Currently Viewing:
Supplements Easing the Economic and Clinical Burden of Psoriasis and Psoriatic Arthritis: The Role of Managed Ca

Psoriasis and Psoriatic Arthritis Treatment

Alan Menter, MD
Over the past several years, an increased understanding of the pathophysiology of psoriasis and psoriatic arthritis has led to the development of several new biologic therapies.
     Apremilast is an oral inhibitor of phosphodiesterase 4 that indirectly down-regulates the inflammatory response by enhancing the expression of anti-inflammatory cytokines while suppressing the activity of pro-inflammatory cytokines.51,52 In March 2014, apremilast became the first oral biologic drug approved for the treatment of active PsA. Later that year, in September 2014, the FDA expanded the indication for apremilast to include treatment of moderate to severe plaque psoriasis in patients for whom phototherapy or systemic therapy is appropriate.51

The approval of apremilast in PsA and plaque psoriasis was based on the phase 3 PALACE and ESTEEM clinical trial programs.52 PALACE 1 evaluated apremilast in 504 patients with active PsA despite standard treatment with synthetic DMARDs or biologic therapy. At week 16, approximately 30% and 40% of patients treated with apremilast 20 or 30 mg twice daily, respectively, achieved an ACR20 response compared with approximately 20% of those in the placebo group (P <.001).53 The ESTEEM 1 trial compared apremilast 30 mg twice daily or placebo in 844 patients with moderate to severe plaque psoriasis. After 16 weeks, 33% of patients in the apremilast group achieved a 75% or greater reduction in the PASI score compared with 5% of patients in the placebo group (P <.0001).54 Focusing on concomitant PsA and psoriasis, the PALACE 3 trial evaluated apremilast in 505 patients with PsA and current skin involvement. Treatment with apremilast 20 or 30 mg twice daily was associated with clinically meaningful improvements in both PsA and psoriasis measures by week 16, and sustained improvements continued through week 52.51 Apremilast was well tolerated and exhibited a highly acceptable safety profile. Up to 17% of patients develop gastrointestinal AEs in the first month of therapy.51-54 However, no laboratory monitoring of patients on apremilast is required.

     Tofacitinib is a novel oral Janus kinase (JAK) inhibitor currently approved for the treatment of rheumatoid arthritis; it shows promising activity in both psoriasis and PsA.16,55 In a placebo-controlled phase 2 trial of patients with moderate to severe psoriasis (N = 197), twice-daily treatment with tofacitinib 2, 5, or 15 mg was associated with significant dose-dependent improvements in multiple patient-reported outcomes, including dermatologyrelated quality of life, itch severity, and Short Form-36 psychological and physical domains.55

Two recent identical phase 3 trials confirmed the safety and efficacy of tofacitinib in patients with psoriasis. In total, 1861 patients were randomly assigned 2:1 to treatment with oral tofacitinib (5 or 10 mg) or placebo twice daily. After 28 weeks, 55.6% and 68.8% of patients in the tofacitinib 5-mg and 10-mg groups, respectively, achieved a PASI 75 response; 54.7% and 65.9% of patients, respectively, achieved clear/almost clear status by PGA. Treatment efficacy was sustained in most patients through 24 months. The most common AEs were nasopharyngitis (18.8%) and upper respiratory tract infection (12.6%). Overall, 10.1% of patients developed serious AEs, and 10.7% discontinued treatment due to AEs.56
     In a phase 3 noninferiority trial, tofacitinib 10 mg twice daily was noninferior to etanercept 50 mg twice weekly and superior to placebo in terms of PASI 75 response and clear/almost clear PGA response in patients with moderate to severe plaque psoriasis. The safety analysis showed similar AE rates at 12 weeks in patients treated with tofacitinib or etanercept, with 2% of patients developing
serious AEs and 1% to 3% of patients discontinuing treatment due to AEs.57
In patients with PsA, tofacitinib appears to reduce synovial inflammation and other markers of PsA disease activity.58 In a randomized, double-blind, phase 3 trial of patients with psoriasis and/or PsA (N = 99), treatment with tofacitinib 5 mg or 10 mg twice daily was associated with high response rates, as measured by PASI 75 response (63% and 73%, respectively) and a clear/almost clear PGA response (67% to 68%). In addition, all patients with PsA (N = 12) achieved an ACR20 response by treatment week 12. Four patients (4.3%) developed serious AEs, including 3 cases of herpes zoster infection.59 Overall, these findings support the potential therapeutic role of JAK inhibition in patients with PsA (similar to rheumatoid arthritis, for which tofacitinib FDA approved). A topical formulation of tofacitinib ointment is currently under development for the treatment of chronic plaque psoriasis.60

