Additional Resources

Atul A. Deodhar, MD, MRCP, FACR, FACP, is Professor of Medicine and Medical Director of Rheumatology Clinics in the Division of Arthritis & Rheumatic Diseases at Oregon Health & Science University in Portland. He is board-certified in Internal Medicine and Rheumatology and is a Fellow of the American College of Rheumatology (ACR) and the American College of Physicians.

Dr. Deodhar is Past Chair of SPARTAN, an organization of North American rheumatologists dedicated to education and research in the field of axial spondyloarthritis. He also serves on the ACR treatment guidelines subcommittee and is Associate Editor for the Advanced Rheumatology Course by the Association of Rheumatology Professionals (ARP). He has served the ACR in various other capacities,including as Vice Chair of the annual meeting planning committee, a member of the peripheral MRI task force and the nominating committee, and a developer of the ARP online Advanced Rheumatology Course. Dr. Deodhar serves on the Rheumatology Board for the American Board of Internal Medicine.

Dr. Deodhar is a reviewer for Arthritis & Rheumatology, Annals of the Rheumatic Diseases, and Annals of Internal Medicine, among several other journals. His research interests are axial spondyloarthritis and psoriatic arthritis. Dr. Deodhar has authored three books, more than 150 peer-reviewed articles, and several book chapters and editorials. He has been a guest editor for Best Practice & Research: Clinical Rheumatology and Current Opinion in Rheumatology. He has been a principal or co-investigator in more than 100 clinical trials, mostly focused on therapies for ankylosing spondylitis, psoriatic arthritis, and rheumatoid arthritis.

Dr. Deodhar completed a fellowship in Rheumatology at Oregon Health & Science University and a research fellowship in Rheumatology at the Royal Cornwall Hospital in Truro, United Kingdom. He completed a residency in Internal Medicine and Geriatrics at the Royal Cornwall Hospital as well as at Sassoon General Hospital and King Edward Memorial Hospital in Pune, India. He received his medical degree from the University of Pune and is a Master of the Royal College of Physi-cians in London, United Kingdom.

Atul A. Deodhar, MD, MRCP, FACR, FACpProfessor of Medicine,Medical Director of Rheumatology Clinics,Division of Arthritis & Rheumatic DiseasesOregon Health & Science UniversityPortland, Oregon

Faculty

Joseph F. Merola, MD, MMSc, is Associate Professor at Harvard Medical School in Boston, Massachusetts. He also serves as Vice Chair of Clinical Trials and Innovation in Dermatology, Director of the Center for Skin and Related Musculoskeletal Diseases, Director of the Clinical Unit for Research Innovation and Trials (CUReIT) in Dermatology in the Departments of Dermatology and Medicine in the Division of Rheumatology at Brigham and Women’s Hos-pital in Boston. Dr. Merola earned his medical degree at the New York University School of Medicine in New York, New York, followed by his Master of Medical Sciences degree at Harvard Medical School. He completed an intern-ship in Internal Medicine at the Hospital of the University of Pennsylvania in Philadelphia, followed by a residency in Dermatology at New York University Medical Center. Dr. Merola continued with a residency in Internal Medicine and a fellowship in Rheumatology at Brigham and Women’s Hospital. He is board-certified in Dermatology, Internal Medicine, and Rheumatology.

Dr. Merola is a member of the medical board of the National Psoriasis Foundation, the board of the International Dermatology Outcome Measures Group, the Executive Committee for GRAPPA (Group for Research and Assess-ment of Psoriasis and Psoriatic Arthritis), and the board of the Lupus Foundation of America. He is also a board member and Founding President of the Psoriasis and Psoriatic Arthritis Clinics Multicenter Advancement Network Consortium (PPACMAN).

Joseph Merola, MD, MMScAssociate Professor, Harvard Medical School Vice Chair of Clinical Trials and Innovation, Dermatology Director, Center for Skin and Related Musculoskeletal Diseases Director, Clinical Unit for Research Innovation and Trials (CUReIT), DermatologyDepartments of Dermatology and Medicine Division of Rheumatology Brigham and Women’s Hospital Boston, Massachusetts

Faculty

Sheetal Desai, MD, MSEd, received her medical degree from the Keck School of Medicine of USC and completed a residency in Internal Medicine and a fellowship in Rheumatology at the University of California, Los Angeles. She has a master’s degree in Medical Education from the USC Rossier School of Education. She has served as a rheumatologist at the University of California, Irvine (UCI) for the past 11 years and focuses on medical education, lupus, scleroderma, and myositis. Dr. Desai also serves as the Director of the Lupus Clinic, Rheumatology Fellowship Program Director, and Chair of the Division of Rheumatology at UCI.

