient was not a candidate for thrombectomy due to her age and frailty; therefore, they decided to treat the PVT medically with anticoagulation therapy. Due to the shorter half-life of unfractionated heparin (1.5 hours), resulting in a quicker cessation of anticoagulation, the consulting neurologist recommended anticoagulation therapy using intravenous (i.v.) unfractionated heparin over enoxaparin and a blood pressure target less than 135/80 mmHg. Unfractionated heparin i.v. infusion was initiated at 18 units/kg/hr without a bolus dose, due to enoxaparin dose in the ED, and was titrated according to the institutional protocol (Table 2) to achieve an activated partial thromboplastin time (aPTT) between 60 and 90 seconds (Figure 1). Anticoagulation with warfarin 5 mg p.o. daily was also initiated on hospital day two, with an INR goal of 2-3 (Figure 2). INR was 2.8 on hospital day seven and unfractionated heparin i.v. infusion was discontinued. INR decreased to subtherapeutic levels on hospital day 10. Enoxaparin, dosed at 70 mg s.c. every 12 hours (1 milligram per kilogram every 12 hours for a creatinine clearance above 30 milliliters per minute), was started on hospital day 12 as the patient’s INR remained subtherapeutic and the patient did not have any bleeding due to anticoagulation therapy. Enteral nutrition was held initially on hospital day 2 and oral feeding with pureed diet was attempted, this could have contributed to her increased INR seen at initiation of warfarin therapy due to inadequate oral intake. Enteral nutrition (DiabetiSource® AC) was restarted on hospital day 13.

During the hospital stay, the patient had no signs or symptoms of bleeding or adverse events associated with the anticoagulation therapy. The patient had anemia with hemoglobin levels between 9-10 g/dL since the previous admission, but maintained stable hemoglobin levels with a hemoglobin of 9.4 g/dL on discharge. A subsequent CT of the head, on hospital day eight, showed continual resolution of the hemorrhage despite anticoagulating the patient for one

17tshp.org | TSHP

week. The fecal occult blood test was obtained to evaluate the cause of chronic anemia on hospital day 3 and 14 and was negative. The patient’s neurologic examinations remained stable during the hospitalization; however, warfarin was discontinued on hospital day 16 for suprapubic catheter insertion as an outpatient three days after discharge. The patient was discharged to a skilled nursing facility on hospital day 18 and resumption of warfarin therapy with enoxaparin as bridging therapy was planned after the urologic procedure. Her home medications were resumed at discharge. Patient was also instructed to follow up with her primary care physician in three months to re-evaluate the anticoagulation therapy for PVT.

Table 2. Intravenous Unfractionated Heparin Infusion Protocol at the Institutiona

aPTTb Infusion Titration< 35 seconds IV bolus 80 units/kg

Increase rate by 4 units/kg/hrNotify PhysicianDraw aPTT in six hours

35 – 59 seconds IV Bolus 40 units/kgIncrease rate by 2 units/kg/hrDraw aPTT in 6 hours

60 – 90 seconds TherapeuticRedraw aPTT in 6 hoursaPTT daily if 2 consecutive therapeu-tic aPTT values

91 – 120 seconds Decrease rate by 2 units/kg/hrDraw aPTT in 6 hours

121 – 150 seconds Hold infusion for 30 minutesDecrease rate by 3 units/kg/hrDraw aPTT in 6 hours

> 150 seconds Hold Infusion for 60 minutesDecrease rate by 4 units/kg/hrNotify physicianDraw aPTT in 6 hours

a The initial unfractionated heparin infusion rate is 18 units/kg/hr with a bolus dose of 80 units/kg. aPTT is obtained every 6 hours until two consecutive therapeutic aPTT (60-90 seconds). aPTT monitoring will then be reduced to once daily. Nurses adjust the unfractionated heparin infusion rate based on the titration table. b aPTT = activated partial thromboplastin time

Figure 1. aPTT Values During the Intravenous Unfractionated Heparin Infusiona

a aPTT = activated partial thromboplastin timeb aPTT Goal 60 to 90 seconds

Figure 2. INR and Hemoglobin Levels During Warfarin Anticoagulationa


DiscussionThis case raises a clinical dilemma of using anticoagulation therapy for PVT in a patient with a recent history of intracranial hemorrhage. Case reports describe the etiology of PVT as lung cancer, lung transplantation, lobectomy, radiofrequency catheter ablation for atrial fibrillation, and atrial fibrillation with mitral valve regurgitation.3-10 Our patient also had a history of paroxysmal atrial fibrillation with a CHADS2 score of 2 for which chronic anticoagulation therapy would be indicated; however, the benefit of long-term anticoagulation therapy should be balanced against the risk of worsening or recurrent intracranial hemorrhage.2 The cause of our patient’s PVT was most likely a combination of atrial fibrillation and mitral valve regurgitation.9 The clinical presentation of PVT is nonspecific such as dyspnea, pleuritic chest pain, non-productive cough, and crackles in the lungs.4,7 Our patient presented with dyspnea without signs or symptoms of peripheral embolization. Case reports have demonstrated complete or partial dissolution of the thrombus in PVT after two to three months of anticoagulation therapy; however, no widely accepted therapy has been established.5,6,8-10 Since our patient was deemed unsuitable for surgical intervention, anticoagulation was the only therapeutic option.

Our patient had a basal ganglial hemorrhagic stroke with intraventricular extension diagnosed one-month prior to admission. The risk of recurrent bleeding or hemorrhagic expansion of an intracerebral hemorrhage (ICH) is the highest within the first 24 hours, but some case reports state that the risk extends for several weeks.11,12 The rate of recurrent ICH is 2.1% to 3.7% per patient-year and the risk is increased by nearly three-fold with anticoagulation therapy.13,14 However, the risk of recurrence is less frequent if the location of the hemorrhage is characteristic of hypertensive vasculopathy, such as the basal ganglial, and if the blood pressure is reduced to less than 140/90 mmHg.13,15,16

ConclusionOur patient was at risk for ischemic stroke, myocardial infarction and other thromboembolic events due to peripheral embolization from PVT; thus, the benefit of preventing further symptomatic ischemic events from PVT outweighed the risk of bleeding. Residual left sided hemiplegia, age, and urinary incontinence contributed to her high fall risk; therefore, lifelong anticoagulation therapy for atrial fibrillation alone would not be appropriate due to her increased risk of recurrent ICH.

The patient needs to be monitored closely for bleeding while continuing on anticoagulation therapy. Cessation of warfarin therapy should be considered once the PVT has resolved which should be assessed in three months via CT angiogram of the chest. 5, 6, 8-10

References1. Gage BF, Waterman AD, Shannon W, et al. Validation

of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA. 2001; 285:2864-70.

2. Guyatt GH, Akl EA, Crowther M, et al. American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel. Executive summary: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012; 141:7S-47S.

3. Cavaco RA, Kaul S, Chapman T, et al. Idiopathic pulmonary fibrosis associated with pulmonary vein thrombosis: a case report. Cases J. 2009; 2:9156.

4. Garcia MJ, Rodriguez L, Vandervoort P. Pulmonary vein thrombosis and peripheral embolization. Chest. 1996; 109:846-7.

5. Kinsella JA, MacCarthy AJ, Kiernan TJ, et al. Transesophageal echocardiographically-confirmed pulmonary vein thrombosis in association with posterior circulation infarction. Case Rep Neurol. 2010; 2:24–31.

6. Miranda JA. Pulmonary vein thrombosis presenting as myocardial infarction. Chest. 2006; 130:344S.

7. Alexander GR, Reddi A, Reddy D. Idiopathic pulmonary vein thrombosis: a rare cause of massive hemoptysis. Ann Thorac Surg. 2009; 88:281-83.

8. Kim NH, Roldan CA, Shively BK. Pulmonary vein thrombosis. Chest. 1993; 104:624-26.

9. Mumoli N, Cei M. Idiopathic pulmonary vein thrombosis. J Emerg Med. 2012; 42:182-3.

10. Selvidge SD, Gavant ML. Idiopathic pulmonary vein thrombosis: detection by CT and MR imaging. AJR Am J Roentgenol. 1999; 172:1639-41.

11. Bae HG, Lee KS, Yun IG, et al. Rapid expansion of hypertensive intracerebral hemorrhage. Neurosurgery. 1992; 31:35-41.

12. Wijdicks EF, Fulgham JR. Acute fatal deterioration in putaminal hemorrhage. Stroke. 1995; 26:1953-5.

13. Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2010; 41:2108-29.

14. Vermeer SE, Algra A, Franke CL, et al. Long-term prognosis after recovery from primary intracerebral hemorrhage. Neurology. 2002; 59:205-9.

15. Bailey RD, Hart RG, Benavente O, et al. Recurrent brain hemorrhage is more frequent than ischemic stroke after intracranial hemorrhage. Neurology. 2001; 56:773-7.

16. Parker D Jr, Rhoney DH, Liu-DeRyke X. Management of spontaneous nontraumatic intracranial hemorrhage. J Pharm Pract. 2010; 23:398-407.

19tshp.org | TSHP

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Optimizing Infection Prevention Practices with Medication Deliveries

Depending on your wholesaler, compounding pharmacy or manufacturer, you may be receiving your medication orders in re-usable plastic totes, cardboard boxes, shrink wrap packaging, and/or postal containers. Some TSHP members have reported is-sues with the cleanliness of the re-usable plastic totes or other delivery materials.

