ADDITIONAL RESOURCES. Friday, September 14, Encore at Wynn Las Vegas, Nevada TABLE OF CONTENTS

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1 ADDITIONAL RESOURCES Friday, September 14, 2018 Encore at Wynn Las Vegas, Nevada TABLE OF CONTENTS Faculty Bios... 2 Pretest/Posttest Explanations Key References Generic Trade Name Identification Guide Tools for Shared Decision-Making This activity is supported by an educational grant from Lilly. For further information concerning Lilly grant funding, visit This symposium is independently organized and not an official part of The 11th Perspectives in Rheumatic Diseases conference.

2 FACULTY BIOS Daniel E. Furst, MD Professor of Rheumatology, University of Washington School of Medicine, Seattle, Washington University of Florence Medical School, Florence, Italy Carl Pearson Professor of Medicine, Professor Emeritus, David Geffen School of Medicine at UCLA, Director of Research, Arthritis Associates of Southern California, Los Angeles, California Daniel E. Furst, MD, is Professor of Medicine Emeritus in the Department of Medicine in the Division of Rheumatology at the David Geffen School of Medicine. He is also Adjunct Professor at the University of Washington School of Medicine in Seattle and Research Professor at the University of Florence in Italy. He has part-time practices at the Arthritis Associates of Southern California and the Seattle Rheumatology Associates in Seattle, Washington. Dr. Furst received his MD from Johns Hopkins University, where he also completed his internship and residency. He completed fellowships in Rheumatology at UCLA Medical Center and in Clinical Pharmacology at the University of California, San Francisco Medical Center. After serving as Assistant Professor of Medicine/Rheumatology at the UCLA Medical Center and as Associate Professor of Internal Medicine/Rheumatology at the University of Iowa Carver College of Medicine, he became Clinical Professor in the Department of Medicine in the Division of Rheumatology and Connective Tissue Research at the University of Medicine and Dentistry of New Jersey. He later served as Director of Clinical Research Programs and the Arthritis Clinical Research Unit at the Virginia Mason Medical Center in Seattle. He has served on a number of national committees and was a Fellow in the American College of Rheumatology and the American Society of Clinical Pharmacology & Therapeutics. He has also been a member of the Arthritis Advisory Committee for the US Food and Drug Administration. He has served on the editorial boards of Inpharma, Clinical Drug Investigation, Drugs, the Journal of Clinical Rheumatology, and The Journal of Rheumatology. Additionally, he is an editorial reviewer for professional publications including Arthritis & Rheumatism, The New England Journal of Medicine, the Journal of Clinical Investigation, Pharmacotherapy, and the Annals of the Rheumatic Diseases. His research interests include the clinical pharmacology of antirheumatic drugs and biologics and the pathophysiology and treatment of systemic sclerosis. Disclosure: Daniel E. Furst, MD: grant/research support from AbbVie, Actelion, Amgen, BMS Corbus, NIH, Novartis, Pfizer, Roche/Genentech; consultant for AbbVie, Actelion, Amgen, BMS, Cytori, Novartis, Pfizer, Roche/Genentech; and on the speakers bureau of CMC Connect, (McCann Health Company) Linda L. Grinnell-Merrick, MS, NP-BC Nurse Practitioner, Division of Allergy, Immunology, and Rheumatology University of Rochester Medical Center Rochester, New York Linda L. Grinnell-Merrick, MS, NP-BC, is a nurse practitioner in the Division of Allergy, Immunology, and Rheumatology at the University of Rochester Medical Center in New York. She received her Bachelor of Science in Nursing and her Master of Science in Nursing degrees from the University of Rochester. Ms. Grinnell-Merrick is a board-certified Adult Nurse Practitioner. Ms. Grinnell-Merrick is the current president of the Rheumatology Nurses Society and member of the American College of Rheumatology. She has lectured regionally and nationally in the field of rheumatology. She has been a nurse for more than 30 years, working on medical surgical units, hemodialysis, peritoneal dialysis, and solid organ transplantation before finding her home in Rheumatology. Disclosure: Linda Grinnell-Merrick, MS, NP-BC: advisory board for AbbVie, Novartis, Pfizer, Horizon; contracted research for Novartis; and on the speakers bureau for AbbVie, Celgene, Novartis and Janssen 2