Sheetal Desai, MD, MSEdChief of Rheumatology, Rheumatology Fellowship Program Director,Director, Lupus ClinicAssociate Clinical Professor of Medicine,Division of RheumatologyUniversity of California, IrvineIrvine, California

Faculty

Posttest With Explanations

Question 1. The centrality of IL-23 and IL-17A to PsA pathogenesis has resulted in many new biologic therapies targeting these cytokines. Which drug inhibits the interaction of IL-17A with the IL-17 receptor?

A. AdalimumabB. ApremilastC. IxekizumabD. TofacitinibE. Ustekinumab

Correct Answer: C. Ixekizumab

Explanation:

Ixekizumab inhibits the interactions of IL-17A with the IL-17 receptor. Ustekinumab is a monoclonal antibody that inhibits the p40 subunit common to IL-12 and IL-23, thereby decreasing the activities of both the Th1 and Th17 pathways. Adalimumab binds to TNF,α inhibiting activation of the TNF receptor. Apremilast inhibits PDE4, preventing the degradation of cyclic adenosine monophosphate (cAMP). Tofacitinib, the first approved JAK inhibitor, is relatively selective for JAK3, but may also inhibit JAK1, JAK2, and TYK2.

• Blauvelt A, Chiricozzi A. The immunologic role of IL-17 in psoriasis and psoriatic arthritis pathogenesis. Clin Rev Allergy Immunol. 2018;55(3):379-390.

• Fragoulis GE, McInnes IB, Siebert S. JAK-inhibitors. New players in the field of immune-mediated diseases, beyond rheuma-toid arthritis. Rheumatology (Oxford). 2019;58:i43-i54.

• Mease PJ, Gladman DD, Ritchlin CT, et al. Adalimumab for the treatment of patients with moderately to severely active psori-atic arthritis: Results of a double-blind, randomized, placebo-controlled trial. Arthritis Rheum. 2005;52(10):3279-3289.

• Zerilli, T., & Ocheretyaner, E. (2015). Apremilast (Otezla): a new oral treatment for adults with psoriasis and psoriatic arthritis. P T. 2015; 40(8), 495–500.

Posttest With Explanations

Question 2.Enthesitis is an early manifestation of PsA that is associated with increased disease activity and reduced quality of life. Which cytokine is thought to activate T cells within the entheses promoting inflammation, osteogenesis, and bone loss and remodeling?

A. TNF-αα

B. IL-12

C. IL-17

D. IL-22

E. IL-23

Correct Answer: E. IL-23

Explanation:

Thus far, two lymphocyte populations have been defined at the human enthesis. Innate lymphoid cells are part of the IL-23-responsive T cells which are residents of the healthy enthesis. Gamma delta T cells are also resident at the enthesis. The activation of resident T cells within the enthesis by IL-23 may promote inflammation, osteogenesis, and bone loss and remodeling. These lymphocyte populations may release different cytokines including IL-17 and IL-22 and TNF-α.

• Watad A, Cuthbert RJ, Amital H, McGonagle D. Enthesitis: much more than focal insertion point inflammation. Curr Rheumatol Rep. 2018;20(7):41.

Question 3. In PsA pathogenesis, activated macrophages secrete TNF-α which activate fibroblast-like synoviocytes (FLS) and upregulate the surface expression of RANKL thus initiating downstream signaling that mediates osteoclastogenesis. In addition to this immune inflammation cascade, which answer choice best describes the pathophysiology underlying bone erosion in PsA?