An electronic Hospital Pharmacy Delivery Survey was sent via Zoomerang to the TSHP membership in August 2012 to solicit input and feedback regarding optimum phar-

maceutical delivery & receipt practices and infection prevention or particulate contamination risk. Forty-seven members replied to at least one survey question. The results are as follows:

Fig. 1. In your opinion, do these types of deliveries to a hospital pharmacy represent a potential source of particulate con-tamination and infection?

Fig. 2. Which of the following represent a possible contamination threat in your hospital?

AutHor

Carrie A Berge MS, Pharm.D.TSHP Professional Affairs Council

21tshp.org | TSHP

Fig. 3. Has your facility’s infection control committee raised this as a potential issue?

Fig.4. Has your hospital developed specific policies and procedures to minimize potential contamination from these sources?

The survey asked several open- ended questions. • The first requested what hospitals were doing to minimize contamination. Strategies regarding brown cardboard

boxes or totes were reported: Do not allow them in patient care areas. • Create segregated areas within the pharmacy to store IV boxes away from clean room. • Boxes should not be opened/stored in the same areas where meds are dispensed• Remove them entirely from all pharmacy and patient care areas-having a separate breakdown area to remove all

outer wrappings.• Do not place any cardboard boxes directly on the floor• Re-usable totes should be placed on shelf just inside of pharmacy entrance, unpack them there and store there for

pick up. • Empty totes immediately when delivered and send them back with the driver so they are not stored.

Decontamination strategies reported were:• Cleaning the counter with germicidal wipes after drugs are removed from cardboard boxes.• Products are decontaminated before entering aseptic areas.• Clean products with ETOH before storage. Discard packing boxes.• Follow 797 standards in taking product out of carton/over-wrap and wiping off in anteroom.

Another question asked was for members’ recommendations for processes that might help minimize this risk. Their sug-gestions included:

• Ask wholesalers to clean/wash bins prior to reuse including removing sticker residue.• Standardize cleanliness of delivery trucks.• Use plastic wrapped packing boxes to avoid picking up contaminants on delivery routes.• Identify a staging or separate receiving area for medications to be removed from boxes separate from pharmacy

production or patient care areas.• Open bins and remove medications immediately. Send totes back with driver. • Use hard sided storage devices that can be cleaned with sanitizing wipes prior to handling or after usage in a patient

care area that comes back to pharmacy for restocking.


• Hand washing at regular intervals in the pharmacy even if unsoiled due to touch contamination.

TSHP Professional Affairs Council Recommendation

We thank those members who shared their experiences and best practices in the survey. Based on this survey the TSHP Professional Affairs Council has two recommendations:

1. Include expectations of delivery method in your vendor service level agreements (i.e. wholesaler, compounding pharmacy, etc.).

• Newly packaged cardboard boxes or shrink wrapped original manufacturer packaging are preferred.• If the vendor must use the plastic totes, a written standard of cleanliness should be established with a per-

formance threshold expectation. • The pharmacy department should monitor and report any issues immediately to the vendor. • The contract should discuss resolution for any damaged or contaminated products due to dirty totes.

2. Have a segregated medication order receipt & breakdown area outside of pharmacy production or patient care areas to remove all outer containers prior to allowing medications into pharmacy areas.

“I have been a pharmacist for almost 20 years. During this time, I have seen the pharmacists’ role evolve and become more focused on the clinical aspect of care. As a result, the smooth and efficient operation of today’s pharmacy requires the expertise of a Certified Pharmacy Technician. When considering to hire someone, I look for the familiar PTCB CPhT. When I see that initiative, I know that the applicant has, at a minimum, the basic knowledge to meet the needs of my department.”

—Laura M. Forbes, RPh, Director of Pharmacy Services, Gov. Juan F. Luis Hospital and Medical Center, Christiansted, U.S. Virgin Islands

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23tshp.org | TSHP

ABSTRACTPurpose: The purpose of this study is to assess the impact of prescriber education on optimizing the selection of patients for acid suppressive therapy.

Methods: A prospective cohort study was conducted to compare the use of stress ulcer prophylaxis (SUP) in 300 patients admitted to the internal medicine teaching services before and after prescriber education. Medical residents were educated by pharmacist through noon conference, one-on-one education, pocket cards, notes left on the chart, and e-mail notification. Education consisted of appropriate, evidence-based use of acid suppressive therapy including US Food and Drug Administration (FDA)-labeled indications, gastrointestinal (GI) bleeding, and the American College of Cardiology Foundation/ American College of Gastroenterology/ American Heart Association (ACCF/ACG/AHA) 2008 Expert Consensus statement on the steps for minimizing GI bleeding in patients on NSAIDs or antiplatelet therapy. SUP was considered inappropriate if patient did not have documented FDA-labeled indications, GI bleeding, or did not meet the 2008 Expert Consensus.

Results: Of the 150 patients admitted in each group, 114 (76%) in the pre-education compared to 78 (52%) in the post-education group were on acid suppressive therapy during hospitalization. Following prescriber education, inappropriate SUP was reduced from 47% to 21% (p < 0.001). Secondary outcomes showed a reduction in the use of acid suppressive therapy in patients with SUP initiated during hospitalization on acute care floor (33% vs 15%, p < 0.001) and transferred from the ICU and kept on acid suppressive therapy (5% vs 0, p = 0.007). The annualized cost savings from the prescriber education was approximately $1,040.

Conclusions: Prescriber education by pharmacists on optimizing the selection of patients for acid suppressive therapy showed a reduction of inappropriate SUP use and thus a reduction in drug costs and number of medications administered.

INTRODUCTIONStress ulcer prophylaxis (SUP) guidelines are typically intended for critically ill patients and do not directly address patients on acute care medicine floors.1 SUP initiated in the intensive care unit (ICU) is often continued on transfer to acute care floors despite reduction in gastrointestinal (GI) bleeding risk and frequently continued at the time of discharge unnecessarily.2-4 In one study, 55% of non-critically ill patients received unjustified SUP.2 Common drugs used for SUP include histamine-2 receptor antagonists, proton pump inhibitors, and sucralfate.

AutHors

Rafael Felippi, PharmD, BCPSClinical Pharmacist, Physicians’

Alliance for Quality

Anila Thomas, PharmD, BCPSClinical Pharmacist, Department

of Pharmacy Services

Kathryn Pidcock, PharmD, BCPSClinical Pharmacist, Department

of Pharmacy Services

Facility:The Methodist Hospital,

Houston, TX

Evaluation of Prescriber Education on the Use of Stress Ulcer Prophylaxis in Non-ICU Patients


The use of SUP in non-ICU patients is widespread and prescribers may overestimate the risks of stress-induced GI bleeding, underestimate potential harm associated with the use of SUP, and have misunderstandings about appropriate SUP indications.5,6 The incidence of clinically significant GI bleeding in the ICU is relatively low at 3.7% of patients with risk factors and only 0.1% of patients without risk factors.7 In the non-ICU setting, the number needed to treat to prevent one episode of nosocomial GI bleeding was 770 patients.8 It is therefore important to limit the use of acid suppressive therapy to high risk populations.

The overuse of SUP can increase the number of medications administered, adverse reactions, drug-drug interactions, and overall cost.9,10 Moreover, recent studies have shown that acid suppressive therapy can increase risk of Clostridium difficile infections, bone fractures, and community- and hospital-acquired pneumonia.11-14 In order to reduce complications from acid suppressive therapy, candidates for SUP should be thoroughly evaluated.

Studies have shown that a large percentage of patients are prescribed SUP medications on acute care floors.2,5,15 Clinical pharmacists at our institution have also observed similar inpatient prescribing practices. The objectives of this study

were to evaluate the inappropriate use of SUP in hospitalized patients on an acute care medicine floor and assess the impact of prescriber education on optimizing the selection of patients for acid suppressive therapy.

MATERIALS AND METHODSSettingThe study was conducted at a 900-bed teaching institution located in the Texas Medical Center in Houston, Texas. The focus was on a 30-bed acute care medicine unit.

Study Design and PatientsWe performed a prospective cohort study of 300 adult patients (> 17 years of age), as a convenience sample, admitted consecutively to the internal medicine teaching services. The study consisted of two phases with 150 patients in each phase. The pre-intervention phase was between September 8 and October 15, 2011. The post-intervention phase was between January 13 and March 10, 2012. To minimize bias, all patients admitted to the internal medicine teaching services on an acute care medicine floor were included; none were excluded. Approval for the study was obtained from the hospital Institutional Review Board and informed consent was waived.

USE OF ACID SUPPRESSIVE THERAPY ON ACUTE CARE FLOOR

Steps for minimizing gastrointestinal bleeding: Need for NSAID or Antiplatelet

Assess GI Risk

History of Ulcer Complication

History of Ulcer Disease (non-bleeding)

GI Bleeding

(active or history of)

Dual Antiplatelet Therapy

(ex. Aspirin, clopidogrel, prasugrel, ticagrelor)

Treatment-Dose Anticoagulant Therapy

Test for H. pylori and treat if infected

Yes

YesFamotidine or Pantoprazole1

More Than One Risk Factor:Age 60 Years or More

Famotidine or Pantoprazole1

No

Yes

Figure 1. Pocket reference card.

