Demystifying Drug Interactions with
Combined Analgesics Across Various
Therapeutic Classes
September 19, 2017
Jeffrey Fudin, PharmD, DAIPM, FCCP, FASHP
President & Director, Scientific & Clinical Affairs,Remitigate, LLC, Delmar, NY
Adjunct Associate Professor,Western New England University College of
Pharmacy, Springfield, MA
Adjunct Associate Professor of Pharmacy Practice & Pain Management,
Albany College of Pharmacy & Health Sciences,
Clinical Pharmacy Specialist & Director,PGY2 Pain & Palliative Care Residency,Stratton VA Medical Center, Albany, NY
Larry C. Driver, MD
University of Texas Distinguished Teaching Professor,
Professor, Department of Pain Medicine,
Professor, Section of Integrated Ethics,
The University of Texas M.D. Anderson Cancer Center,
Houston, TX
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Accreditation and
Credit Designation
• Accreditation:
The American Academy of Pain Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
• Credit Designation:
The American Academy of Pain Medicine designates this live activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Dr D
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Speaker and Planning Committee
Disclosures
Speakers:
AstraZeneca: Speakers BureauClarity: Consultant Collegium: Consultant Daiichi Sankyo: Advisory Board Depomed: Advisory Board, Speakers Bureau Egalet: Consultant, Advisory BoardEndo: Consultant, Speakers BureauIroko Pharmaceuticals: Speakers BureauPernix Therapeutics: Consultant Quest Labs: Advisory Board Remitigate, LLC: Owner
Jeffrey Fudin, PharmD, DAIPM, FCCP, FASHPPresident & Director, Scientific & Clinical Affairs, Remitigate, LLC Adjunct Associate Professor, Western New England
University College of Pharmacy, Adjunct Associate Professor of Pharmacy Practice &
Pain Management, Albany College of Pharmacy & Health Sciences, Clinical Pharmacy Specialist & Director, PGY2 Pain & Palliative Care Residency, Stratton VA Medical Center
Larry C. Driver, MDUniversity of Texas Distinguished
Teaching Professor,Professor, Department of Pain Medicine,Professor, Section of Integrated Ethics,The University of Texas M.D.
Anderson Cancer CenterNo relevant financial relationships
Reviewer:
Michael Harned, MD
University of Kentucky
Medtronic: Honorarium,
Speaker & Fellow
Education
St. Jude: Honorarium,
Speaker & Fellow
Education
Planners:
Jennifer Westlund, MSWDirector of Education, AAPMNo relevant financial relationships
Angela CaseyVP, Medical Director, PharmaCom GroupNo relevant financial relationships
Stephanie LeeMeetings Manager, PharmaCom GroupNo relevant financial relationships
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Target Audience
• The overarching goal of PCSS-O is to offer evidence-based trainings on the safe and effective prescribing of opioid medications in the treatment of pain and/or opioid addiction
• Our focus is to reach providers and/or providers-in-training from diverse healthcare professions including physicians, nurses, dentists, physician assistants, pharmacists, and program administrators
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Educational Objectives
• At the conclusion of this activity, participants should be able to:
1. Classify cytochrome P450 (CYP450) system nomenclature and describe role of CYP450 and p-glycoprotein in pharmacokinetics
2. Recognize key CYP450 mediated drug-drug interactions
3. Identify potential drug-drug interactions and important considerations when prescribing various analgesic classes and adjuvants
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Common Mechanisms for
Drug-Drug Interactions
• Similar or overlapping pharmacological activity
Opioids / Benzodiazepines and sedation
Opioids / TCAs and constipation
NSAIDs / SNRIs / Steroids and bleed risk
• Protein binding and free drug
NSAIDs and albumin
Amitriptyline and alpha-glycoprotein
• CYP450 induction, inhibition, autoinduction, substrates
Carbamazepine/methadone, codeine or tramadol/sertraline
• P-glycoprotein
Morphine/rifampin, methadone/telaprevir
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Adverse Outcomes Due to Drug-Drug
Interactions in Stable Patients
• Often occur after the addition of a new drug that increases or decreases the effect of a drug a patient is already taking
• Time course varies depending on the pharmacokinetics of the drugs involved
Most adverse outcomes manifest themselves within the first week or two of starting therapy with a new drug
Adverse outcomes can also occur in patients who have been stabilized on interacting drugs for weeks or months
Horn JR, Hansten PD. Pharmacy Times. March 20, 2017.