A. Activated Th17 cells secrete IL-17 promoting the expression of receptor activator of NF-κβ (RANKL) on osteoblasts and then

activates RANK signaling in osteoclasts leading to osteoclastogenesis

B. Activated Th2 cells secrete inflammatory cytokines IL-4, IL-13, IL-5, and IL-31

C. Activated macrophages release IL-6 which activates Th17 cells initiating downstream signaling that

mediates osteoclastogenesis

D. A and C

E. B and C

Correct answer: D. A and C

Explanation:

Both A and C describe processes leading to bone erosion in PsA. Activated Th17 cells secrete IL-17 promoting the expression of receptor activator of NF-κβ (RANKL) on osteoblasts and then activates RANK signaling in osteoclasts leading to osteoclastogenesis. Activated macrophages release IL-6 which activates Th17 cells initiating downstream signaling that mediates osteoclastogenesis.

• Merola JF, Espinoza LR, Fleischmann R. Distinguishing rheumatoid arthritis from psoriatic arthritis. RMD Open. 2018;4(2):e000656.

• Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM. Mechanisms of TNF-alpha- and RANKL-mediated osteoclastogen-esis and bone resorption in psoriatic arthritis. J Clin Invest. 2003;111(6):821-831.

• Robert M, Miossec, P. IL-17 in rheumatoid arthritis and precision medicine: from synovitis expression to circulating bioactive levels. Frontiers in Medicine. 2019;5:364.

Posttest With Explanations

Question 4. A 35-year-old man with history of hypertension and obesity presents with complaints of pain and swelling of fingers for the past 4 months. He smokes half-a-pack a day, and has recently started exercising to lose weight. He feels well but on review of systems he says that he has noticed anterior chest wall discomfort during a workout, which he attributes to heavy lifting. On physical examination, his BMI is 35 kg/m2, BP is 150/96, pulse is 88/mt, regular. Anterior chest wall is tender, he has dactylitis of left fourth finger, has nail pitting, and has psoriasis in scalp and umbilicus. You diagnose him with psoriatic arthritis, and send him for hand X-ray, and lab tests (CBC, CMP, CRP). What is the next best step to address his chest discomfort?

A. Prescribe NSAIDs for costochondritis

B. Prescribe diclofenac cream for application on chest wall

C. Refer him to cardiology for stress test

D. Order chest x-ray

E. Order an ECG

Correct Answer: C. Refer him to cardiology for stress test

Explanation:

While a diagnosis of costochondritis is reasonable given reproducible chest pain on examination, evaluation for possible cardiac etiologies is most appropriate in this setting. Patients with PsA have been shown to have an increased risk of cardiovascular morbidity when compared with the general population and this risk is greater than expected when predicted by Framingham Risk Scoring. A chest X-ray will not show the etiology of his chest pain, and a resting ECG is likely to be normal in a patient with angina pectoris.

• Husni ME. Comorbidities in psoriatic arthritis. Rheum Dis Clin North Am. 2015;41(4):677-698. • Ogdie A, Schwartzman S, Husni ME. Curr Opin Rheumatol. Recognizing and managing comorbidities in psoriatic arthritis.

2015;27(2):118-126.

Posttest With Explanations

Question 5. A 28-year-old woman with known PsA for 3 years presents with left second and third toe dactylitis with mild tendonitis on the right Achilles tendon. She has been on adalimumab for the past year. She has a history of severe depression and suicidal thoughts, which required hospitalization 4 years ago. Additionally, she has gastroesophageal reflux disease with a history of a peptic ulcer at 26 years of age. More recently, she had unexplained abdominal pain, and a colonoscopy showed patch erythema and aphthous ulcers in the ileum, consistent with Crohn’s disease. She had a recent bout of uveitis 3 weeks ago, which was treated with steroid eye drops. She has no history of back pain. The patient and her husband would like to start family within the next year. The adalimumab is discontinued for lack of efficacy. Which would be the next best medication for this patient?

A. Apremilast

B. Diclofenac

C. Methotrexate

D. Secukinumab

E. Ustekinumab

Correct answer: E. Ustekinumab

Explanation:

With a history of severe depression and suicidal thoughts, apremilast is not a suitable drug for her. Peptic ulcer and desire to be pregnant makes diclofenac and methotrexate contraindicated. Recent history of active Crohn’s disease is a contraindication for starting secukinumab. Ustekinumab is category risk B for pregnancy and is the right choice.

• Secukinumab prescribing information • Ustekinumab prescribing information

Posttest With Explanations

Question 6. 26-year-old man with psoriasis is recently diagnosed with PsA. He has only peripheral disease and no axial disease, but he has enthesitis, which causes limping and interferes with daily activities. What is the best initial treatment for this patient?

