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TABLE OF CONTENTS Faculty Biographies ............................................................................................ 2 Posttest Questions With Explanations................................................................ 3 FDA-Approved Biologic and New Small Molecule Systemic Therapies for Psoriasis, Psoriatic Arthritis, and Atopic Dermatitis ...................... 8 HoloLens Experience: Legend .......................................................................... 9 Atopic Dermatitis ............................................................................................. 10 Psoriasis ............................................................................................................ 11 Psoriatic Arthritis............................................................................................... 12 References ........................................................................................................ 13 ADDITIONAL RESOURCES FOCUSING IN-DEPTH ON TREATMENT STRATEGIES FOR PSORIASIS, PSA, AND AD

ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

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Page 1: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

TABLE OF CONTENTSFaculty Biographies ............................................................................................ 2

Posttest Questions With Explanations................................................................ 3

FDA-Approved Biologic and New Small Molecule Systemic Therapies for Psoriasis, Psoriatic Arthritis, and Atopic Dermatitis ...................... 8

HoloLens Experience: Legend .......................................................................... 9

Atopic Dermatitis ............................................................................................. 10

Psoriasis ............................................................................................................ 11

Psoriatic Arthritis ............................................................................................... 12

References ........................................................................................................ 13

ADDITIONAL RESOURCES

FOCUSING IN-DEPTH ON TREATMENT STRATEGIES FOR PSORIASIS, PSA, AND AD

Page 2: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

2

FEATURED FACULTY

JOEL GELFAND, MD, MSCE Professor of Dermatology and of Epidemiology,Vice Chair of Clinical Research and Medical Director,Dermatology Clinical Studies UnitDirector, Psoriasis and Phototherapy Treatment CenterPerelman School of MedicineUniversity of PennsylvaniaPhiladelphia, Pennsylvania

Joel Gelfand, MD, MSCE, is Professor of Dermatology and Epidemiology (with tenure) at the University of Pennsylvania’s Perelman School of Medicine in Philadelphia, where he is also Vice Chair of Clinical Research, Medical Director of the Dermatology Clinical Studies Unit, and Director of the Psoriasis and Phototherapy Treatment Center. He is a nationally and internationally recognized expert in psoriasis, clinical epidemiology, drug safety, and clinical trials. Dr. Gelfand is the author of over 260 scientific publications, editorials, reviews, and text book chapters (cited over 18,000 times, H index 60) which appear in journals such as JAMA, BMJ, European Heart Journal, Annals of Rheumatic Disease, JAMA Dermatology, the Journal of the American Academy of Dermatology, and The Journal of Infectious Diseases. He is the recipient of the American Skin Association’s Psoriasis Achievement Award, PENN’s New Investigator Marjorie Bowman Award, and the Lady Barbara Colyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology Teaching Award, the National Psoriasis Foundation’s Inaugural Award for Scientific Achievement, and is an elected member of the American Society for Clinical Investigation.

He has given over 10 named lectureships and keynote addresses including the Society for Investigative Dermatology’s Eugene M. Farber lecture and the American Academy of Dermatology’s Marion B. Sulzberger lecture. He has received grant support from the National Institutes of Health, the FDA, the Patient-Centered Outcomes Research Institute, the Dermatology Foundation, the American Skin Association, the National Psoriasis Foundation, and numerous pharmaceutical companies to support his independent research program. The overarching goal of his research and clinical practice is to improve psoriasis patient outcomes in the skin and joints, while lowering the risk of diabetes, CV disease, and mortality.

Richard Martin, MD, MA, is Professor of Medicine and Rheumatology at the Michigan State University College of Human Medicine in East Lansing, Michigan. He earned his medical degree at the Michigan State University College of Human Medicine. He completed an Internal Medicine residency at the University of Rochester in New York and a fellowship in Rheumatology at the Mayo Clinic in Rochester, Minnesota. In addition, Dr. Martin has completed postgraduate research training at Michigan State University, earning a Master of Arts degree in Educational Psychology and Instructional Design, as well as a National Institutes of Health-funded postdoctoral fellowship in Clinical Epidemiology and Community-Based Research.

Dr. Martin has a translational research thread developing and validating decision aids for patients considering biologics. He has conducted more than 65 clinical trials of biologic therapies, yielding more than 80 publications, which have over 8000 citations.