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Adverse Outcomes Due to Drug-Drug
Interactions in Stable Patients
• Pharmacodynamic DDIs Risk may continue as long as a patient receives the 2 drugs; eg,
increased risk of bleeding when SSRIs are given with warfarin
• Addition of third drug Sometimes a patient is on long-term therapy with 2 interacting
drugs with no adverse outcomes, but a reaction occurs when a third drug is added
• Stopping a drug If a drug is titrated to effect in the presence of an inhibitor or
inducer, when the inhibitor or inducer is stopped, the drug concentrations may become subtherapeutic or excessive
• Change in renal function Some DDIs are more likely to result in adverse outcomes in
patients with impaired renal function
Horn JR, Hansten PD. Pharmacy Times. March 20, 2017.
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Cytochrome P450 Review
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CYP450 Nomenclature
• Cytochrome is designated CYP
• CYP (#) - # identifying the enzyme family
• CYP (#) (A,C) - subfamily designation
• CYP (#) (A,C) (#) - individual enzyme(based on when enzyme was discovered)
• Examples:
CYP3A4
CYP2D6
CYP1A2
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Cytochrome P450 Enzyme Tree
1 2 3 4 5 7 11 17 19 21 27
1A 1B
1A1 1A2
1B1
2F2D2C2B 2E2A
2A6 2A7
2B6 2B7P
2C8 2C9 2C18 2C19
2D6 2D7P 2D8P
4A 4B 4F
4B1
4F2 4F3
11A 11B
11A1
11B1 11B2
21A
21A1P 21A2
4A9 4A11
3A
3A3 3A4 3A5 3A5P 3A7
2E1
2F1
Adapted from: Riddick DS. Drug biotransformation. In: H Kalant, W Roschlau (Ed), Principles of Medical Pharmacology, 6th ed, Oxford University Press: NY, 1997.
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Terminology
• Inducer
3 weeks
• Inhibitor
48 hours
• Substrate
• Genetic polymorphism
Poor metabolizer
Intermediate metabolizer
Extensive metabolizer*
Ultrarapid metabolizer
• Autoinducer
Carbamazepine
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Warfarin Metabolism by CYP2C9
© RxPrep/Dr Jeffrey Fudin
Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.
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Rifampin Induces CYP2C9
Metabolism of Warfarin
© RxPrep/Dr Jeffrey Fudin
Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.
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Amiodarone Inhibits CYP2C9
Metabolism of Warfarin
Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.
© RxPrep/Dr Jeffrey Fudin
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Paroxetine Inhibits CYP2D6 Conversion
of the Prodrug Codeine to Morphine
Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.
© RxPrep/Dr Jeffrey Fudin
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p-Glycoprotein (pGP) Efflux Pumps
• pGP efflux pumps “pump” drugs (pGP substrates) back into the gut
Decreases movement of some drugs across biological barriers, which decreases the amount of drug available in the blood
• pGP pumps located in the liver, gut wall, brain, and kidney
pGP inducerCauses creation of more pGP: blood drug levels go down. pGP inducers also reduce amount of some toxin ingestion, by pumping them back into the gut.
pGP inhibitorInhibits the drug-pump-inhibitor and, consequently, blood drug levels increase.
Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. 2014 ed.
© RxPrep/Dr Jeffrey Fudin
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Polling Question
Drug A is a substrate of enzyme X.
Drug B is an inducer of enzyme X.
A patient has been using Drug A with good results.
The patient has now started therapy with Drug B. What will happen to the concentration of Drug A?
a) Increase
b) Decrease
c) Stay the same
d) Not enough information is given
e) None of the above
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Polling Question
Drug A is a substrate of enzyme X.
Drug B is an inhibitor of enzyme X.
A patient has been using Drug A with good results.
The patient has now started therapy with Drug B. What will happen to the concentration of Drug A?
a) Increase
b) Decrease
c) Stay the same
d) Not enough information is given
e) None of the above
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Opioid Pharmacokinetics and
Drug-Drug Interactions
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Opiates and Opioid Metabolism
Shown in red are the major CYP450 enzymes involved in phase I metabolism; patterns of drug metabolites may reflect the metabolic profile of the patient. Actual proportions of individual metabolites will vary.