A. Combination methotrexate and TNF inhibitor

B. Methotrexate

C. Sulfasalazine

D. TNF inhibitor

Correct answer: D. TNF inhibitor

Explanation:

According to the GRAPPA recommendations, TNF inhibitors are the first-line therapy for enthesitis-related PsA. There are no data to support initial treatment for PsA using a combination of methotrexate and TNF inhibitor. This combination should be considered if the patient needs step up treatment for his arthritis in the future.

• Coates LC, Kavanaugh A, Mease PJ, et al. Group for Research and Assessment of Psoriasis and Psoriatic Arthritis recommen-dations for psoriatic arthritis. Arthritis Rheumatol. 2016;68 (5):1060-1071.

Posttest With Explanations

Question 7. Patient-provider shared decision making about treatment is most accurately defined as:

A. Collaborative process in which a patient and a clinician make a treatment decision together by integrating evidence and patient

preferences and values

B. Education of a patient by a clinician about the disease and treatment options

C. Communication between the patient and the provider where a decision aid is used

D. Informed consent, where a patient gives permission to a clinician for treatment with full knowledge of the possible risks

and benefits

E. Multi-step process involving the patient, health care team, and caregiver to implement evidence-based care

Correct answer: A. Collaborative process in which a patient and a clinician make a treatment decision together by integrating evidence and patient preferences and values

Explanation:

“ Instead of assuming that decisions should be guided by scientific consensus about effectiveness, shared decision making proposes that informed preferences—by which is meant what matters to patients and families—should play a major role in decision making processes. Shared decision making is more than being attentive to patients’ needs or concerns: it represents an important shift in the roles of both patients and clinicians” (Elwyn G, et al, 2017). It goes beyond the minimal requirement of providing informed consent, which is simply educating the patient about risks, benefits, and alternatives. Sharing decisions means moving away from the view that “doctor knows best” to decisions informed by the best available evidence and considerations for how recommendations might align with what matters to patients.

• Elwyn G, Durand MA, Song J, et al. A three-talk model for shared decision making: multistage consultation process. BMJ. 2017;359: j4891.

• Elwyn G, Frosch D, Thomson R, et al. Shared decision making: a model for clinical practice. J Gen Intern Med. 2012;27(10):1361-1367.

Posttest With Explanations

FDA-Approved Biologic and New Small Molecule Targeted Therapies for Psoriatic Arthritis and Psoriasis

Approved Medication Approved for PsA Approved for Psoriasis

TNFi

Adalimumab Yes Yes

Certolizumab Yes Yes

Etanercept Yes Yes

Golimumab Yes

Infliximab Yes Yes

PDE4i

Apremilast, small molecule Yes Yes

IL-12/23i

Ustekinumab Yes Yes

IL-17i

Ixekizumab Yes Yes

Secukinumab Yes Yes

Brodalumab Yes

CTLA4

Abatacept Yes

JAK 2/3i

Tofacitinib, small molecule Yes

IL-23i

Guselkumab Yes

Tildrakizumab Yes

Risankizumab Yes

HoloLens Experience: Legend

Dendritic cell

IL-12

Th1 cell

IL-12

TNF-α

Macrophage

RANKL

Fiberblast-like synoviocyte

Osteoclast precursors

Osteoclast

IL-23/IL-17 Inflammatory Pathway

Adalimumab Ixekizumab Ustekinumab Apremilast

Joint Cross Section Tofacitinib

IL-12 Inflammatory Pathway

Adalimumab

TNF-α

TNF-α receptor

Ixekizumab

IL-17AFIL-17AA

IL-17RC receptor

IL-17RA receptor

Ustekinumab

Receptor

IL-12 p40 subunit

IL-23

Apremilast

cAMP

PDE4

JAK1TYK2

JAK2JAK3

Tofacitinib

Cytokine

STAT

Bone

Normal Late PsA

Enthesis

Synovial membrane

Synovial fluid

Receptors

IL-23

Th17 cell

IL-17 RANKL

Osteoblast Osteoblast precursors

Dendritic cell

TNF-α

Psoriatic Arthritis

Coates LC, et al. Arthritis Rheumatol. 2016;68(5):1060-1071. 1

NSAI

Ds a

nd IA

cor

ticos

tero

ids

as in

dica

ted

Asse

ss A

ctiv

ity, I

mpa

ct, a

nd P

rogn

ostic

Fac

tors

DMARDs (MTX, SSZ, LEF),

TNFi or PDE4i

Biologics (TNFi, IL12/23i, IL17i)

or PDE4i

Switch biologic (TNFi, IL12/23i,

or IL17i)