RICHARD MARTIN, MD, MA Professor of Medicine and Rheumatology,Michigan State University College of Human MedicineEast Lansing, Michigan

Page 3: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Posttest Question 1 Which mediator of chronic inflammation does guselkumab directly target?

A. TNF

B. IL-4

C. IL-12

D. IL-17

E. IL-23

Correct Answer: E. IL-23

EXPLANATIONGuselkumab is IL-23 inhibitor. IL-23 consists of the p19 subunit and the p40 subunit. The p19 subunit is unique to IL-23, whereas the p40 subunit is common to both IL-12 and IL-23. Guselkumab targets the p19 subunit of IL-23.

• Guselkumab prescribing information

POSTTEST WITH EXPLANATIONS

3

Page 4: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Posttest Question 2A known side effect of dupilumab treatment for atopic dermatitis is:

A. Demyelinization

B. Tuberculosis reactivation

C. Lymphoma

D. Varicella virus reactivation

E. Conjunctivitis

Correct Answer: E. Conjunctivitis

EXPLANATIONConjunctivitis in one of most common adverse reactions for dupilumab. It was observed in 10% of patients with atopic dermatitis on dupilumab monotherapy.

• Dupilumab prescribing information

4

POSTTEST WITH EXPLANATIONS

Page 5: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Posttest Question 3A 25-year-old patient with a history of optic neuritis and active Crohn’s disease presents with thick plaques of psoriasis affecting her scalp, trunk, extremities, and finger nails. Which mechanism of action would be most appropriate in treating this patient?

A. TNF

B. IL-12/23

C. IL-17

D. IL-23

E. PDE4

Correct Answer: B. IL-12/23

EXPLANATIONUstekinumab targets IL-12/23 and is approved for Crohn’s disease and psoriasis. Some TNF inhibitors are approved for psoriasis and Crohn’s disease (adalimumab, infliximab, certolizumab) but this class can induce or aggravate multiple sclerosis and the patient has a history of optic neuritis. Treatments that target IL-17 could exacerbate or even trigger Crohn’s disease. Agents that target IL-23 or PDE4 are not currently approved for Crohn’s disease.

• Paramsothy S, Rosenstein AK, Mehandru S, Colombel JF. The current state of the art for biological therapies and new small molecules in inflammatory bowel disease. Mucosal Immunol. 2018; 11(6): 1558–1570.

5

POSTTEST WITH EXPLANATIONS

Page 6: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Posttest Question 426-year-old man with psoriasis is recently diagnosed with psoriatic arthritis. He has only peripheral disease and no axial disease, but he has enthesitis. 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

EXPLANATIONAccording to the GRAPPA recommendations, TNF inhibitors are the first line therapy for enthesitis related psoriatic arthritis. There are no data to support initial treatment for psoriatic arthritis using a combination of methotrexate and a 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 Recommendations for Psoriatic Arthritis. Arthritis Rheumatol. 2016;68 (5):1060-1071.

6

POSTTEST WITH EXPLANATIONS

Page 7: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Posttest Question 5Good decision aids are designed to accomplish all of the listed features EXCEPT:

A. Help clinician explain patient why a particular option is the best for the patient

B. Provide specific probabilities about outcomes to aid comparison of options

C. Encourage and structure patient reflection on options after office visit with support persons

D. Gives a consistent script for the care team to reinforce patient education content

E. Create a standard operating procedure that reduces documentation to clicking an EMR macro

Correct Answer: A. Help clinician explain patient why a particular option is the best for the patient

EXPLANATIONThe correct answer is A. Decision aids are tools intended to structure and support a dialogue, not to persuade the use of a particular option. Shared decision making is useful in equipoise—when there is more than one medically reasonable option. In that case, the patient’s preference for one or more drug attribute, ie, route of administration, avoidance of certain risks, desire for maximum potency, etc, would motivate the patient to find a particular treatment most desirable. In complex medication dialogues there can be an overload of information. Patients often have limited ability and motivation to sustain attention and deliberation. Reduced health literacy, age and general health-related cognitive impairment, risk aversion, and non-native language skill all reduce patients’ ability to participate in decision making. This emphasizes the need to simplify complex concepts and risk propositions to patient’s level. Decision aids can lengthen the time of deliberation beyond the office visit and increase the involvement of support persons. The goal of increasing patient engagement is to reduce going for the default option, “whatever you recommend doctor.”