Treatment Selection in Practice: 2016 GRAPPA PsA Treatment Algorithm
     In 2016, the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) published updated guidelines on the management of patients with PsA, including those with psoriasis. The new guidance defines the 6 major domains of PsA: peripheral arthritis, axial disease, enthesitis, dactylitis, skin involvement, and nail disease. While many patients with PsA exhibit multiple manifestations, the selection of therapy should be driven by the most severe component of each patient’s clinical presentation (Figure 21).1

Peripheral Arthritis
     Traditional DMARDs and biologic therapies are strongly recommended for the treatment of PsA. In particular, biologics should be initiated early in patients with poor prognostic factors, such as high inflammatory markers and multiple active joints. For patients with an inadequate response to their first biologic therapy, switching to a second biologic agent is recommended. The GRAPPA guideline supports the conditional use of NSAIDs and corticosteroids to control the signs and symptoms of PsA but also indicates that these agents should be used with caution due to the potential for AEs. If needed, corticosteroids should be given in the lowest doses (eg, <7.5 mg/day) and for short periods of time to provide symptomatic control.1

Axial Disease
     Given the lack of clinical trial data in PsA-specific axial disease, the GRAPPA recommendations rely on experience in ankylosing spondylitis. Appropriate firstline therapy for axial disease can include NSAIDs, sacroiliac injections, and physiotherapy. However, traditional DMARDs show poor efficacy against axial manifestations. Therefore, patients with PsA with predominant axial disease who require treatment intensification should consider early initiation of anti-TNF therapy.1

     Standard first-line treatment for enthesitis involves NSAIDs. As with axial disease, there is a lack of evidence to support the use of DMARDs to treat enthesitis. Therefore, for patients with an inadequate response to NSAIDs alone, biologics are the recommended second-line therapies. In that group, TNF inhibitors and ustekinumab appear to be highly effective in reducing the tendon and ligament inflammation characteristic of enthesitis. Preliminary evidence also supports the use of secukinumab and apremilast to treat enthesitis in patients with PsA.1

     Traditional DMARDs are recommended as first-line therapy for patients with dactylitis. If needed, corticosteroid injections are also effective at controlling digit inflammation. Clinical trial data support the
use of biologic therapies, particularly TNF inhibitors, ustekinumab, secukinumab, and apremilast. To date, however, there is little evidence to guide further treatment adjustments for patients with an inadequate response to initial biologic therapy.

Skin Involvement
     Topical medications are recommended for the first-line treatment of psoriasis, particularly in patients with mild and/or limited disease. Phototherapy and DMARDs provide improved control of psoriatic skin lesions; they should be considered for use in combination with topical medications as initial treatment in patients with more extensive disease. Systemic and biologic therapies are the next step for patients with widespread skin involvement who experience an inadequate response to topical medications, DMARDs, and phototherapy. Until patients find a combination regimen that provides optimal disease control, switching among DMARDs and biologic agents may be necessary.1

Nail Disease
     Patients with PsA and moderate to severe nail disease respond well to first-line treatment with TNF inhibitors and other biologics, including ustekinumab, anti-IL17 therapy, and apremilast. For patients with milder psoriatic nail disease or contraindications to biologic therapy, treatment options include topical medications, nonbiologic DMARDs, and intralesional corticosteroid injections.1

Preventing Complications
    Preventing complications in patients with psoriasis and PsA begins with a thorough medical history, with a review of systems covering cutaneous, musculoskeletal, immune, hematologic, cardiac, gastrointestinal, neurologic, reproductive, and family and social history.16 When selecting systemic therapy, the contraindications, precautions, and side-effect profiles of each agent should be considered
(Table 117-26). Clinicians should consider risk-aversion strategies, such as avoiding therapies with a significant risk of liver toxicity in patients with chronic alcohol use or a history of hepatitis (Table 216). The potential for drug–drug interactions should be assessed and addressed. Patient education and counseling can ensure that patients are willing to attempt the prescribed therapy and have realistic expectations regarding efficacy, tolerability, cost, and convenience.16