Phys

ioth

erap

y an

d NS

AIDs NSAIDs

only

TNFi, IL17i,or IL12/23i*

Switch biologic (TNFi, IL17i,or IL12/23i*)

No direct evidence for therapies in axial PsA;

recommendations based on axial SpA literature

Phys

ioth

erap

y

NSAIDs

Biologics (TNFi, IL12/23i, IL17i)

or PDE4i

Switch biologic (TNFi, IL12/23i, IL17i) or PDE4i

CS injections: consider on an individual basis due to potential for

serious side effects; no clear evidence for efficacy

Corti

cost

eroi

d In

ject

ions

as

indi

cate

d NSAIDs

DMARDs (MTX, LEF, SSZ)

or PDE4i

Biologics (TNFi, IL12/23i)

Switch biologic (TNFi, IL12/23i, IL17i) or PDE4i

Topi

cals

as

indi

cate

d

Topicals (keratolytics, steroids, vitamin D

analogues, emollients,

calcineurin i)

Phototherapy or DMARDs (MTX, CSA, acitretin, fumaric acid

esters) or PDE4i

Biologics (TNFi, IL12/23i, IL17i)

or PDE4i

Switch biologics (TNFi, IL12/23i, IL17i) or PDE4i

Topical or procedural or DMARDs (CSA, LEF,

MTX, acitretin)

Switch biologics (TNFi, IL12/23i, IL17i) or PDE4i

Consider previous therapy, patient choice, other disease involvement, and comorbidities. Choice of therapy should address as many domains as possible. Treat, periodically re-evaluate, and modify therapy as required.

Biologics (TNFi,

IL12/23i,IL17i)

or PDE4i

Standard therapeutic route Expedited therapeutic routeBlue text identifies conditional recommendations for drugs that do not currently have regulatory approvals or for which recommendations are based on abstract data only. GRAPPA=Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. NSAIDs=nonsteroidal anti-inflammatory drugs. IA=intra-articular. DMARDs=disease-modifying antirheumatic drugs. MTX=methotrexate. SSZ=sulfasalazine. LEF=leflunomide. TNFi=tumor necrosis factor inhibitor. PDE-4i=phosphodiesterase 4 inhibitor (apremilast). IL=interleukin. SpA=spondyloarthritis. CS=corticosteroid. CSA=cyclosporin A. IL-12/23i=interleukin-12/23 inhibitor.

Which Domains Are Involved?

Peripheral Arthritis Axial Disease Enthesitis Skin Nails

Key:

Dactylitis

References

Azfar RS, Gelfand JM. Psoriasis and metabolic disease: epidemiology and pathophysiology. Curr Opin Rheumatol. 2008;20(4):416-422.

Blauvelt A, Chiricozzi A. The immunologic role of IL-17 in psoriasis and psoriatic arthritis pathogenesis. Clin Rev Allergy Immunol. 2018;55(3):379-390.

Charles C, Gafni A, Whelan T. Shared decision-making in the medical encounter: what does it mean? (or it takes at least two to tango). Soc Sci Med.1997;44(5):681-692.

Coates LC, Kavanaugh A, Mease PJ, et al. Group for Research and Assessment of Psoriasis and Psoriatic Arthritis recom-mendations for psoriatic arthritis. Arthritis Rheumatol. 2016;68 (5):1060-1071.

Cosentyx (secukinukab) [package insert]. East Hanover, NJ: Novartis; 2015.

Cutolo M, Myerson GE, Fleischmann RM, et al. A phase III, randomized, controlled trial of apremilast in patients with psori-atic arthritis: results of the PALACE 2 Trial. J Rheumatol. 2016;43(9):1724-1734.

Deodhar A, Gottlieb AB, Boehncke WH, et al. (2018). Efficacy and safety of guselkumab in patients with active psoriatic arthritis: a randomised, double-blind, placebo-controlled, phase 2 study. Lancet. 2018;391 (10136), 2213–2224.