FDA-Labeled Indications for Acid-Suppressive Therapy and GI Bleeding:

• GERD• GI ulcer (PUD,

gastric, duodenal)• H. pylori infection• Erosive esophagitis• Pathological

hypersecretory conditions (e.g., Zollinger-Ellison syndrome)

• NSAID-associated gastritis or prophylaxis in patients at risk (age ≥ 60 years and/or history of GI ulcer)

• GI bleedingAdapted from: ACCF/ACG/AHA 2008 Expert consensus statement on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use. Circulation 2008;118:1894-1909. NSAID = non-steroidal anti-inflammatory drug; GI = gastroin-testinal; GERD = gastroesophageal reflux disease; PUD = peptic ulcer disease. 1. Pantoprazole and famotidine were listed here based on the institution’s formulary.

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OutcomeThe primary outcome of this study was the proportion of patients receiving acid-suppressive therapy for SUP before and after prescriber education. Secondary outcomes were percentage of patients with SUP initiated during hospitalization, patients transferred from the ICU and kept on SUP, patients discharged home on SUP initiated in the hospital, and drug costs. InterventionThe intervention consisted of education provided by the pharmacist to medical residents on appropriate, evidence-based use of acid suppressive therapy in patients on acute care floors. The teaching services consisted of an attending physician, upper level resident, and interns. Medical residents were educated through one-on-one education, pocket cards (Figure 1), notes left on the chart, e-mail notification, and noon conference presented by the pharmacist study investigator. Modes of education varied among residents as they rotate throughout the hospital and noon conference was presented once prior to data collection to internal medicine residents. The content of education consisted of indications for SUP as described in the ASHP guidelines for ICU patients,1

risks versus benefits of initiating, continuing, and discharging patients on SUP, US Federal and Drug Administration (FDA)-labeled indications for acid suppressive therapy, and steps for minimizing GI bleeding in patients on NSAIDs or antiplatelet therapy according to the American College of Cardiology Foundation/ American College of Gastroenterology/ American Heart Association (ACCF/ACG/AHA) 2008 expert consensus statement.1,16 Medical residents were instructed to investigate indication and document findings in the medical record for each patient on acid suppressive therapy. If patient was on dual antiplatelet therapy or NSAIDs, residents were educated on the suggested steps for minimizing GI bleeding according to the 2008 expert consensus. If the patient did not have a FDA-labeled indication or did not meet the criteria for the use of acid suppressive therapy, medical residents were encouraged to discontinue therapy. As part of prescriber education, data describing the overuse of SUP during the pre-intervention phase was presented at noon conference, including number of patients with SUP initiated during hospitalization and patients discharged home on SUP initiated at the hospital. Data CollectionData were collected from electronic and paper medical records which included age, gender, length of stay, comorbidities, prior use of acid suppressive therapy (defined as proton pump inhibitors, H2-receptor antagonists, sucralfate, and antacids) at home or in the ICU, discharge prescriptions for acid suppressive therapy, indications, and the use of NSAIDs, antiplatelets, systemic corticosteroids, and anticoagulants. SUP was defined as use of acid suppressive therapy without

documented FDA-labeled indication or GI bleeding during patient’s current hospitalization. Patients who were on SUP were further evaluated to verify appropriate use based on the 2008 expert consensus. To avoid bias, study definitions were pre-determined and kept consistent for both groups (Figure 1).

Statistical AnalysisWe utilized the chi-squared test to evaluate categorical data for trend analysis. For continuous nonparametric variables, the Mann-Whitney test was performed. For continuous parametric variables, the two-sample t-test was used. A p-value of less than 0.05 was considered statistically significant. All statistics were analyzed using Minitab (2010, Minitab Inc., State College, PA) software.

RESULTSPatient CharacteristicsThe study examined 300 patients admitted to the internal medicine teaching services on an acute care floor. The two groups consisting of 150 patients each were similar in baseline characteristics. The only differences were a shorter length of stay and higher documented GI bleeding in the post-education group at baseline. Prior to hospitalization, 43 patients (29%) in the pre-education and 39 (26%) in the post-education group were taking acid suppressive therapy (Table 1).

Table 1. Characteristics of Study PopulationCategory Pre-Ed-

ucation(n = 150)

Post-Ed-ucation(n = 150)

P value

Mean age (range) 57 (21-91) 56 (19-97) 0.4Gender: Male, n (%) 75 (50) 75 (50) 1Average total length of stay

5.3 days 3.5 days 0.0013

Average length of stay on acute care floor

4.4 days 3.4 days 0.0283

Patients on acid sup-pressive therapy prior to admission, n (%)

43 (29) 39 (26)

Documented FDA-labeled and GI bleeding indications for acid-sup-pressive therapy, n (%):GERDGI ulcerNSAID-associated gastric ulcer or prophylaxis in patients at riskGI bleeding

18 (12)12 (8)

2 (1)

3 (2)

14 (9)11 (7)

0

14 (9)

0.70.5

0.5

< 0.001


Table 1. Characteristics of Study PopulationCategory Pre-Ed-

ucation(n = 150)


P value

Comorbidities, n (%):CardiovascularEndocrinologicGastrointestinal (e.g., hepatitis, inflamma-tory bowel disease, constipation)NeurologicPsychiatricOncologicOthers (e.g., re-nal, ophthalmic)

66 (44)35 (23)25 (17)

19 (13)19 (13)16 (11)54 (36)

61 (41)35 (23)29 (19)

28 (19)19 (13)12 (8)70 (47)

NSAID = non-steroidal anti-inflammatory drug; GI = gastrointestinal; GERD = gastroesophageal reflux disease; PUD = peptic ulcer disease.

OutcomesOf the 150 patients admitted in each group, 114 (76%) in the pre-education compared to 78 (52%) in the post-education group were on acid suppressive therapy during hospitalization. Compared to pre-education group, an increase in the percentage of patients on acid suppressive therapy with documented FDA-labeled indication or GI bleeding was observed in the post-education group (28% vs 21%, p < 0.001).

For the primary outcome, the percentage of patients on SUP who did not meet the 2008 Expert Consensus was reduced from 47% to 21% following prescriber education (p < 0.001) (Table 2).

Table 2. Primary OutcomePre-Edu-cation(n = 150)


P value

Patients on acid suppressive therapy, n (%)

114 (76) 78 (52) < 0.001

Patients on acid suppressive therapy with documented FDA-labeled indication or GI bleeding, n (%)

31 (21) 42 (28) < 0.001

Patients on acid suppressive therapy for, n (%):SUP1

2008 Expert Consensus only2

SUP without Expert Con-sensus

83 (55)12 (8)

71 (47)

36 (24)5 (3)

31 (21)

< 0.0010.08

< 0.001

1. SUP indicates patients on acid suppressive therapy who did not have documented FDA-labeled indication or GI bleeding.

2. Patients on SUP but use of acid suppressive therapy is acceptable according to ACCF/ACG/AHA 2008 Expert Consensus.16

Secondary outcomes analysis demonstrated a reduction in the use of acid-suppressive therapy in patients with SUP initiated during hospitalization on acute care floor (33% vs 15%, p < 0.001), transferred from the ICU and kept on acid-suppressive therapy (5% vs 0, p = 0.007), and those discharged home on acid suppressive therapy initiated in the hospital (7% vs 3%, p = 0.17) (Table 3).

Table 3. Secondary OutcomesPre-Ed-ucation( n = 150)


P value

Patients with acid suppressive therapy initiated during hospi-talization on acute care floor:SUP1


SUP without Expert Consensus56 (37)7 (5)

49 (33)

24 (16)2 (1)

22 (15)

< 0.0010.17

< 0.001

Patients transferred from the ICU and kept on acid suppres-sive therapy:SUP1


SUP without Expert Consensus

10 (7)2 (1)

8 (5)

00

0

0.0020.5

0.007

Patients discharged home on acid suppressive therapy initi-ated at the hospital:SUP1


SUP without Expert Consensus

13 (9)3 (2)

10 (7)

5 (3)1 (1)

4 (3)

0.050.62

0.17

1. SUP indicates patients on acid suppressive therapy who did not have documented FDA-labeled indication or GI bleeding.2. Patients on SUP but use of acid suppressive therapy is acceptable according to ACCF/ACG/AHA 2008 Expert Consensus.16

The most common class of SUP agents prescribed was proton pump inhibitor (98%), followed by H2-receptor antagonist (2%). The cost of acid suppressive drugs used without documented FDA-labeled indications for 150 patients on a 30-bed acute care floor was $1,588 before education compared to $547 after education, using average drug wholesale prices (Morris Dickson® WebPortal), leading to a cost savings of

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$1,040 post intervention.

DISCUSSIONOur study investigated the impact of prescriber education on optimizing the selection of patients for acid suppressive therapy. Current ASHP guidelines for SUP were published in 1999 and a review update is expected to be released later this year.1,17 Despite these ICU-specific guidelines, acid suppressive drugs have been over-prescribed for SUP in non-ICU patients.

Studies have shown that 60% to 73% of patients lacked an indication for acid suppression on general medical floors.18,19 In our study, after prescriber education, use of acid suppressive therapy for SUP in patients who also did not meet the expert consensus criteria was reduced from 47% to 21%. Khalili and colleagues observed a reduction in overall use of acid suppressive therapy from 81% to 47% among non-ICU patients after the introduction of a treatment guideline for SUP by clinical pharmacists.20 The internal guideline implemented in their study, however, used similar ASHP indications for SUP as in ICU patients, which are not recommended for patients who are on non-ICU floors.1,20 Similar educational interventions in the ICU setting have also shown significant reduction in the use of non-indicated SUP after discharge.9,21,22

Nardino et al found that acid suppressive therapy for SUP was initiated in 50% of patients on an acute care floor during hospitalization.15 In our study, after prescriber education, a reduction of SUP initiated during hospitalization (33% vs. 15%) was observed.