Pharmacogenetics testing is available for CYP2D6
Phase II reactions (eg, glucuronide conjugation) are not shown but are prominent for most compounds.
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Medication Metabolism
Phase of
metabolismKey enzymes involved
Examples of opioid
medication metabolized
Phase I
• CYP450
• Examples:
CYP2D6, CYP2C19,
CYP2B6, CYP2C9,
CYP3A4, and CYP3A5
Codeine, hydrocodone,
oxycodone, tramadol,
fentanyl, methadone,
buprenorphine
Phase II
• Uridine 5’-diphospho-
glucuronosyltransferase
(UDP-
glucuronosyltransferase, UGT)
• Examples:
UGT2B7 and UGT2B15
Morphine,
oxymorphone,
hydromorphone,
tapentadol, levorphanol
Smith HS. Mayo Clin Proc. 2009;84:613-24.
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Tramadol Metabolism
• 6,000 X weaker binding affinity to mu opioid receptors compared to morphine
• Serotonin and norepinephrine activity
Tramadol
CYP2D6
O-desmethyltramadol (M1)(active)
N-desmethyltramadol (M2)(inactive)
CYP2B6CYP3A4
N,N,-didesmethyl
tramadol (M3)
N,O-didesmethyl tramadol (M5)
CYP2B6CYP3A4
CYP2B6CYP3A4
CYP2D6
O-desmethyl tramadol
glucuronide (M5)
UGT2B7UGT1AB
Gong L, et al. Pharmacogenet Genomics. 2014;24:374-80.
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Common CYP3A4
Inhibitors and Inducers
CYP3A4 Inhibitors CYP3A4 Inducers
Aprepitant Grapefruit juice Armodafinil Griseofulvin
Amiodarone Indinavir Barbiturates Nafcillin
Atazanavir Itraconazole Bicalutamide Oxcarbazepine
Cimetidine Ketoconazole Carbamazepine* Phenobarbital
Clarithromycin Nefazodone Dexamethasone Phenytoin
Diltiazem Ritonavir Efavirenz Primidone
Erythromycin Telithromycin Etravirine Rifabutin
Fluconazole Verapamil Fosamprenavir Rifampin
Fosamprenavir Voriconazole Fosphenytoin St. John’s Wort
Horn JR, Hansten PD. Pharmacy Times. September 1, 2008.Horn JR, Hansten PD. Pharmacy Times. December 16, 2015.
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Polling Question
Oxycodone is metabolized by CYP3A4.
A patient has been using oxycodone with good results.
The patient has now started therapy with clarithromycin, which is a CYP3A4 inhibitor.
What is the likely result?
a) The patient could suffer fatal respiratory depression
b) The patient experiences a subtherapeutic analgesic response
c) Not enough information is given
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CASE: JB
• 45-year-old Caucasian male
History of cervical stenosis at C5-6 with myelopathy
Has been on tramadol for a number of years, but comes to you for assistance with optimal control of neuropathic pain
You initiate carbamazepine 100 mg PO daily x 7 days, then 200 mg PO daily
• 3 weeks later: JB calls the clinic in distress
Reports being in the worst pain he has experienced in years
• Why is JB suddenly in pain?
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Polling Question
JB has been on tramadol for several years.
Tramadol is metabolized by CYP3A4 and CYP2B6 to the inactive metabolite and by CYP2D6 to the active metabolite.
You add carbamazepine to treat JB’s neuropathic pain.
What is the likely cause of JB’s sudden pain?
a) Carbamazepine is a CYP3A4 inducer. It increases metabolism of tramadol by CYP3A4 to an inactive metabolite
b) Carbamazepine is a CYP2D6 inducer. It increases metabolism of tramadol by CYP2D6 to an active metabolite
c) Not enough information is given
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Common CYP2D6
Inhibitors
CYP2D6 Inhibitors CYP2D6 Inducers
Amiodarone Haloperidol • There are no known
CYP2D6 inducers
• Genetics, rather than drug
therapy, accounts for most
ultrarapid CYP2D6
metabolizers
Bupropion Imatinib
Celecoxib Paroxetine
Cinacalcet Quinidine
Diphenhydramine Terbinafine
Fluoxetine Thioridazone
Horn JR, Hansten PD. Pharmacy Times. July 1, 2008.