Edwards CJ, Blanco FJ, Crowley J, et al. Apremilast, an oral phosphodiesterase 4 inhibitor, in patients with psoriatic arthritis and current skin involvement: a phase III, randomised, controlled trial (PALACE 3). Ann Rheum Dis. 2016;75(6):1065-1073.

Elwyn G, Durand MA, Song J, et al. A three-talk model for shared decision making: multistage consultation process. BMJ. 2017;359: j4891.

Elwyn G, Frosch D, Thomson R, et al. Shared decision making: a model for clinical practice. J Gen Intern Med. 2012;27(10):1361-1367.

Fischhoff B, Brewer NT, Downs JS, eds. Communicating Risks and Benefits: An Evidence-Based User’s Guide. FDA. 2011. Available at: https://www.fda.gov/media/81597/download. Accessed October 16, 2019.

Fragoulis GE, McInnes IB, Siebert S. JAK-inhibitors. New players in the field of immune-mediated diseases, beyond rheu-matoid arthritis. Rheumatology. 2019;58:i43-i54.

Garber K. Psoriasis: from bed to bench and back. Nat Biotechnol. 2011;29(7):563-566.

Genovese MC, Mease PJ, Thomson GT, et al. M02-570 Study Group. Safety and efficacy of adalimumab in treatment of patients with psoriatic arthritis who had failed disease modifying antirheumatic drug therapy. J Rheumatol. 2007;34(5):1040-1050.

Gladman DD, Rigby W, Azevedo V, et al. Efficacy and Safety of Tofacitinib, an Oral Janus Kinase Inhibitor, in Patients with Active Psoriatic Arthritis and an Inadequate Response to Tumor Necrosis Factor Inhibitors: OPAL Beyond, a Randomized, Double Blind, Placebo-Controlled, Phase 3 Trial [abstract 10L]. Arthritis Rheumatol. 2016;68(suppl 10):4371-4375.

References

Husni ME, Merola JF, Davin S. The psychosocial burden of psoriatic arthritis. Semin Arthritis Rheum. 2017;47(3):351-360.

Husni ME. Comorbidities in psoriatic arthritis. Rheum Dis Clin North Am. 2015;41(4):677-698.

Kavanaugh A, Mease PJ, Gomez-Reino JJ, et al. Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor. Ann Rheum Dis. 2014;73(6):1020-1026.

Kopf M, Bachmann MF, Marsland BJ. Averting inflammation by targeting the cytokine environment. Nat Rev Drug Discov. 2010;9(9):703-718.

Martin RW, McCallops K, Head AJ, Eggebeen AT, Birmingham JD, Tellinghuisen DJ. Influence of patient characteristics on perceived risks and willingness to take a proposed anti-rheumatic drug. BMC Med Inform Decis Mak. 2013;13(89):1-9.

Martin RW, Head AJ, René J, et al. J Rheumatol. Patient decision-making related to antirheumatic drugs in rheumatoid arthritis: the importance of patient trust of physician. 2008;35(4):618-624.

McInnes IB, Kavanaugh A, Gottlieb AB, et al. PSUMMIT 1 Study Group. Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial. Lancet. 2013; 382(9844);780-789.

McInnes JB, Mease PJ, Kirkham B, et al. FUTURE 2 Study Group. Secukinumab, a human anti-interleukin-17A monoclonal antibody, in patients with psoriatic arthritis (FUTURE 2): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet. 2015;386(9999):1137-1146.

Mease PJ, Kellner H, Morita A, et al. Efficacy and safety of risankizumab, a selective IL-23P19 inhibitor, in patients with active psoriatic arthritis over 24 weeks: results from a phase 2 trial [abstract OP037}. Arthritis Rheumatol. 2017;69(suppl 10): 200.

Mease P, Gladman DD, van Den Bosch F, et al. Filgotinib, an Oral, Selective Janus Kinase 1 Inhibitor, Is Effective in Psoriatic Arthritis Patients with an Inadequate Response to Conventional Disease-Modifying Anti-Rheumatic Drugs: Results from a Randomized, Placebo-Controlled, Phase 2 Study [abstract 1821]. Arthritis Rheumatol. 2018; 70 (suppl 9):2026.