Carey et al evaluated the impact of having pharmacy students on internal medicine teams and demonstrated a reduction of 1.5 days in duration of inappropriate therapy.23 However, the study did not show statistically significant difference in the proportion of hospitalized patients discharged home on acid suppressive therapy initiated at the hospital (9.4% vs. 6.1%, p = 0.07).23 In our study, we observed similar findings in the number of patients discharged home on new acid suppressive therapy between the groups (7% vs. 3%, p = 0.17).

The post-education group had significantly increased number of documented GI bleeding episodes compared to the pre-education group (9% vs. 2%, p < 0.001) at baseline. This difference is attributed to increased prescriber documentation after pharmacist intervention. Because patients had a short length of stay averaging approximately 4 days and our study was not designed to assess effectiveness of SUP, the long-term incidence of GI bleeding was not investigated. There were no inpatient reports of GI bleeding as a result of discontinuation of acid-suppressive therapy.

Some common reasons identified by medical residents for the inappropriate use of acid suppressive therapy were pancreatitis, vomiting, and parenteral nutrition; none were considered FDA approved indications or SUP.

The cost savings for 150 patients in this study after prescriber education was approximately $1,040. When extrapolated to annualized cost savings according to our current discharge rate, the cost avoidance is projected to be approximately $30,000 annually for one 30-bed acute care floor. Heidelbaugh and colleagues observed that the annual estimated cost of inpatient SUP in non-ICU patients was over $44,000.5 This is an avoidable cost and a potential underestimation since it does not include costs involved with medication processing and administration, costs involved with impact from potential adverse effects and drug interactions, as well as treatment of C. diff diarrhea, pneumonia, or osteoporosis that could potentially occur due to use of acid suppressive therapy as shown in recent studies.11-14

Based on the results of this pilot study, we plan to expand education hospital-wide regarding appropriate use of acid suppressive therapy. The long-term impact of prescriber education remains to be investigated. Moreover, our institution’s Pharmacy and Therapeutics committee approved the removal of SUP standing orders from non-ICU order sets. Newer SUP guidelines, especially addressing patients on acute care floors, are needed as we now have more recent studies available on risks and benefits of acid suppressive therapy.

One limitation of this study is that education was restricted to medical residents who might be more inclined to change prescribing habits compared to attending level physicians. Moreover, out of 300 patients, only 18 (6%) were transferred from the ICU. Since current guidelines only address use of SUP in ICU patients, it would be interesting to see the impact of prescriber education on an acute care floor with high volume of transfers from ICU, such as step-down acute care units.

Another limitation was inconsistent prescriber documentation. Patients were considered to be on SUP if there was no other written indication for acid suppressive therapy. This lack of documentation was more prominent among patients who were on therapy prior to hospitalization. Medical residents were encouraged to investigate the need of acid suppressive therapy regardless of when it was initiated and more frequent documentation was noted in the second phase of the study.

Lastly, prescriber education may not have been uniform as medical residents rotate monthly and education was done by various approaches such as noon conference, pocket cards, one-on-one education, and e-mail notification. This study did not evaluate which education method was the most effective.


In conclusion, prescriber education by pharmacists on optimizing the selection of patients for acid suppressive therapy showed a reduction of inappropriate SUP use and thus a reduction of drug costs and number of medications administered.

REFERENCES

1. ASHP report. ASHP therapeutic guidelines on stress ulcer prophylaxis. Am J Health-Syst Pharm. 1999;56:347-379.

2. Hwang KO, Kolarov S, Cheng L et al. Stress ulcer prophylaxis for non-critically ill patients on a teaching service. J Eval Clin Pract. 2007;13:716-721.

3. Guda NM, Noonan M, Kreiner MJ et al. Use of intravenous proton pump inhibitors in community practice: an explanation for the shortage? Am J Gastroenterol. 2004;99:1233-1237.

4. Farrell CP, Mercogliano G, Kuntz CL. Overuse of stress ulcer prophylaxis in the critical care setting and beyond. J Crit Care. 2010;25:214-220.

5. Heidelbaugh JJ, Inadomi JM. Magnitude and economic impact of inappropriate use of stress ulcer prophylaxis in non-ICU hospitalized patients. Am J Gastroenterol. 2006;101:2200-2205.

6. Hussain S, Stefan M, Visintainer P et al. Why do physicians prescribe stress ulcer prophylaxis to general medicine patients? South Med J. 2010;103:1103-1110.

7. Cook DJ, Fuller HD, Guyatt GH et al. Risk factors for gastrointestinal bleeding in critically ill patients. Canadian Critical Care Trials Group. N Engl J Med. 1994;330:377-381.

8. Herzig SJ, Vaughn BP, Howell MD et al. Acid-suppressive medication use and the risk for nosocomial gastrointestinal tract bleeding. Arch Intern Med. 2011;171:991-997.

9. Nasser SC, Nassif JG, Dimassi HI. Clinical and cost impact of intravenous proton pump inhibitor use in non-ICU patients. World J Gastroenterol. 2010;16:982-986.

10. Perwaiz MK, Posner G, Hammoudeh F et al. Inappropriate use of intravenous PPI for stress ulcer prophylaxis in an inner city community hospital. J Clin Med Res. 2010;2:215-219.

11. Laheij RJ, Sturkenboom MC, Hassing RJ et al. Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs. JAMA. 2004;292:1955-1960.

12. Howell MD, Novack V, Grgurich P et al. Iatrogenic gastric acid suppression and the risk of nosocomial Clostridium difficile infection. Arch Intern Med. 2010;170:784-790.

13. Yu EW, Bauer SR, Bain PA et al. Proton pump inhibitors and risk of fractures: a meta-analysis of 11 international studies. Am J Med. 2011;124:519-526.

14. Herzig SJ, Howell MD, Ngo LH et al. Acid-suppressive medication use and the risk for hospital-acquired pneumonia. JAMA. 2009;301:2120-2128.

15. Nardino RJ, Vender RJ, Herbert PN. Overuse of acid-suppressive therapy in hospitalized patients. Am J Gastroenterol. 2000;95:3118-3122.

16. Bhatt DL, Scheiman J, Abraham NS et al. ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. Circulation. 2008;118:1894-1909.

17. A m e r i c a n S o c i e t y o f H e a l t h - S y s t e m Pharmacists . Therapeutic Guidel ines. www.a s h p . o r g / I m p o r t / p r a c t i c e a n d p o l i c y /P o l i c y P o s i t i o n s G u i d e l i n e s B e s t P r a c t i c e s /BrowsebyDocumentType/TherapeuticGuidelines.aspx. Accessed May 01, 2012.

18. Zink DA, Pohlman M, Barnes M et al. Long-term use of acid suppression started inappropriately during hospitalization. Aliment Pharmacol Ther. 2005;21:1203-1209.

19. Martin-Echevarria E, Pereira Julia A, Torralba M et al. Assessing the use of proton pump inhibitors in an internal medicine department. Rev Esp Enferm Dig. 2008;100:76-81.

20. Khalili H, Dashti-Khavidaki S, Hossein Talasaz AH et al. Descriptive analysis of a clinical pharmacy intervention to improve the appropriate use of stress ulcer prophylaxis in a hospital infectious disease ward. J Manag Care Pharm. 2010;16:114-121.

21. Hatch JB, Schulz L, Fish JT. Stress ulcer prophylaxis: reducing non-indicated prescribing after hospital discharge. Ann Pharmacother. 2010;44:1565-1571.

22. Coursol CJ, Sanzari SE. Impact of stress ulcer prophylaxis algorithm study. Ann Pharmacother. 2005;39:810-816.

23. Carey KM, Cross JE, Silva MA et al. Pharmacy student impact on inappropriate prescribing of acid suppressive therapy. Am J Pharm Educ. 2011;75:175.

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IntroductionChildhood obesity has become an epidemic among children and adolescents in the United States (US) and presents medi-cal, psychosocial, and economic challenges. Obesity is a serious, preventable disease characterized by a sedentary lifestyle accompanied by an unhealthy diet, con-

tributing to a decline in the quality of life in children, which often carries into adulthood. Obesity can be attributed to factors such as a lack of nutritional education with increases in caloric intake and less nutritious foods, minimal physical activity with sedentary behavior, and decreased knowledge about health associated complications.1

Childhood obesity has risen over the past thirty years, although rates have more recently leveled off.1 However, obesity rates continue to remain above the goal of 5% set by the National Health and Nutrition Examination Survey (NHANES).1 The 2010 Healthy People Program set goals simi-lar to those set by NHANES to reduce child obesity to < 5% of the population and lower than 10% by 2020.2 In 2009-10, 16.9% of US children 2 to 19 years of age were identified as obese, while one in five children older than five years were obese.3,4 Obesity results in a large socio-economic impact on society as well as on families, with health care financial issues secondary to medical complications.

The Centers for Disease Control and Prevention (CDC) growth charts with body mass index (BMI) percentiles incorporate the height and weight of children aged 2 to 20 years to determine the amount of body fat in an inexpensive and noninvasive screening, and compare children of the same sex and age. In the US, children and adolescents are considered obese if

they are in the ≥ 95th percentile range of BMI, overweight in the 85th to < 95th percentile range of BMI, normal weight in the 5th to < 85th percentile range of BMI, and underweight in the < 5th percentile range of BMI.5-7 These growth charts help to evaluate the weight of a child in comparison to physical growth and may alert healthcare professionals if a child is at risk for obesity.