3 PRETEST/POSTTEST EXPLANATIONS Question 1 Psoriatic arthritis may be associated with specific musculoskeletal and cutaneous features, such as synovitis, pustulosis, acne, hyperostosis, osteitis syndrome, and other features. Which of the following clinical manifestations is less likely to be a manifestation of psoriatic arthritis? 1. Dactylitis 2. Enthesitis 3. Grinding or clicking during movement 4. Peripheral edema 5. Psoriatic onycho-pachydermo periostitis Correct Answer: 3. Explanation: Grinding or clicking during movement is specific to osteoarthritis. Dactylitis or sausage digit is the complete swelling of a single digit in the hand or foot and occurs in 30-40% of patients during the course of the disease. Enthesitis refers to the inflammatory lesions at the insertion of tendon into bone. Symptomatic enthesitis occurs in 20-40% of patients with psoriatic arthritis. Peripheral edema is frequently asymmetric, preferentially affects the lower limbs, can occur anytime during the course of the disease, and is thought to be associated with extensor tenosynovitis. Local enthesitis with the edema is found along the course of the involved tendon. This type of edema is usually responsive to oral corticosteroids. SAPHO syndrome of synovitis, acne, pustulosis, hyperostosis, and osteitis is an uncommon but recognized subgroup of psoriatic arthritis. Clinically, less than 3% of patients with psoriatic arthritis are found to have SAPHO at initial evaluation but at least 67% of all patients with SAPHO syndrome have psoriasis vulgaris or palmoplantar pustulosis. Psoriatic onycho-pachydermo-periostitis is a rare manifestation that refers to severe involvement of one or more terminal phalanges with associated severe nail dystrophy, soft tissue swelling, and marked periosteal reaction of the distal phalanx, which can be seen on radiographs. Goupile P, Laulan J, Védère V, et al. Psoriatic onycho-periostitis. Report of three cases. Scand J Rheumatol, 1995;24(1): Hayem G, Bouchaud-Chabot A, Benali K, et al. SAPHO syndrome: a long-term follow up study of 120 cases. Semin Arthritis Rheum, 1999;29: Scarpa R. Peripheral enthesopathies in psoriatic arthritis. J Rheumatol. 1998; 25: Veale D, Rodgers S, Fitzgerald O. Classification of clinical subsets in psoriatic arthritis. Br J Rheumatol. 1994;33:

4 PRETEST/POSTTEST EXPLANATIONS (CONT.) Question 2 Current FDA-approved biologic therapies for PsA are 1. Five TNFi (adalimumab, certolizumab, etanercept, golimumab, infliximab), one IL12/23i (ustekinumab), one CTLA4 fusion protein (abatacept), one PDE4i (apremilast), and two IL-17i (ixekizumab, secukinumab). 2. Five TNFi (adalimumab, certolizumab, etanercept, golimumab, infliximab), one IL12/23i (ustekinumab), one PDE4i (apremilast), and one IL-17i (secukinumab). 3. Four TNFi (adalimumab, certolizumab, etanercept, infliximab), one IL12/23i (ustekinumab), one CTLA4 fusion protein (abatacept), one PDE4i (apremilast), and one IL-17i (secukinumab). 4. Five TNFi (adalimumab, certolizumab etanercept, golimumab, infliximab), one IL12/23i (ustekinumab), one CTLA4 fusion protein (abatacept), one PDE4i (apremilast), and one IL-17i (secukinumab). Correct Answer: 1. Explanation: Currently nine biologic disease-modifying antirheumatic drugs (DMARDs) and one Jak2/3i (tofacitinib, a synthetic small molecule) have been approved. An IL-17i (ixekizumab) has recently been approved for psoriatic arthritis in addition to psoriasis; secukinumab was the first IL-17i approved for psoriatic arthritis and psoriasis. An additional IL-17i (brodalumab) has been approved for psoriasis; however, its use has been limited due to concerns about an increased risk of suicide in patients who have used this drug. An IL23i (guselkumab) has also been approved for psoriasis but is not yet approved for psoriatic arthritis. Latest FDA approvals and indications may be found at 4

5 PRETEST/POSTTEST EXPLANATIONS (CONT.) Question 3 Out of those approved for psoriatic arthritis, which biologic DMARD is least effective in psoriasis? Choose from the list below. 1. Adalimumab 2. Golimumab 3. Infliximab 4. Secukinumab 5. Ustekinumab Correct Answer: 2. Explanation: Three TNFi are approved for psoriasis adalimumab, infliximab, and etanercept. Golimumab (subcutaneous and IV) is approved only for PsA due to poor skin response in trials. Efficacy of golimumab for psoriasis is PASI-75 in 40% at week 14. Ustekinumab trials show great response in psoriasis, and the same is true for secukinumab, adalimumab, and infliximab, which are FDA approved for psoriasis. Menter A, Korman NJ, Elmets CA,et al; American Academy of Dermatology Work Group. Guidelines of care for the treatment of psoriasis and psoriatic arthritis:case-based presentations and evidence-based conclusions. J Am Acad Dermatol Jul;65(1):