Mease PJ, Gottlieb AB, van der Heijde D, et al. Efficacy and safety of abatacept, a T-cell modulator, in a randomised, dou-ble-blind, placebo-controlled, phase III study in psoriatic arthritis. Ann Rheum Dis. 2017;76(9):1550-1558

Mease PJ, van der Heijde D, Ritchlin CT, et al ; SPIRIT-P1 Study Group. Ixekizumab, an interleukin-17A specific monoclonal antibody, for the treatment of biologic-naive patients with active psoriatic arthritis: results from the 24-week randomised, double-blind, placebo-controlled and active (adalimumab)-controlled period of the phase III trial SPIRIT-P1. Ann Rheum Dis. 2017;76(1):79-87.

Mease PJ, Gladman DD, Ritchlin CT, et al. Adalimumab for the treatment of patients with moderately to severely active pso-riatic arthritis: Results of a double-blind, randomized, placebo-controlled trial. Arthritis Rheum. 2005;52(10):3279-3289.

Mease PJ, Hall S, FitzGerald O, et al. Efficacy and Safety of Tofacitinib, an Oral Janus Kinase Inhibitor, or Adalimumab in Patients with Active Psoriatic Arthritis and an Inadequate Response to Conventional Synthetic Dmards: A Randomized, Placebo-Controlled, Phase 3 Trial [abstract 2983]. Arthritis Rheumatol. 2016;68(suppl 10): 3978.

References

Mease PJ, Genovese MC, Greenwald MW, et al. Brodalumab, an anti-IL17RA monoclonal antibody, in psoriatic arthritis. N Engl J Med. 2014;370(24):2295-2306.

Mease PJ. Biologic therapy for psoriatic arthritis. Rheum Dis Clin North Am. 2015;41(4):723-738.

Mease PJ, Gottlieb AB, van der Heijde D, et al. Efficacy and safety of abatacept, a T-cell modulator, in a randomised, dou-ble-blind, placebo-controlled, phase III study in psoriatic arthritis. Ann Rheum Dis. 2017;76(9):1550-1558.

Mehta NN, Azfar RS, Shin DB, Neimann AL, Troxel AB, Gelfand JM. Patients with severe psoriasis are at increased risk of cardiovascular mortality: cohort study using the General Practice Research Database. Eur Heart J. 2010;31(8):1000-1006.

Menter A, Disch D, Clemens J, et al. A phase 2b trial of baricitinib, an oral JAK inhibitor, in patients with moderate to severe psoriasis [abstract P7941]. J Am Acad Dermatol. 2014;70(5):AB162.

Merola JF, Espinoza LR, Fleischmann R. Distinguishing rheumatoid arthritis from psoriatic arthritis. RMD Open. 2018;4(2):e000656.

Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361(5):496-509.

O’Connor AM. Validation of a decisional conflict scale. Med Decis Making.1995;15(1):25-30.

Ogdie A, Schwartzman S, Husni ME. Curr Opin Rheumatol. Recognizing and managing comorbidities in psoriatic arthritis. 2015;27(2):118-126.

Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM. Mechanisms of TNF-alpha- and RANKL-mediated osteoclasto-genesis and bone resorption in psoriatic arthritis. J Clin Invest. 2003;111(6):821-831.

Robert M, Miossec, P. IL-17 in rheumatoid arthritis and precision medicine: from synovitis expression to circulating bioactive levels. Frontiers in Medicine. 2019;5:364.

Sakkas LI, Zafiriou E, Bogdanos DP. Mini review: new treatments in psoriatic arthritis. focus on the IL-23/17 axis. Front Pharmacol. 2019;10:872-872.

Shuai K, Liu B. Regulation of JAK-STAT signalling in the immune system. Nat Rev Immunol. 2003;3(11):900-911.

Stelara (ustekinumab) [package insert]. Horsham, PA: Janssen Biotech; 2016.

Watad A, Cuthbert RJ, Amital H, McGonagle D. Enthesitis: much more than focal insertion point inflammation. Curr Rheumatol Rep. 2018;20(7):41.

Zerilli T, Ocheretyaner E. Apremilast (Otezla): a new oral treatment for adults with psoriasis and psoriatic arthritis. P T. 2015;40(8):495–500.