Health Complications Childhood obesity predisposes children to future health complications due to metabolic issues, as well as respira-tory and cardiovascular illnesses, when compared to normal weight children. Weight gain is inevitable with the continual growth of children, but the implementation of strategies to minimize the risk of becoming overweight or obese may decrease secondary health complications (SHC) of diabetes, hypertension and hypercholesterolemia previously confined to the adult population.8,9

Increases in SHC diagnoses in the pediatric population encour-age assessment if a child has two or more cardiometabolic risk factors.8 In a study of pediatric patients 5 to 17 years of age, 26% demonstrated at least one risk factor for cardiovascular disease after evaluating triglycerides, high-density lipopro-tein cholesterol, low-density lipoprotein cholesterol, fasting insulin, systolic blood pressure, and diastolic blood pressure.10 Davis et al11 found aerobic exercise training in children 7 – 11 years of age decreased diabetes and cardiometabolic risks. Cardiovascular disease is the most significant health com-plication that may affect obese or overweight children, and is often preventable with exercise and nutrition education.

Children Most AffectedPreventing and controlling excess weight and obesity in children is of vital importance. Obesity disproportionately impacts lower economic classes and minorities such as Latinos and African Americans, highlighting the great need to target these groups with education to decrease obesity and other associated complications.12 Not only are health problems linked with obesity, but psychological problems and peer teasing can result in isolation or poor self-esteem.13

Pharmacist’s Role in Child ObesityAutHors

Ashley Gutierrez, Pharm.D. Candidate

Janie Robles, Pharm.D., AE-C

Facility:School of Pharmacy, Texas Tech University

Health Sciences Center, Lubbock, Texas


Poverty plays a significant factor in the fight against obesity due to decreased access to nutritious food or physical activ-ity in lower income families. The 2009 US census reported poverty at its highest level in the previous 51 years.10 Access to markets with healthier options tends to be limited in poorer communities, and healthier food choices are often more expensive.

Unsafe neighborhoods or the lack of well-developed or well-kept parks and facilities in this population is attributed to decreases in physical activity. Reduced incomes minimize the likelihood of enrollment in extracurricular activities that may decrease weight in children. Additionally, parent occupations with odd shift hours require an increase in the amount of time children spend in daycare facilities or in residences, which may fur-ther contribute to sedentary lifestyles and increase the obesity risk in lower income families.

After-school Programs and Nutrition Knowledge Public school systems house the majority of children for seven to eight hours of each school day, providing a great opportunity to influence many children with exercise and nu-trition knowledge at one time. After-school exercise interven-tion programs with a combination of aerobic and resistance exercises that are appropriate for children’s developmental age have had measurable outcomes when implemented at least three months to prevent rebound weight gain.d

Studies show that school-based programs have reduced blood lipids, increased aerobic activity and activity levels, de-creased television time, and improved selection of healthier food choices with the implementation of year-round pro-grams with after-school exercise and nutritional education.5,14

Kid’s Choice Program found that a school-based intervention increases health behaviors in average weight children and promotes weight loss in overweight children.6 Farris et al1

studied obese or overweight children 6 to 12 years of age in a 12-week intervention program and demonstrated statistically significant differences in serum glucose, triglycerides, blood pressure and body measurements.1 School-based exercise and nutrition programs are not readily available, but phar-macists can help provide educational information found in these programs to children at risk.

Pharmacist’s RoleParents or caregivers are important facilitators in nutrition education and exercise interventions to ensure long-term effects, but there are other healthcare professionals that can assist.15 Pharmacist roles continue to expand in differ-ent areas within the healthcare field predominantly in the adult population, but the pediatric population would also benefit from these accessible healthcare professionals to help combat obesity. They can be an essential resource that provides non-pharmacologic educational information includ-

ing materials on nutrition and exercise to pediatric patients and their caregivers. The most limiting factor for Texas community pharmacists was identified by O’Donnell et al16 that found a lack of time was the most significant barrier in providing counseling on obesity education.

Changes in diet and exercise habits that help to prevent obesity can improve the fu-ture health of the pediatric population. Nutrition edu-cation include interpreting nutrition facts labels; identi-fying and choosing low-fat, nutritious foods; creating consistent, scheduled meals; reducing sugary foods; limit-

ing saturated fat; selecting water as a beverage over sugared drinks; and, identifying appropriate portion sizes.17-20 Exer-cise education include incorporating at least 60 minutes of appropriate daily exercise in children greater than 6 years; identifying different types of physical activities (swimming, walking, biking, hiking, dancing, and sports); and, reducing sedentary behaviors of television time, computer time, phone time, texting time, and video games with two or less hours of screen time per day.17,20-22 The information provided to children by pharmacists can help them make better choices at school and at home to help reduce the risk of obesity despite the challenges pharmacists encounter due to a lack of time. Pharmacists could provide that education during patient counseling sessions for other medications to encour-age lifelong lifestyle nutrition and exercise awareness. SummaryChildhood obesity is a growing problem affecting a consider-able number of children in the US, with numbers well above goal levels. This may result in obesity-related comorbidities, lower quality of life and fewer friendships, or psychological issues. School-based programs that combat obesity are ben-

Photo credit: ktheory / Foter.com / CC BY

31tshp.org | TSHP

eficial if incorporated with school physical activity, nutritional knowledge, and parenteral involvement. These programs can promote a lifelong healthy lifestyle by encouraging healthy behaviors. Pharmacists can be important healthcare profes-sional resources to provide nutritional and exercise educa-tion in making these lifestyle changes to decrease obesity in pediatrics.

References1. Farris JW, Taylor L, Williamson M, et al. A 12-week

interdisciplinary intervention program for children who are obese. Cardiopulm Phys Ther J. 2011; 22:12-20.

2. Centers for Disease Control and Prevention. Health People 2010: Nutrition and Overweight. http://www.cdc.gov/nchs/data/hpdata2010/hp2010_final_review_focus_area_19.pdf (accessed 2013 7 March)

3. Centers for Disease Control and Prevention. Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963–1965 Through 2009–2010. http://www.cdc.gov/nchs/data/hestat/obesity_child_09_10/obesity_child_09_10.pdf (accessed 2012 5 December).

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5. Centers for Disease Control and Prevention. About BMI for children and teens. www.cdc.gov/healthyweight/ assessing/bmi/childrens_bmi/ about_childrens_bmi.html (accessed 2012 30 November).

6. Hendy HM, Williams KE, Thomas CS. Kid’s choice program improves weight management behaviors and weight status in school children. Appetite. 2011;56(2):484-494.

7. Wang Y, Beydoun MA, Liang L et al. Will all Americans become overweight and obese? Estimating the progression and cost of the US obesity epidemic. Obesity (Silver Spring). 2008; 16(10):2323-2330.

8. Li C, Ford ES, Zhao G et al. Prevalence of pre-diabetes and its association with clustering of cardiometabolic risk factors and hyperinsulinemia among US adolescents: NHANES 2005–2006. Diabetes Care. 2009;32:342–347.

9. Zorba E, Cengiz T, Karacabey K. Exercise training improves body composition, blood lipid profile and serum insulin levels in obese children. J Sports Med Phys Fitness. 2011; 51(4):664-9. Pediatrics. 2007;120;S164.

10. Freedman DS, Zuguo M, Srinivasan SR et al. Cardiovascular risk factors and excess adiposity among overweight children and adolescents: the Bogalusa Heart Study. J Pediatrics. 2007; 150(1):12–17.

11. Davis CL, Pollock NK, Waller JL et al. Exercise Dose and Diabetes Risk in Overweight and Obese Children A Randomized Controlled Trial. JAMA. 2012;308(11):1103-1112.

12. Caprio S, Daniels SR, Drewnowski A et al. Influence of race, ethnicity, and culture on childhood obesity: implications for prevention and treatment. Obesity (Silver Spring). 2008;16(12):2566-2577.

13. Wang Y. Disparities in pediatric obesity in the United States. Adv Nutr. 2011; 2:23-31.

14. Carrel AL, Logue J, Deininger H et al. An after-school exercise program improves fitness, and body composition in elementary school children. JPESM. 2011;2(3):32-36.

15. Golan M, Crow S. Targeting Parents Exclusively in the Treatment of Childhood Obesity: Long-Term Results. Obes Res. 2004; 12: 357–361.

16. O’Donnell DC, Brown CM, Dastani HB. Barriers to Counseling Patients with Obesity: A Study of Texas Community Pharmacists. J Am Pharm Assoc. 2006;46(4):465-471.

17. Centers for Disease Control and Prevention. How much physical activity do children need? http://www.cdc.gov/healthyweight/children/index.html (accessed 2012 30 November).

18. United States Department of Agriculture. Printable Materials & Ordering. http://www.choosemyplate.gov/print-materials-ordering.html (accessed 2012 30 November).

19. United States Department of Health and Human Services. Dietary Guidelines for Americans 2010. http://www.cnpp.usda.gov/Pujanieblications/DietaryGuidelines/2010/PolicyDoc/PolicyDoc.pdf (accessed 2012 30 November).

20. Barlow SE. Expert Committee Recommendations Regarding the Prevention, Assessment and Treatment of Child and Adolescent Overweight and Obesity: Summary Report. Pediatrics. 2007;120(4):S164-192.

21. Centers for Disease Control and Prevention. Tips for Parents- Ideas to Help Children Maintain a Healthy Weight. http://www.cdc.gov/physicalactivity/everyone/guidelines/children.html (accessed 2012 30 November).