• An introduction to patient decision aids. BMJ. 2013;347:f4147. • Dartmouth-Hitchcock Center for Shared Decision Making. Step 4: Decision Support Tools. https://med.

dartmouth-hitchcock.org/csdm_toolkits/step_4_tools.html

7

POSTTEST WITH EXPLANATIONS

Page 8: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

NOTE• Crisaborole, an FDA-approved, small-molecule, PDE4 inhibitor for treatment of atopic dermatitis, is not included in the chart because

it is a topical medication• FDA-approved conventional systemic pharmacotherapies include: acitretin, cyclosporine, and methotrexate for psoriasis; leflunomide,

methotrexate, and sulfasalazine for psoriatic arthritis; and systemic corticosteroids for atopic dermatitis• Systemic immunomodulatory agents—cyclosporine, methotrexate, mycophenolate mofetil, azathioprine, and interferon gamma—although

not approved in the United States for the treatment of atopic dermatitis, are used for cases with severe, difficult-to-manage symptoms

8

Approved Medication Approved for Psoriasis Approved for PsA Approved for AD

TNFi

Adalimumab Yes Yes

Certolizumab Yes Yes

Etanercept Yes Yes

Golimumab Yes

Infliximab Yes Yes

PDE4i

Apremilast, small molecule

Yes Yes

IL-4

Dupilumab Yes

IL-12/23i

Ustekinumab Yes Yes

IL-23i

Guselkumab Yes

Tildrakizumab Yes

Risankizumab Yes

IL-17i

Ixekizumab Yes Yes

Secukinumab Yes Yes

Brodalumab Yes

CTLA4

Abatacept Yes

JAK 2/3i

Tofacitinib, small molecule

Yes

FDA-APPROVED BIOLOGIC AND NEW SMALL MOLECULE SYSTEMIC THERAPIES FOR PSORIASIS, PSORIATIC ARTHRITIS, AND ATOPIC DERMATITIS

Page 9: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

9

HOLOLENS EXPERIENCE: LEGEND

IL-4

Inflammatory Pathways in Psoriasis

Inflammatory Pathways in Atopic Dermatitis

MOA of Dupilumab in Atopic Dermatitis

MOAs of Therapies for Psoriasis

Skin Barriers Psoriatic Skin Atopic Dermatitis Skin

Ixekizumab

Apremilast

Guselkumab

Adalimumab

Microbiome Barrier Neutrophils

Th17 cell

Th1 cell

Tc1 cell

Th22 cell

AMP

Spongiosis

Lymphocyte clusters

Th22 cell

Neutrophil

Neutrophil

MacrophageNaive T cell

IL-12

IL-23

Th17 cell

Th1 cell

TNF-α

TNF-α

IFNƔ

IL-17

IL-22Myeloid

dendritic cell

KerationcyteIL-17AF

Ixekizumab

IL-17A Receptor

IL-17C Receptor

IL-17AAGuselkumab

IL-12 Receptor

IL-23 Receptor

IL-23 (p19 and p40 subunits)

Apremilast

cAMP

PDE4

TNF-α

Adalimumab

TNF-α Receptor

Keratinocyte

Neutrophil

IL-4

Th2 cell

Eosinophil

Mast cell

Basophil

Th22 cell

IL-4

IL-13

IL-5

IL-31

TNF-α

IL-13

IL-13 Receptor

IL-4 Receptor

IL-4Rα subunit of IL-4 Receptor

IL-4Rα subunit of IL-13 Receptor

Dupilumab

Page 10: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

10

Step-Up Care in AD

Advance from mild to moderate therapy when patients are symptomatic despite appropriate use of low-to-medium potency TCS and adherence to basic management recommendations.