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Methadone Metabolism
Gerber JG, et al. Chirality. 2004;16:36-44.
CYP3A4R-methadone
parent drug
EDDP
inactive metabolite
S: Sorrowing outcome (cardiotoxic effects, QT prolongation with potential of Torsade de pointes
CYP2B6S-methadone
parent drug
EDDP
inactive metabolite
R: Responsible for analgesia
CYP2B6 selectively metabolizes S-enantiomerPotential risk?
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QTc Prolonging Drugs
QTc prolonging
drugs
Quinolone antibiotics
Macrolide antibiotics
Amiodarone/ Sotalol
Sertraline/ Citalopram
Venlafaxine
Fluconazole/ Ketoconazole
Ondansetron
Quetiapine
Buprenorphine
Methadone
Fudin J, Pratt Cleary J, Gottwald J. Pharmacy Times. Mar 22, 2016.
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QTc Prolonging Drugs:
Buprenorphine
• Buprenorphine buccal film
900 mcg Q12H (maximum dose)
− QTc 450-480 msec for 2% of patients
Up to 9.2 msec QT prolongation
• Buprenorphine transdermal patch
20 mcg/hour (maximum dose)
No QTc prolongation seen in trials at this dose
Fudin J, Pratt Cleary J, Gottwald J. Pharmacy Times. Mar 22, 2016.
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0 5 10 15 20 25 30 35 40
Haloperidol 15 mg/d
Buccal buprenorphine 3 mg/naltrexone 50 mg
Antidepressants (SSRI vs TCA)
Olanzapine 20 mg/d
Escitalopram
Buprenorphine transdermal patch 40 mcg/hr
Citalopram
Risperidone 16 mg/d
Moxifloxacin 400 mg
Quetiapine 750 mg/d
Ziprasidone 160 mg/d
Thioridazine 300 mg/d
QT prolongation (msec)
Fudin J, Pratt Cleary J, Gottwald J. Pharmacy Times. Mar 22, 2016.
• Note, these data are: Not meant for direct comparisons between the
various agents because of differences in study design, QT correction strategies, and population variations
Provided as context for the current landscape of QT-prolonging drugs
QT Prolongation of Various
Medications
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Methadone vs Levorphanol
Methadone Both Levorphanol
< kappa opioid agonist
Serotonin reuptake inhibitor
Mu opioid agonist
NMDA antagonist
Norepinephrine reuptake inhibitor
> kappa opioid agonist
Delta opioid agonist
CYP450 metabolism
pGP substrate
Phase II glucuronidation
Not a known pGPsubstrate
t1/2 = 15-60 hours
Up to 150 hours in polymorphic outliers
t1/2 = 11-16 hours
QTc prolongation No QTc prolongation
Pham TC, Fudin J, Raffa RB. Pain Med. 2015;16:1673-9.
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Pharmacogenetics
• Drug metabolism and variability among patients in terms of drug response can sometimes be explained by genetic variations within CYP450 enzymes
2 patients: same gender, weight, height, and race on oxycodone ER 10 mg Q12H
− Patient A’s serum oxymorphone level: as expected
− Patient B’s serum oxymorphone level: elevated
Patients A and B are genetically tested:
Gene
Predicted phenotype
Patient A Patient B
CYP3A4/3A5 Normal metabolizer Normal metabolizer
CYP2D6 Normal metabolizer Ultrarapid metabolizer
Naginewicz T, Archer K, Raouf M, Fudin J. Pharmacy Times. August 24, 2017.
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The Perfect Storm: Opioid Risks
and “The Holy Trinity”
• Opioids, benzodiazepines, and carisoprodol have overlapping side effects
Drowsiness, respiratory depression (opioid), confusion, tremor, and seizures risk
• Combined, these drugs are synergistic in causing respiratory depression
Could collectively result in death
Opioid
Wolf AA, Fudin J. Pharmacy Times. September 24, 2014.