22. Physical Activity Guidelines Advisory Committee. Physical Activity Guidelines Advisory Committee Report, 2008. Washington, DC: U.S. Department of Health and Human Services, 2008. http://www.health.gov/paguidelines/report/pdf/committeereport.pdf (accessed 2012 4 December).


The 2013 TSHP Annual Seminar and associated events hit new records and raised the bar for excitement, involvement and new ideas. Beginning with the Alcáldé Southwest Residency Conference on April 24-25, the entire event was filled with record breaking attendance. A total of 262 individuals registered for the showcase, including 179 residents and 80 pharmacists/preceptors. The abstracts of all platform presentations are posted on the TSHP R&E Foundation website as well as additional details about the meeting. Overall seminar registration hit a record 993 individuals, including a record number of pharmacists (285), new practitioners (103), and students (232). Over 100 posters were displayed during the TSHP/TSHP R&E Poster Competition, and a record 156 students and residents (78 teams) participated in the Clinical Skills and Disease State Management Competitions. Winners of the Poster Competition were:

• Resident/PGY 1 - Christine Lang, Pharm.D., Evaluation of Medication Error Reduction with Pharmacist-Conducted Admission Medication Reconciliation in an Emergency Department

• Resident PGY 2 - Zachary R. Smith, Pharm.D., The University of Texas: MD Anderson Cancer Center, Houston, Texas, Development of a Combination Antibiogram for Pseudomonas aeruginosa Bacteremia

• Student - Catherine Pharm, The University of Texas at Austin College of Pharmacy, Austin, Texas, Findings of medication review services provided by a student pharmacist-led community outreach program

• Technician - Dianna Little, Memorial Hermann

Hospital, Sugar Land, TX, Pharmacy Technician Preventing Medication Errors Through Medication History Interview At Admission

• Practitioner/Administrative - Jacinto Villarreal, Pharm.D., Children’s Hospital of San Antonio, San Antonio, Texas, The Birth of an Innovative Obstetrics APPE Experience

• Practitioner/Clinical - Bradi L. Frei, Pharm.D., University of the Incarnate Word, San Antonio, TX, A Cost Comparison of Consumer Price Per Unit of Common Nonprescription Drugs and Durable Medical Equipment at Different Types of Pharmacies

• Practitioner/Education - Marissa Quinones, Pharm.D., Parkland Health & Hospital System, Dallas, TX, Applicant Selection Process for PGY1 Pharmacy Residency

Individuals recognized for the Clinical Skills & Disease State Management Competition include:

• Residents - Samuel Akinyele and Kady Phe, St. Luke’s’ Episcopal Hospital

• P1 - P2 Students 1st place - Heidi Michaels & Jisha Jacob, Texas Tech University Health Science Center School of Pharmacy. Honorable mention - Elaine Lo & Linda Yang, The University of Texas at Austin College of Pharmacy

• P3 - P4 Students 1st place - Jesse Castillo & Martin Strait, Texas A&M Health Science Center Irma Lerma Rangel College of Pharmacy. Honorable mention - Sumon Sen & Sarah Ryu, The University of Texas at Austin College of Pharmacy.

• Disease State Management 1st place - Madeline King, Texas A&M Health Science

2013 Annual Seminar

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Center Irma Lerma Rangel College of Pharmacy. Honorable mention - Nola Finke, Texas A&M Health Science Center Irma Lerma Rangel College of Pharmacy.

The Seminar is traditionally the end and beginning of the TSHP organizational year. Outgoing President Brian Cohen reviewed the year in his President’s Message at the Opening General Session. The full TSHP Annual Report is available on the TSHP website, under the ‘Publications’ drop down. A solid and varied program of professional education was developed by the TSHP Council on Education Affairs, under the leadership of Chair Bob Talbert and Vice Chair Andrea Ries. Up to 5 concurrent educational tracks provided over 19 hours (1.925 CEUs) of continuing pharmacy education from a selection of over 51 total hours. “Practical,” “Better than ASHP Mid-Year,” and “Best ever!” were among the evaluation comments received. New officers for the coming year were installed, including:

• President Emory Martin, Scott & White, Temple, TX • President-Elect Larry Egle, MedAssets, Houston, TX• Treasurer Linda Haines, The Methodist Hospital,

Houston, TX

The TSHP R&E Foundation added a “wine toss” to its fund raising activities and brought new fun to the exhibit area. Prior to the meeting, the Foundation board approved awarding $14,500 in scholarships for 2012-2013. A full list of the scholarship recipients is available in the Foundations’ 2012 Annual Report.

The Foundation’s 2012 Annual report, list of scholarship recipients, and contributors for the year are available on the R&E Website. With tremendous support from members, friends and TSHP local chapters, a record amount of donations and pledges were received by R&E during the 3-day event. Entering the Installation Luncheon, the total assets of the Foundation were approaching $500,000. With an appeal to the attendees, R&E President Sarah Lake Wallace helped push the total fund to just over the half million dollar level, assuring the Foundation’s place as the largest state society-based foundation in the nation.


Effectiveness of Lovaza Compared to OTC Fish Oil in Reducing Hypertriglyceridemia:

A Retrospective Analysis

IntroductionHypertriglyceridemia is defined as the p r e s e n c e o f a n excessive amount of triglycerides (TG) in the blood.1 The National Cholesterol Education Program A d u l t Tre at m e nt Panel (NCEP ATP III) states that the goal triglyceride level is less than 150mg/dL.2

Hypertriglyceridemia is a commonly encountered lipid abnormality. Hypertriglyceridemia’s prevalence in the United States is thought to be close to 30%.1 Hypertriglyceridemia can be either primary or secondary in nature. Primary hypertriglyceridemia is caused by various genetic factors that result in altered triglyceride metabolism. Secondary hypertriglyceridemia is due to acquired causes such as a high fat diet, obesity, diabetes, hypothyroidism, and medications.1 Getting a patient’s triglycerides to goal can be problematic as it often involves therapeutic lifestyle changes (TLC) and the use of multiple medications (HMG-3-CoA reductase inhibitors, fibric acid derivatives, niacin and fish oil/omega-3 fatty acids). Fish oil is thought to decrease triglycerides in the body through several pathways; however the exact mechanism is not completely understood. Fish oil contains EPA and DHA (omega-3 fatty acids) which inhibit acyl CoA:1,2-diacylglycerol acyltransferase (resulting in decreased triglyceride synthesis) and increases peroxismal beta-oxidation in the liver (which results in the up-regulation of fatty acid metabolism). Additionally, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) inhibit the esterification and release of other fatty acids because they have a high affinity, however they serve as poor substrates, for enzymes that produce triglycerides (effectively blocking their synthesis). They are also thought to increase lipoprotein lipase activity to triglyceride clearance.3 Most fish oil supplements have a lower EPA/DHA content than the prescription fish oil product Lovaza. However, to date there have been no head-to-head trials comparing over-the-counter (OTC) fish oil supplements

to Lovaza to determine if the decreased EPA/DHA content of the OTC products results in a clinically significant effect on patients with hypertriglyceridemia. This retrospective analysis aims to shed some light on this subject in comparing Lovaza (EPA content of 465mg and DHA content of 375mg per capsule) and an OTC fish oil product (EPA content of 180mg and DHA content of 120mg per capsule).

BackgroundLovaza’s effects were evaluated in two randomized, placebo-controlled, double-blind, parallel-group clinical trials of 84 adult patients (42 patients on Lovaza, 42 patients on placebo).4 Only patients’ whose baseline triglycerides were between 500-2000mg/dL were enrolled. The median baseline triglyceride, LDL and HDL levels for the studied patients were 792mg/dL, 100mg/dL and 23mg/dL, respectively. Compared to placebo, Lovaza decreased triglycerides by 51.6%, increased LDL by 49.3% and increased HDL by 9.1%.4 The effects of Lovaza have also been studied as an adjunct to statin therapy in adult patients with persistently high triglycerides (200 to 499mg/dL). In an eight week study, 254 patients (122 on Lovaza and 132 on placebo) received either Lovaza plus simvastatin or placebo plus simvastatin. The median baseline triglyceride, LDL and HDL levels for these patients’ were 268mg/dL, 89mg/dL and 45mg/dL, respectively. After 8 weeks the Lovaza plus simvastatin group was found to have significantly reduced triglycerides (by 23.2%), significantly increased HDL (by 4.6%) and insignificantly increased LDL (by 3.5%, p=0.05).4 Lovaza is currently indicated for hypertriglyceridemia in adjunct to diet in adults with triglyceride levels of 500mg/dL or higher, at a dose of 4g once daily or divided into two doses. It’s most common side effects are gastrointestinal in nature including: burping, indigestion and taste sense alterations.5 While Lovaza generally contains more EPA and DHA than OTC fish oil products, it is much more costly, so some patients are forced to use an OTC fish oil product instead.