(Basic management)1. Skin Care

• Liberal, frequent moisturizer use

• Daily warm bath/shower, followed by moisturizer

2. Trigger Avoidance• Common irritants;

allergens if proven• Consider comorbidities

(Basic management + topical anti-inflammatory medication)1. Add bleach baths

• 2-7 times weekly based on severity and tendency to develop crusting at sites of excoriation

2. Maintenance TCS• Medium potency, 2-3 times weekly

(“proactive”) to recurrently active areas of involvement

• Low potency, 1-2 times daily3. Maintenance TCI

• 1-2 times daily (especially to sensitive areas)

• 2-3 times weeklya (proactive approach)4. Crisaborole 2%, twice daily

Mai

nten

ance

Trea

tmen

tA

cute

Trea

tmen

t

MILD

MODERATE

OR

OR

SEVERE

Apply TCS to Inflamed Skin• Low-to-medium potency TCS,

twice daily for 3-7 days beyond clearance

• Consider crisaborole 2% or TCI

Apply TCS to Inflamed Skin• Medium-to-high potency TCS, twice daily

for 3-7 days beyond clearance• Lower potency for sensitive areas or consider

crisaborole 2% or TCI• If unresolved after 7 days, reconsider next step

(Basic management + referral to AD Specialist)1. Phototherapy2. Dupilumab3. Systemic immunosuppressants

• Cyclosporine A• Methotrexate• Mycophenolate mofetil• Azathioprine• Corticosteroids

4. Consider acute treatment for some patients to help gain control• Wet wrap therapy• Short-term hospitalization

Apply TCS to Inflamed Skin• Medium-to-high potency TCS, twice daily for

3-7 days beyond clearance• Lower potency for sensitive areas or consider

crisaborole 2% or TCI• If unresolved after 7 days, reconsider next step

• Nonadherence• Infection• Misdiagnosis• Contact allergy

to medications• Referral

aNot an FDA-approved dose of pimecrolimus or tacrolimus.FDA=US Food and Drug Administration. TCS=topical corticosteroids. TCI=topical calcineurin inhibitor.Adapted from Boguniewicz M, et al. Ann Allergy Asthma Immunol. 2018;120(1):10-22. 11

Step-Up Care in AD (cont.)When Is It Time for Systemic Therapy?

QoL=quality of life.Simpson EL, et al. J Am Acad Dermatol. 2017;77(4):623-633.

Does the patient have moderate to severe AD?

• Consider eczema severity• Assess impact on QoL and daily functioning

Have alternative diagnoses been considered?

• Have infections been adequately managed?• Is referral to an allergy specialist required?

Has adequate patient education been provided?

Has adequate patient education been provided?

Does the patient still have persistent moderate to severe disease/impaired QoL despite intensive topical therapy?

Is phototherapy unsuccessful, unsuitable, or unavailable?

Consider phototherapy in selected patient groups

Discuss systemic therapy with the patient/caregiver

12

ATOPIC DERMATITIS

Page 11: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Factors to Consider When Selecting a Systemic Treatment (cont.)

40

Class of Drugs Drug/Special Population Pregnancy Pediatric Anti-HCVAb+ HbsAg+ Anti-Hbc+ HIV Latent TB

TNF-α inhibitors Etanercept + ++ ++* - +/-* +* -Adalimumab + ++ +* - +/-* +* -Infliximab + + +* - +/-* +* -Certolizumab ++ + +* - +/-* +* -Golimumab + ++ - - +/-* +* -

IL-12/23 inhibitor Ustekinumab + ++ - - ?/+* +/ -IL-17 inhibitorsAnti–IL-17A Secukinumab ?/+ ?/+ ?/+* ?/+* ?/+* ?/+* +Anti–IL-17A Ixekizumab ?/+ ?/+ ?/+* ?/+* ?/+* ?/+* +Anti–IL-17A receptor Brodalumab ?/+ ?/+ ?/+* ?/+* ?/+* ?/+* +IL-23 inhibitors Guselkumab ? ?/+ ? ? ? ? ?

Tildrakizumab ? ?/+ ? ? ? ? ?Risankizumab ? ?/+ ? ? ? ? ?Mirikizumab ? ?/+ ? ? ? ? ?