Benzodiazepine
Carisoprodol
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Non-Opioid
Drug-Drug Interactions
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Acetaminophen
• Metabolism Pediatrics: sulfation
Adults: glucuronidation
CYP2E1: conversion to N-acetyl-p-benzoquinone imine (NAPQI)
− Hepatotoxic metabolite
• Drug-drug interactions Avoid concomitant hepatotoxic therapies
Imatinib, dasatinib, and sunitinib inhibit glucuronidation− Max acetaminophen dose: 1,300 mg/day
Warfarin− Possibly: CYP2C9, NAPQI, and/or hepatoxicity
− Increased anticoagulant effect: INR
McGill MR, Jaeschke H. Pharm Res. 2013;30:2174-87.Zhang Q, et al. Eur J Clin Pharmacol. 2011;67:309-14.Sasu-Tenkoramaa J, Fudin J. Practical Pain Management. 2013;13:50-64.
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NSAIDs
• Bleeding
COX-1 vs COX-2
• Renally cleared
Lithium
− Which NSAIDs are safest?
Methotrexate
ACE inhibitors/diuretics
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Arachidonic acid
Prostaglandins Prostaglandins
COX-1 COX-2
Inhibit gastric acid secretion
GI mucus
Renal perfusion
Platelet activation
Pain, inflammation
NSAID NSAID
GI side effectsUlceration
Water retentionHyperkalemia
Interstitial nephritis
Anti-coagulation AnalgesiaAnti-inflammatory
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Skeletal Muscle Relaxants
• CNS depressants
• Tizanidine
CYP1A2 inhibitors – increased exposure
− Ciprofloxacin
− Birth control
− Verapamil
• Cyclobenzaprine
Cardiac toxicity
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Antidepressants
• SNRIs Duloxetine
− CYP2D6 and CYP1A2
Venlafaxine− CYP3A4
• SSRIs CYP2D6 Fluvoxamine
− CYP1A2
• Bupropion CYP2B6
• Tricyclic antidepressants Cardiotoxic medications Cyclobenzaprine
Medication CYP activity
Duloxetine 2D6 inhibitor (weak)
pGP inhibitor
Venlafaxine 2D6 inhibitor (weak)
Desvenlafaxine 2D6 inhibitor (weak)
Bupropion 2D6 inhibitor (strong)
Cyclobenzaprine vs Amitriptyline
https://pubchem.ncbi.nlm.nih.gov
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Case Assessment
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CASE: MK
• 69-year-old African American male
Chronic low back pain s/p laminectomy
• Current medications:
− Acetaminophen 1000 mg PO TID
− Methadone 5 mg PO QID
− Dabigatran 150 mg PO BID
− Metoprolol tartrate 50 mg PO BID
− Lisinopril 10 mg PO daily
− Atorvastatin 40 mg PO daily
• What drug-drug interactions are you concerned about?
− Docusate/senna 4 tabs PO QHS
− Celecoxib 100mg PO BID
− Omeprazole 20mg PO QAM
− Venlafaxine 100mg PO BID
− Metformin 500mg PO TID
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CASE: MK
• MK reports to the ED with complaints of productive cough x 1 week with bright green sputum
Diagnosed with community-acquiredpneumonia
• Which of the following drug or dugs do you want to avoid and why?
Amoxicillin/clavulanic acid
Cefdinir
Sulfamethoxazole/trimethoprim
Levofloxacin
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Conclusions
• Considering drug-drug interactions is key in selecting the safest and most efficacious therapies
• Understanding pharmacology is essential to appropriately identify drug-drug interactions
• Pharmacogenetic differences among patients can highly impact efficacy, drug interactions, and ability to tolerate medications
Dr D
References
• Fudin J, et al. Drug interactions. In Shapiro K, Brown SA, McNatty D. RxPrep Course Book. A Comprehensive Course for the NAPLEX and CPJE. 2014 ed.
• Fudin J, Pratt Cleary J, Gottwald J. A brief review of buprenorphine products. Pharmacy Times. Mar 22, 2016. www.pharmacytimes.com/contributor/jeffrey-fudin/2016/03/a-brief-review-of-buprenorphine-products
• Gerber JG, Rhodes RJ, Gal J. Stereoselective metabolism of methadone N-demethylation by cytochrome P4502B6 and 2C19. Chirality. 2004;16:36-44.
• Gong L, Stamer UM, Tzvetkov MV, Altman RB, Klein TE. PharmGKB summary: tramadol pathway. Pharmacogenet Genomics. 2014;24:374-80.