MethodsThe study was approved by the Chickasaw Nation Medical Center Institutional Review Board. The Chickasaw Nation Medical Center offers a dyslipidemia pharmacy based

AutHors

Thomas Ross Clark, Pharm.D., Inpatient Pharmacy Clinical Coordinator

Facility:Chickasaw Nation

Medical Center, Ada, OK

35tshp.org | TSHP

clinical service on a voluntary provider referral basis. This clinical service offers counseling on the patient’s dietary and exercise habits along with the management of their dyslipidemia medications. The clinic maintains a list of current and past patients that have been enrolled in this service. A retrospective search was conducted of these patients’ electronic health records (EHR). In order for a patient to be included they must have met the following criteria: 1) have a baseline triglyceride value available before starting either OTC fish oil therapy or Lovaza; 2) they must have shown a compliance rate of at least 75% within the past year based on refill history (if the patient had been on their therapy for less than 1 year their compliance must have been at least 75% for the time they had been on fish oil or Lovaza); 3) they must have been on their fish oil therapy for a minimum of 3 months. Once it was determined that a patient could be included in the study their baseline triglyceride value was recorded. Their most recent triglyceride value was recorded as well. The patient’s length of therapy was determined by the date of the first fill of their fish oil medication (available through EHR) up to the point of their most recent triglyceride lab value measurement. A percent difference was determined between their baseline value and most current value.

ResultsEighty out of a total of 106 clinic patients were found to have been on OTC fish oil or Lovaza; 19 of whom were found to be eligible for the study with non-compliance being the most common reason for exclusion (42 of 61 excluded patients were excluded for this reason). The OTC fish oil group consisted of 11 patients and the Lovaza group consisted of eight patients. There were some differences in baseline characteristics (% male/female, % concurrently on fibrates, % concurrently on niacin) (Table 1). Eighteen of the patients were dosed 2g twice daily with one Lovaza patient being dosed 1g twice daily due to tolerance issues.

Table 1 Baseline patient characteristicsO T C F i s h O i l (n=11)

Lovaza (n=8)

Age 59 Years 60 Years% Male 63.6% 25%% Female 36.4%q 75%% Diabetic 72.7% 75%% Concurrently on Statins

81.8% 87.5%

% Concurrently on Fibrates

90.9% 62.5%

% Concurrently on Niacin

9.1% 25%

The average length of therapy and baseline triglycerides did vary between the OTC fish oil and Lovaza group (3.04 years vs. 1.03 years) and the baseline triglyceride levels varied as well. Table 2 shows the baseline lipid characteristics of the patients included in the study. The patients who were only on the OTC fish oil experienced a 20% decrease in their TG level where as the Lovaza patients experienced a 57.9% decrease.

Table 2 Comparison of changes in triglyceride levelsOTC Fish Oil Lovaza

Average Length of Therapy

3.04 years 1.03 years

Average Baseline TG

280 426

Average Current TG

224 179

Average % Change in TG

-20.0% -57.9%

Of the patients who were on Lovaza, two had never been on any type of fish oil product prior to the initiation of their Lovaza therapy. Six of the Lovaza patients had been on OTC fish oil and were switched to Lovaza after an average of 2.57 years of being on OTC fish oil therapy. However, the baseline characteristics of the fish oil naïve patients were not highly comparable to the patients who were switched from OTC fish oil to Lovaza (Table 3).

Table 3 Baseline characteristics of Lovaza patientsBaseline Fish Oil Previously

(n=6)Fish Oi l Naïve (n=2)

Age 62.8 52.5% Male 16.6% 50%% Female 83.3% 50%% Diabetic 66.7% 100%% Statin Use 83.3% 100%% Fibrate Use 66.7% 50%% Niacin Use 16.7% 50%

The patients who were switched from OTC fish oil to Lovaza had a baseline TG level of 363.2. After an average of 2.57 years on OTC fish oil their TGs ended up at 510. At this point they were switched to Lovaza. After an average of 0.96 years on Lovaza therapy, the patient’s TG levels decreased by 61% to 200. The patients who had never been on any type of fish oil (this includes the one patient who was on 1g twice daily) had a baseline TG level of 172.5 and were treated for an average of 1.25 years. After this treatment period these patients’ TG levels were reported to be an average of 117.5 (a 31.9% decrease).


The patients’ LDL values were also measured to determine if the fish oil had any effect on LDL, since it is the primary target of dyslipidemia therapy. The baseline LDL for patients before being started on OTC fish oil was measured at 102; at the time that they ended their OTC fish oil therapy (or their most current LDL value if the patient is still on OTC fish oil) it was measured at 94 (a 7.8% decrease). The baseline LDL for patients before being started on Lovaza therapy was measured at 94, at the time of their most recent LDL measurement it was measured at 82 (a 12.7% decrease). After pooling all of the patients’ data together, the baseline LDL was measured at 105 and their most recent LDL values averaged out at 89 (a 15.2% decrease). LDL changes in patients who were on statins and a fish oil product versus patients who were just on fish oil are compared below (Table 4), several patients in this study were either on simvastatin/ezetimibe or ezetimibe in addition to rosuvastatin or atorvastatin (1 patient was on ezetimibe without a statin) and were excluded from this part of the analysis. Rosuvastatin (n=4) and simvastatin (n=4) were the most commonly used statins with atorvastatin being used slightly less (n=3).

Table 4 Comparison of LDL levels on patients with or with-out statin therapy

Baseline LDL Endpoint LDLNo Statin therapy (n=2)

112.5 116.5

Statin therapy (n=11)

83.5 73.7

DiscussionThis retrospective analysis compared the efficacy of OTC fish oil to Lovaza to determine the clinical significance of differing levels of EPA/DHA in reducing hypertriglyceridemia. This analysis was conducted to determine if the use of Lovaza in our clinic actually provided more benefit in triglyceride lowering than OTC fish oil, given the expense of Lovaza. The data suggests that the use of Lovaza imparts a more significant reduction in triglycerides (20% for OTC fish oil; 57.9% for Lovaza). Lovaza clinical trials found a 44.9% reduction in triglycerides when not used in conjunction with a statin and a 29.5% reduction when used in conjunction with a statin.4 A comparison of patients who were started on the OTC fish oil product and switched to Lovaza or patients who were initially started on Lovaza was also conducted. The baseline characteristics of these patients were not highly comparable. The Lovaza only patients showed smaller decreases in their triglycerides, but this is most likely attributable to their lower baseline triglyceride levels. Additionally, one patient was using Lovaza 1g twice daily (as compared to the 2g twice daily that all other patients in the analysis were taking). An analysis of the included patients’ LDL was also conducted to determine if the fish oil in these patients had caused elevations that have

been previously reported in the literature.6-8 Overall, patients saw a small decrease in their LDL. This is likely due to the fact that a high percentage of patients in this study were concurrently on statins. The literature has also reported that fish oil may not raise a patient’s LDL if used concurrently with statin medications.4,9-11 An analysis of patients who were on statins versus patients who were not on statins reflect that data. Small elevations in LDL were noted (3.6%) in the patients who were not on statin therapy, but this level of LDL increase is likely not of any clinical significance. This is in contrast to placebo-controlled Lovaza clinical trial that showed a 44.5% increase in LDL. However, further studies have found this percentage LDL increase to be similar.12

The results of this study were shared with the pharmacists who managed the clinic to give them an idea of the differences in triglyceride and LDL changes in patients on our two different fish oil products. It is unknown at this time if this affected prescribing habits within the clinic. Vascepa (icosapent ethyl), which is an ultra-purified ethyl EPA fish oil product, has yet to be used within our facility, but given the negligible LDL increases seen while using Lovaza or OTC fish oil I do not think it is likely that it will be used within our clinic in the foreseeable future.13 More investigation into this subject matter would be needed to determine the full clinical relevance of using Lovaza or an OTC fish oil product.

As with any retrospective analysis there are multiple confounders and weaknesses. In the case of this analysis we were unable to control for the patients diets. However, every dyslipidemia clinic patient receives dietary counseling at every visit. The use of refill history as a marker of compliance may not be 100% reflective of how the patient is actually taking the medication. It is assumed that all patients were fasting at the time their lipid panel was drawn, and level of diabetic control was also not assessed by this analysis. Additionally, the sample size in this study was small (n=19) and was only able to include 24% of clinic patients who were on a fish oil product due mostly to non-compliance.

ConclusionIn summary, this analysis suggests that the use of Lovaza may produce more pronounced reductions in triglycerides than using an OTC fish oil product with lower amounts of EPA/DHA. This analysis also suggests that the use of fish oil may not result in LDL elevations if the patient is concurrently using a statin medication. However, these LDL elevations may have been blunted by the dietary counseling provided.

References1. Pejic RN, Lee DT. Hypertriglyceridemia. J Am Board Fam

Med. 2006;19(3):310-316.2. Third Report of the Expert Panel on Detection,

Evaluation, and Treatment of High Blood Cholesterol

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in Adults (Adult Treatment Panel III). U.S. Department of Health and Human Services. Available at: http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm. Accessed April 25, 2011.

3. Koski, RR. Drug Forecast. Omega-3-acid Ethyl Esters (Lovaza) For Severe Hypertriglyceridemia. P&T. 2008;33(5):271-303.

4. Lovaza Full Prescribing Information. GSK Source. Available at: https://www.gsksource.com/gskprm/htdocs/documents/LOVAZA-PI-PIL.PDF. Accessed February 25, 2013.

5. Omega-3-Acid Ethyl Esters. Micromedex Healthcare Series, (electronic version). Thompson Micromedex, Greenwood Village, Colorado, USA. Available at: http://www.thompsonhc.com. Accessed February 25, 2013.

6. Harris WS, Ginsberg HN, Arunakul N, et al. Safety and Efficacy of Omacor in Severe Hypertriglyceridemia. Journal of Cardiovascular Risk. 1997;4:385-391.