Oral novel Apremilast ? ?/+ ?/+* ? ? +* +Oral traditional Methotrexate X + X X X X X

Cyclosporine + + +/-* X X X XAcitretin X + + + + + +

Note: 2 plus symbols (++) indicates preferred agents; 1 plus symbol (+) indicates that the agent can be used; 1 plus symbol and 1 minus symbol (+/-) indicate that the drug can be used but is controversial; 1 minus symbol and 1 plus symbol (-/+) indicates that the drug is not preferred but can be used; 1 question mark and 1 plus symbol (?/+) indicates that there are not enough data but that the drug is likely safe to use; 1 question mark (?) indicates that there are not enough data; 1 minus symbol (-) indicates that use of that drug is controversial because there are not enough data; and X indicates that a drug is contraindicated.*Additional monitoring required.Anti-Hbc=Antibody to hepatitis B core. anti-HCV=antibody to hepatitis C virus. HbsAg=hepatitis B surface antigen. Kaushik SB, Lebwohl MG. J Am Acad Dermatol. 2019;80:43-54.

Factors to Consider When Selecting a Systemic Treatment

39

Class of drugs Drug/Comorbidity PsA CD Cancer Obesity Cardiac CHF MS Lupus

TNF-α inhibitors Etanercept ++ + - + ++ -/+ X +/-Adalimumab ++ ++ - + ++ -/+ X +/-

Infliximab ++ ++ - ++ ++ -/+ X +/-Certolizumab ++ ++ - + ++ -/+ X +/-

Golimumab + ++ - ++ + ++ + + IL-12/23 inhibitor Ustekinumab + ++ + ++ + ++ + +IL-17 inhibitorsAnti-IL-17A Secukinumab ++ - ?/+ ++ ? ++ + ?/+Anti-IL-17A Ixekizumab ++ - ?/+ ++ ? ++ + ?/+

Anti-IL-17 receptor Brodalumab + - ?/+ ++ ? ++ + ?/+IL-23 inhibitors Guselkumab ? + ?/+ ++ ? ++ ?/+ ?/+

Tildrakizumab ? + ?/+ ++ ? ++ ?/+ ?/+Risankizumab ? + ?/+ ? ? ++ ?/+ ?/+

Mirikizumab ? + ?/+ ? ? ++ ?/+ ?/+ Oral novel Apremilast + + ?/+ ++ ? ++ ?/+ + Oral traditional Methotrexate + + - X ++ ++ + +

Cyclosporine +/- + X + ?/+ ++ + +/-Acitretin +/- + ++ + ?/+ ++ + +

Note: 2 plus symbols (++) indicates preferred agents; 1 plus symbol (+) indicates that the agent can be used; 1 plus symbol and 1 minus symbol (+/-) indicate that the drug can be used but is controversial; 1 minus symbol and 1 plus symbol (-/+) indicates that the drug is not preferred but can be used; 1 question mark and 1 plus symbol (?/+) indicates that there are not enough data but that the drug is likely safe to use; 1 question mark (?) indicates that there are not enough data; 1 minus symbol (-) indicates that use of that drug is controversial because there are not enough data; and X indicates that a drug is contraindicated.CD=Crohn’s disease. CHF=congestive heart failure. MS=multiple sclerosis. TNF-α=tumor necrosis factor-α.Kaushik SB and Lebwohl MG. J Am Acad Dermatol. 2019;80:27-40

11

PSORIASIS

Page 12: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

GRAPPA Treatment Schema For Active PsA

Blue 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. SpA=spondyloarthritis. CS=corticosteroid. CSA=cyclosporin A. IL-12/23i=interleukin-12/23 inhibitor.

Coates LC, et al. Arthritis Rheumatol. 2016;68(5):1060-1071. 44

NSAI

Ds a

nd IA

cor

ticos

tero

ids

as in

dica

ted

Ass

ess

Act

ivity

, Im

pact

, and

Pro

gnos

tic F

acto

rs

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 route

Which Domains Are Involved?

Peripheral Arthritis Axial Disease Enthesitis Skin Nails

Key:

Dactylitis

12

PSORIATIC ARTHRITIS

Page 13: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Armstrong AW, Harskamp CT, Armstrong EJ. The association between psoriasis and hypertension: a systematic review and meta-analysis of observational studies. J Hypertens. 2013;31(3):433-442.

Azfar RS, Seminara NM, Shin DB, Troxel AB, Margolis DJ, Gelfand JM. Increased risk of diabetes mellitus and likelihood of receiving diabetes mellitus treatment in patients with psoriasis. Arch Dermatol. 2012;148(9):995-1000.