6 PRETEST/POSTTEST EXPLANATIONS (CONT.) Question 4 Which of the following dialogues best represents shared decision-making in medicine? 1. Clinician: This drug can clear your PsA in 4 months; therefore, I m going to prescribe it for you. Patient: Okay. 2. Clinician: What have you heard about oral medicines to treat PsA? Patient: I heard drug X is great. My cousin uses it and loves it. I will have drug X. Clinician: Okay. This is one of the recommended drugs. I m writing the prescription. 3. Clinician: Mr. Jones, because most people are afraid of injections, I m going to assume you are the same way. So why don t we do this oral drug? Patient: Okay. 4. Clinician: Based on the studies, this oral medication typically clears PsA in 25% of patients after 4 months, but it can cause an upset stomach in 2% of the patients. I would recommend this medication, because your PsA is similar to those who have responded to the medicine from our experience. What are your thoughts? Patient: I already have issues with an upset stomach. Can you tell me more about that side effect of the drug? Clinician: I m happy to talk about that in more detail. Correct Answer: 4. Explanation: Both the provider and patient actively participate in shared decision-making. The provider shares facts about treatment, benefits, harms, convenience, and costs. The patient shares values and preferences about treatment attributes. A decision is mutually agreed upon. In this question, D is the best choice, because the clinician is sharing benefits and harms about an oral medication and asks the patient about his/her preferences. The patient expresses his concerns, and the dialogue continues. Elwyn G, Frosch D, Thomson R, et al. Shared decision making: a model for clinical practice. J Gen Intern Med. 2012;27(10): ;27(10):

7 PRETEST/POSTTEST EXPLANATIONS (CONT.) Question 5 What are the essential elements of patient-provider shared decision making? 1. Benefit talk, harms talk, cost talk 2. Choice talk, option talk, decision talk 3. Cognition talk, adherence talk, assessment talk 4. Value talk, preference talk, cost talk Correct Answer: 2. Explanation: The essential elements of shared decision-making are choice talk, option talk, and decision talk or COD. Choice talk refers to ensuring that patients know that reasonable options are available. Option talk is having clinicians provide more detailed information about options, including their benefits, harms, convenience, and cost. Decision talk refers to consideration of patient preferences and deciding what is best through interactive communication between the clinician and the patient. Elwyn G, Frosch D, Thomson R, et al. Shared decision making: a model for clinical practice. J Gen Intern Med. 2012;27(10):