7. Pownall HJ, Brauchi D, Kilinc C, et al. Correlation of Serum Triglycerides and its Reduction by Omega-3 Fatty Acids with Lipid Transfer Activity and The Neutrail Lipid Compositions of High-Density and Low-Density Lipoproteins. Atherosclerosis. 1999;143:285-297.

8. Calabresi L, Donati D, Pazzucconi F, et al. Omacor in Familial Combined Hyperlipidemia: Effects of Lipids and Low Density Lipoprotein Subclasses. Atherosclerosis. 2000;148:387-396.

9. Nordoy A, Hansen JB, Brox J, Svensson B. Effects of Atorvastatin and Omega-3 Fatty Acids on LDL Subfractions and Postprandial Hyperlipidemia in Patients with Combined Hyperlipidemia. Nutr Metab Cardiovasc Dis. 2001;11:7-16.

10. Durrington PN, Bhatnagar D, Mackness MI, et al. An Omega-3 Polyunsaturated Fatty Acid Concentrate Administered For One Year Decreased Triglycerides in Simvastatin Treated Patients With Coronary Heart Disease and Persisting Hypertriglyceridemia. Heart. 2001;85:544-8.

11. Stalenhoef AF, Graaf J, Wittekoek ME, et al. The Effect of Concentrated n-3 Fatty Acids Versus Gemfibrozil on Plasma Lipoproteins, Low Density Lipoprotein Heterogeneity and Oxidizability in Patients with Hypertriglyceridemia. Atherosclerosis. 2000;153:129-138.

12. Maki KC, Lawless AL, Kelley KM, et al. Effects of Prescription Omega-3-Acid Ethyl Esters on Fasting Lipid Profile in Subjects With Primary Hypercholesterolemia. J Cardiovasc Pharmacol. 2011;57:489-494.

13. Vascepa Full Prescribing Information. Vascepa (isocapent ethyl). Available at: http://www.vascepa.com/full-prescribing-information.pdf. Accessed February 25, 2013.


The Power of Mentorship

O n n u m e r o u s occasions, I’ve been asked about the best way to achieve on-going professional accomplishments and recently realized that the consistent thread between each of my

past successes has been due to mentorship. I recall back in my early college days when I was searching for a career suited for my future, I was first informally mentored by my co-worker. She exposed me to the world of pharmacy, walked me through the preparation, application and interview stages for pharmacy school admissions, and still remained there for me throughout the pharmacy curriculum. She graduated pharmacy school one year ahead of me, and still remains my lifelong friend today.

Fast forward into my residency years – I recall carefully picking a formal mentor as a requirement of the program. The person I chose had many positive attributes including a successful career, strong worth ethic and a personality that I truly admired. These were all qualities I aspired to obtain. She was highly influential in helping me succeed through the residency program, and has helped develop and transition me into becoming the practitioner I am today. Whether I was in search of job positions, preparing for interviews or adapting to my first job out of residency, she remained there for me through it all. Still today, we make it a point to keep in contact on a monthly basis.

Through my experiences, I’ve realized the power and importance of mentorship and how greatly it has contributed to my development as I transitioned from student to resident, resident to new practitioner and now, from new practitioner to an experienced practitioner.

Becoming a mentor or mentee is not age-specific, which is a common misconception. Whether you are transitioning from student to resident, resident to new practitioner, new practitioner to experienced practitioner, starting a new job, embarking on a new service or advancing for a job promotion, they all come with their own challenges. Mentorship can play an integral role through each phase of life and help one overcome obstacles in order to succeed.

After realizing this need, the initial step is to select a mentor. Mentors can be selected via “informal” or “formal” means. An informal mentorship requires you to identify your own mentor. As stated in an article from ASHP’s New Practitioner’s forum, “A good mentor will have sufficient professional experience, a history of overall professional success that has not come at the expense of personal happiness, a good professional reputation and history of professional involvement, sufficient time to devote to a mentee, and the willingness to become a mentor.”1 After identifying your potential mentor, it is up to you to develop the relationship. Share knowledge, experiences and perspectives with the realization that true mentorship should provide mutual gains to both the mentor and mentee. It is best to think about not only what you can gain, but also what you can offer to your mentor. Furthermore, realize that not all mentorships result in personal friendships, nor are they always life-long commitments.

TSHP offers a formal mentorship program that has been successful for the past four years. This past year, under the leadership of the New Practitioner Section Chair (Steven Knight, PharmD, BCPS) and Mentor Program Chair (Bonnie Whittington, PharmD, BCPS), the program expanded the matching process to allow for year round application submissions. In addition, the program is enabled to now allow both pharmacy students and new practitioners to apply as mentees.

In the words of Sara White, MS, FASHP, “To be successful, every pharmacist must have at least one mentor and serve as a mentor.” In the profession of pharmacy where pharmacists are lifelong learners and advocacy is of utmost importance, pharmacists must give back and help advance the profession. One way to do this is to serve as mentors. Not only does this lead to professional growth for individuals, it benefits our profession as a whole.

Mentorship is powerful through all phases of life.To sign up as a mentor or mentee or learn about the program, visit TSHP’s website at http://tshp.org/mentor-program.html

References1. Altman JS. The value of mentorship. Am J Health-Syst Pharm. 2005;62:2474-2477.

AutHors

Linda Haines, PharmD, MS TSHP New Practitioners Section

Chair, TSHP Treasurer

39tshp.org | TSHP

Paul F. Davis, R.Ph.Executive Director

Editorial - Speaking of...

Re-inventing Local Chapters

I was filling out one of those ‘association management’ sur-veys recently that asked about what our local chapters do. I had to stop and think about that for a minute . . .

Like most organizations we have a whole spectrum of local chapters. Some are what I would consider among the best in the U.S.; some are almost invisible. Some are bigger than some other state societies, some struggle to get enough members together for a good game of bridge.

And those chapters have a wide range of things they do. Things that only a local chapter can do:

• Regular meetings• Networking opportunities• Continuing pharmacy education programs• Provide a leadership training ground • Idea exchange• Social gatherings• Communications resource (“what’s going on in the world

of pharmacy?”)• Address local health concerns and issues, such as local or-

dinances that impact patient care and pharmacy practice• Community service such as career days, health fairs• PR, as in coordinating responses to local media, under-

taking “pharmacy week” or various health-related public observances

• A place for cooperation and collaboration• Support for the ‘parent organization’

That got me to thinking a bit more. I got to where I am today, partly, because my first ‘volunteer job’ out of phar-macy school was to serve as editor of our local association’s newsletter. How many state, national and specialty leaders in health-system pharmacy, or the bigger world of pharmacy, started out just like that; as a local officer or committee member?

And THAT got me to thinking about just how much has changed in pharmacy, the world and local chapters since I was copying, folding, stapling and mailing that old newsletter.

A lot of locals (not just TSHP’s) took a hit when the free meals

with CPE meetings went away. But thinking back, I’m not sure we were attracting a lot of people even in those days. Even when the meal was at a good steakhouse.

Which is why I think we may be missing the boat when it comes to local chapters, and maybe it’s time to consider re-inventing them.

Between the e-mails, texts, TV, Facebook, electronic games, and the obvious need to focus on professional issues and home life, while continuing to drive on the right side of the road, it’s hard to find time to just share things with other human beings.

We run in circles so fast and for so long that it’s no wonder that we’re all wound up with just getting by. And when that happens we sometimes miss great opportunities to re-evaluate what we’re all about.

Take a local chapter meeting. Many of our locals are now realizing that there are terrific resources right there in their communities and facilities for excellent educational program-ming. You don’t have to have the expert from more than 50 miles away every time you meet. You might even be able to meet without steak, shrimp and wine(!)

There’s a lot to be said about sharing. What about semi-organized open discussions about best practices or how vari-ous institutions have attacked a particular problem? Instead of asking someone to speak for 60 minutes on an issue, how about an idea exchange with short (5 minute?) presentations about a variety of topics. What was your biggest challenge last week? Maybe hold an idea auction, where the best idea of the meeting wins a gift card.

There’s a world beyond those hospital walls – you see it every day on the way to work and going home. What if your local chapter engaged that world a bit and participated, as a group, in a drug take back day, a community project like Habitat, or even looked into taking on some local health challenge (like staffing a community clinic). Some locals do.


Invite your local legislative delegation to a reception. Just a greet and visit thing, or maybe a presentation about a health-care or pharmacy issue pertinent to your community. Do you know your elected state officials? Do they know you, and what you do?

Local journal clubs. A periodic meeting with your colleagues in community practice. A joint meeting with other healthcare professionals – other than doctors. Charter a boat for a group cruise on a lake – if yours hasn’t dried up. Host a 5K fun run for a disease or to support a community effort. Sponsor a sports team. Become visible.

Maybe there are individual jobs that need doing within your local area that just need to have someone asked to take care of it. Who is responsible for welcoming new hospital pharmacists and technicians into your area, and seeing that they get to your local meeting? Who knows who to call at the newspaper or TV station if you had a story to tell or wanted to send out a message about pharmacy week? Who is responsible for finding local news about pharmacy/pharmacists/technicians and sending it to TSHP to include in the E-News? Who edits your chapter newsletter or website? Who handles your ‘politi-cal activities’ such as fund raising for TSHP PAC or seeing that legislators know what a hospital pharmacist is. (You can bet they ALL know their local hospital administrators.)

I think my point is that maybe it’s time to lift our thoughts and eyes out of the regular rut we’ve walked with locals for so long and find ways to re-invigorate and re-invent them using the energy and ideas of a new generation. Who knows where an idea like that might end up?