Balieva FN, Finlay AY, Kupfer J, et al. The role of therapy in impairing quality of life in dermatological patients: a multinational study. Acta Derm Venereol. 2018;98(6):563-569.

Blauvelt A, Papp KA, Griffiths CE, et al. Efficacy and safety of guselkumab, an anti-interleukin-23 monoclonal antibody, compared with adalimumab for the continuous treatment of patients with moderate to severe psoriasis: Results from the phase III, double-blinded, placebo- and active comparator-controlled VOYAGE 1 trial. J Am Acad Dermatol. 2017; 76(3):405-417.

Boguniewicz M, Fonacier L, Guttman-Yassky E, Ong PY, Silverberg J, Farrar JR. Atopic dermatitis yardstick: Practical recommendations for an evolving therapeutic landscape. Ann Allergy Asthma Immunol. 2018;120(1): 10-22.

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.

Cimzia (certolizumab pegol) [package insert]. Smyrna, GA; UCB Inc; 2008.

Clark JD, Flanagan ME, Telliez JB. Discovery and development of Janus kinase (JAK) inhibitors for inflammatory diseases. J Med Chem. 2014;57(12):5023-5038.

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

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

Dartmouth-Hitchcock Center for Shared Decision Making. Step 4: Decision Support Tools. Available at: https://med.dartmouth-hitchcock.org/csdm_toolkits/step_4_tools.html. Accessed October 16, 2019.

Drug and Therapeutics Bulletin. An introduction to patient decision aids. BMJ. 2013;347:f4147.

Dupixant (dupilumab) [package insert]. Tarrytown, NY and Bridgewater, NJ: Regeneron Sanofi Genzyme; 2019.

Elmets CA, Leonardi CL, Davis DMR, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities. J Am Acad Dermatol. 2019; 80(4):1073-1113.

Enbrel (etanercept) [package insert]. Thousand Oaks, CA: Amgen; 1998.

Farahnik B, Beroukhim K, Abrouk M, et al. Brodalumab for the treatment of psoriasis: a review of phase III trials. Dermatol Ther. 2016;6(2):111-124.

Gadina M. Janus kinases: an ideal target for the treatment of autoimmune diseases. J Invest Dermatol Symp Proc. 2013;16(1):S70-S72.

Gelfand JM, Shin DB, Neimann AL, Wang X, Margolis DJ, Troxel AB. The risk of lymphoma in patients with psoriasis. J Invest Dermatol. 2006;126(10):2194-2201.

Gelfand JM, Neimann AL, Shin DB, Wang X, Margolis DJ, Troxel AB. Risk of myocardial infarction in patients with psoriasis. JAMA. 2006;296(14):1735-1741.

13

REFERENCES

Page 14: ADDITIONAL RESOURCESColyton’s Award for Autoimmune Research. He has also received the University of Pennsylvania’s Department of Biostatistics and Epidemiology’s Epidemiology

Guttman E, et al. Primary results from a phase 2b, randomized, placebo-controlled trial of upadacitinib for patients with atopic dermatitis. Late-breaking research oral presentation 6533 at: American Academy of Dermatology Annual Meeting, February 17, 2018. San Diego, CA; 2018.

Guttman-Yassky E, Silverberg JI, Nemoto O, et al. Baricitinib in adult patients with moderate-to-severe atopic dermatitis: A phase 2 parallel, double-blinded, randomized placebo-controlled multiple-dose study. J Am Acad Dermatol. 2018:80(4):913-921.

Hanifin JM, et al. Randomized, double-blind, placebo-controlled, multicenter, multidose phase II study of anti-interleukin-31 receptor A monoclonal antibody CIM331 (nemolizumab) in patients with moderate to severe atopic dermatitis. Late-breaking abstract session FO53 presented at: American Academy of Dermatology Annual Meeting. March 4-8, 2016. Washington, DC; 2016.

Humira (adalimumab) [package insert].North Chicago, IL: AbbVie; 2002

Ilumya (tildrakizumab) [package insert]. Cranbury, NJ: Sun Pharma; 2018

Kaushik SB, Lebwohl MG. Psoriasis: which therapy for which patient: psoriasis comorbidities and preferred systemic agents. J Am Acad Dermatol. 2019;80(1):27-40.

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