8 KEY REFERENCES EULAR Recommendations for CVD Risk Management in Pts With RA and Other Joint Disorders: 2015/2016 Update Overarching Principles a. Clinicians should be aware of the higher risk for CVD in patients with RA compared with the general population; this may also apply to AS and PsA b. The rheumatologist is responsible for CVD risk management in patients with RA and IJD c. The use of NSAIDs and corticosteroids should be in accordance with treatment-specific recommendations from EULAR and ASAS Recommendations Level of evidence Strength of recommendation 1 Disease activity should be controlled optimally in order to lower CVD risk in all patients with RA, AS, or PsA 2b-3 B 9.1 (1.3) CVD risk assessment is recommended for all patients with RA, AS, or PsA at least once every 5 years and should be reconsidered following major changes in antirheumatic therapy CVD risk estimation for patients with RA, AS, or PsA should be preformed according to national guidelines and the SCORE CVD risk prediction model should be used if no national guideline is available TC and HDLc should be used in CVD risk assessment in RA, AS, and lipids should ideally be measured when disease activity is stable or in remission. Non-fasting lipids measurements are also perfectly acceptable Bottom Line: Be Aware do your best to communicate and recommend pt F/U with their other doctors (document) EULAR=European League Against Rheumatism. CVD=cardiovascular disease. Pts=patients. RA=rheumatoid arthritis. AS=ankylosing spondylitis. PsA=psoriatic arthritis. IJD=inflammatory joint diseases. NSAIDs=nonsteroidal antiinflammatory drugs. ASAS=assessment in ankylosing spondylitis. Agca R, et al. Ann Rheum Dis. 2017;76: Level of agreement (SD) 3-4 C 8.8 (1.1) 3-4 C-D 8.7 (2.1) 3 C 8.8 (1.2) 5 CVD risk prediction models should be adapted for patients with RA by a 1.5 multiplication factor, if this is not already included in the model 3-4 C 7.5 (2.2) 6 Screening for asymptomatic atherosclerotic plaques by use of carotid ultrasound may be considered as part of the CVD risk evaluation in patients with RA 3-4 C-D 5.7 (3.9) 7 Lifestyle recommendations should emphasize the benefits of a healthy diet, regular exercise, and smoking cessation for all patients 3 C 9.8 (0.3) 8 CVD risk management should be carried out according to national guidelines in RA, AS or PsA, antihypertensives and statins may be used as in the general population 3-4 C-D 9.2 (1.3) 9 Prescription of NSAIDs in RA and PsA should be with caution, especially for patients with documented CVD or in the presence of CVD risk factors 2a-3 C 8.9 (2.1) 10 Corticosteroids: for prolonged treatment, the glucocorticoid dosage should be kept to a minimum and a glucocorticoid taper should be attempted in case of remission or low disease activity; the reasons to continue glucocorticoid therapy should be regularly checked 3-4 C 9.5 (0.7) 12 Agca R, Heslinga SC, Rollefstad S, et al. EULAR recommendations for cardiovascular disease risk management in patients with rheumatoid arthritis and other forms of inflammatory joint disorders: 2015/2016 update. Ann Rheum Dis. 2017;76(1): Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA): Treatment Guidelines for PsA on the Basis of Severity Peripheral arthritis Skin and nail disease Axial disease Dactylitis Enthesitis Mild NSAID IA STEROIDS TOPICALS PUVA/UVB DMARD NSAID PHYSIO ANALGESIA NSAID INJECTION NSAIDS PHYSIO STEROIDS Moderate to severe DMARDs BIOLOGICS DMARDs BIOLOGICS (ANTI-TNF) DMARDs BIOLOGICS BIOLOGICS BIOLOGICS BIOLOGICS Reassess response to therapy and toxicity if patient fails to demonstrate an acceptable clinical improvement over an appropriate period Kavanaugh A, et al. J Rheumatol. 2006;33: Kavanaugh AF, Ritchlin CT. Systematic review of treatments for psoriatic arthritis: an evidence based approach and basis for treatment guidelines. J Rheumatol. 2006;33(7): Coates LC, Gossec L, Ramiro S, et al. New GRAPPA and EULAR recommendations for the management of psoriatic arthritis. Rheumatology (Oxford). 2017;56(8):

9 KEY REFERENCES (CONT.) Treat to Target: Algorithm to Treat SpA to Target Active SpA* Main target Adapt therapy according to disease activity Remission Adapt therapy if state is lost Sustained Remission Use measures of clinical disease activity and acute phase reactants as needed Use measures of clinical disease activity and acute phase reactants as needed Alternative target Adapt therapy according to disease activity Low disease activity Adapt therapy if state is lost Low disease activity *Axial spondyloarthritis, peripheral spondyloarthritis, or psoriatic arthritis. Coates LC, et al. Arthritis Rheumatol. 2016;68: Coates LC, Helliwell PS. Treating to target in psoriatic arthritis: how to implement in clinical practice. Ann Rheum Dis. 2016;75(4):

10 GENERIC/TRADE NAME IDENTIFICATION GUIDE Generic Name Abatacept Acitretin Adalimumab Apremilast Calcipotriene cream Certolizumab Clobetasol Cyclosporine A Etanercept Golimumab Ibuprofen Infliximab Interferon/ribavirin (INF-RBV) Ixekizumab Leflunomide Levothyroxine Losartan Metformin Methotrexate Naproxen sodium Secukinumab Sulfasalazine Tofacitinib Triamcinolone Ustekinumab Trade Name ORENCIA SORIATANE HUMIRA Otezla Dovonex, Sorilux, Calcitrene CIMZIA CLOBEX, Cormax, Olux, Embeline, Clobevate Neoral, Gengraf, Sandimmune ENBREL SIMPONI, Simponi SIMPONI ARIA MOTRIN, Advil REMICADE Rebetron Taltz Arava Synthroid, Tirosint, Levoxyl, UNITHROID, Levo-T Cozaar GLUMETZA, Glucophage, FORTAMET, Riomet, Glucophage XR Rheumatrex, Trexall, Rasuvo, Otrexup Aleve, Anaprox, Naprelan, Naprosyn COSENTYX Azulfidine XELJANZ Kenalog, Triamcinolone Acetonide in Absorbase, Trianex, Triderm, ZILRETTA STELARA 10

11 TOOLS FOR SHARED DECISION-MAKING SHARE Approach, Agency for Healthcare Research and Quality (AHRQ) Psoriasis Treatment Decision Aid 11