• Horn JR, Hansten PD. Get to know an enzyme: CYP2D6. Pharmacy Times. July 1, 2008. www.pharmacytimes.com/publications/issue/2008/2008-07/2008-07-8624
• Horn JR, Hansten PD. Get to know an enzyme: CYP3A4. Pharmacy Times. Sep 1, 2008. www.pharmacytimes.com/publications/issue/2008/2008-09/2008-09-8687
• Horn JR, Hansten PD. Drug interactions with CYP3A4: an update. Pharmacy Times. Dec 16, 2015. www.pharmacytimes.com/publications/issue/2015/december2015/drug-interactions-with-cyp3a4-an-update
• Horn JR, Hansten PD. Adverse outcomes in stabilized patients. Pharmacy Times. March 20, 2017. www.pharmacytimes.com/publications/issue/2017/march2017/adverse-outcomes-in-stabilized-patients
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References
• McGill MR, Jaeschke H. Metabolism and disposition of acetaminophen: recent advances in relation to hepatotoxicity and diagnosis. Pharm Res. 2013;30:2174-87.
• Naginewicz T, Archer K, Raouf M, Fudin J. Pharmacogenetics: medications do not have doses, people do. Pharmacy Times. Aug 24, 2017. www.pharmacytimes.com/contributor/jeffrey-fudin/2017/08/pharmacogenetics-medications-dont-have-doses-people-have-doses
• Pham TC, Fudin J, Raffa RB. Is levorphanol a better option than methadone? Pain Med. 2015;16:1673-9.
• Riddick DS. Drug biotransformation. In: H Kalant, W Roschlau (Ed), Principles of Medical Pharmacology, 6th ed, Oxford University Press: NY, 1997.
• Sasu-Tenkoramaa J, Fudin J. Drug interactions in cancer patients requiring concomitant chemotherapy and analgesics. Practical Pain Management. 2013;13:50-64.
• Smith HS. Opioid metabolism. Mayo Clin Proc. 2009;84:613-24.
• Wolf AA, Fudin J. The perfect storm: opioid risks and 'the holy trinity.' Pharmacy Times. Sep 24, 2014. www.pharmacytimes.com/contributor/jeffrey-fudin/2014/09/the-perfect-storm-opioid-risks-and-the-holy-trinity
• Zhang Q, Bal-dit-Sollier C, Drouet L, Simoneau G, Alvarez JC, Pruvot S, et al. Interaction between acetaminophen and warfarin in adults receiving long-term oral anticoagulants: a randomized controlled trial. Eur J Clin Pharmacol. 2011;67:309-14.
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PCSS-O Colleague Support
Program and Listserv
• PCSS-O Colleague Support Program is designed to offer general information to health professionals seeking guidance in their clinical practice in prescribing opioid medications.
• PCSS-O Mentors comprise a national network of trained providers with expertise in addiction medicine/psychiatry and pain management.
• Our mentoring approach allows every mentor/mentee relationship to be unique and catered to the specific needs of both parties.
• The mentoring program is available at no cost to providers.
• Listserv: A resource that provides an “Expert of the Month” who will answer questions about educational content that has been presented through PCSS-O project. To join email: [email protected].
For more information on requesting or becoming a mentor visit:
www.pcss-o.org/colleague-support
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PCSS-O is a collaborative effort led by American Academy of Addiction Psychiatry (AAAP) in
partnership with: Addiction Technology Transfer Center (ATTC), American Academy of Neurology
(AAN), American Academy of Pain Medicine (AAPM), American Academy of Pediatrics (AAP),
American College of Physicians (ACP), American Dental Association (ADA), American Medical
Association (AMA), American Osteopathic Academy of Addiction Medicine (AOAAM), American
Psychiatric Association (APA), American Society for Pain Management Nursing (ASPMN),
International Nurses Society on Addictions (IntNSA), and Southeast Consortium for Substance
Abuse Training (SECSAT).
For more information visit: www.pcss-o.org
For questions email: [email protected]
Twitter: @PCSSProjects
Funding for this initiative was made possible (in part) by Providers’ Clinical Support System for Opioid Therapies (grant no.
5H79TI025595) from SAMHSA. The views expressed in written conference materials or publications and by speakers and
moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention of trade
names, commercial practices, or organizations imply endorsement by the U.S. Government.
Dr D
50Please type your questions into the text chat box
Dr D