Addressing Patient Treatment Obstacles
     Nearly 40% of patients with psoriasis are untreated in current clinical practice, and over half of those with severe disease are treated with inadequate therapy (Table 3).61 Even when patients are prescribed guideline-based therapy, adherence is often poor, leading to reduced treatment efficacy.62 For many patients with psoriasis, correct use of topical medications can be time-consuming and burdensome. In one survey of nearly 18,000 patients with psoriasis, patients spent an average of 26 minutes per day applying topical agents.63 Poor adherence can lead to reduced treatment efficacy and the need for more aggressive and/or costly therapy. To support adherence, it is important to select a first-line treatment regimen with enough potency to achieve a favorable clinical response.7
Addressing comorbidities and incorporating patients preferences regarding treatment is essential while also improving adherence. One study showed that comorbidities significantly influenced preferences for treatment among patients with psoriasis. Patients with comorbid PsA prioritized treatment efficacy, while those with cardiovascular disease were primarily concerned with the risk of side effects. Among patients with comorbid depression, the duration and cost of treatment were key treatment concerns.64 Furthermore, it is important to note that patient preferences may change over time, and treatment adjustments may be needed to reflect changing treatment goals.65
     Multiple treatment options are now available to relieve symptoms, protect physical function, and improve quality of life for patients with psoriasis and PsA. Many patients with moderate to severe disease will require combination regimens that may include traditional DMARDs and biologic therapies to provide appropriate control of inflammatory disease activity. To ensure that optimal therapy is provided, clinicians should take time to discuss the true burden of disease with their patients, including the degree to which their disease interferes with both their physical, as well as mental, health. Effective
communication allows patients to have an active role in treatment decisions based on expectations about efficacy, AEs, convenience, and tolerability.

Author affiliation: Baylor University Medical Center, Dallas, Texas.
Funding source: This activity is supported by educational grants from Lilly and Novartis.
Author disclosure: Dr Menter has no relevant financial relationships with commercial interests to disclose.
Authorship information: Concept and design, drafting of the manuscript, and critical revision of the manuscript for important intellectual content.
Address correspondence to:
1. Coates LC, Kavanaugh A, Mease PJ, et al. Group for research and assessment of psoriasis and psoriatic arthritis 2015 treatment recommendations for psoriatic arthritis. Arthritis Rheumatol.  016;68(5):1060-1071. doi: 10.1002/art.39573.
2. Menter A, Gottlieb A, Feldman SR, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 1. Overview of psoriasis and guidelines of care for the treatment
of psoriasis with biologics. J Am Acad Dermatol. 2008;58(5):826-850. doi: 10.1016/j.jaad.2008.02.039.
3. Højgaard P, Glintborg B, Hetland ML, et al. Association between tobacco smoking and response to tumour necrosis factor iinhibitor treatment in psoriatic arthritis: results from the DANBIO registry. Ann Rheum Dis. 2015;74(12):2130-2136. doi:10.1136/annrheumdis-2014-205389.
4. Gottlieb A, Korman NJ, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 2. Psoriatic arthritis: overview and guidelines of care for treatment
with an emphasis on the biologics. J Am Acad Dermatol. 2008;58(5):851-864. doi: 10.1016/j.jaad.2008.02.040.
5. Coates LC, Moverley AR, McParland L, et al. Effect of tight control of inflammation in early psoriatic arthritis (TICOPA): a UK multicentre, open-label, randomised controlled trial. Lancet. 2015;386(10012):2489-2498. doi: 10.1016/S0140-6736(15)00347-5.
6. Armstrong AW, Bagel J, Van Voorhees AS, Robertson AD, Yamauchi PS. Combining biologic therapies with other systemic treatments in psoriasis: evidence-based, best-practice recommendations
from the Medical Board of the National Psoriasis Foundation. JAMA Dermatol. 2015;151(4):432-438. doi: 10.1001/jamadermatol.2014.3456.
7. Menter A, Korman NJ, Elmets CA, et al; American Academy of Dermatology. Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies. J Am Acad Dermatol. 2009;60(4):643-659. doi: 10.1016/j.jaad.2008.12.032.
8. Menter Kamili. Topical treatment of psoriasis. In: Yawalkar N, editor. Current problems in dermatology. Basel, Switzerland:S. Karger AG; 2009.
9. Racz E, Prens EP. Phototherapy and photochemotherapy for psoriasis. Dermatol Clin. 2015;33(1):79-89. doi: 10.1016/j.det.2014.09.007.
10. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 5. Guidelines of care for the treatment of psoriasis with phototherapy
and photochemotherapy. J Am Acad Dermatol. 2010;62(1):114-135. doi: 10.1016/j.jaad.2009.08.026.
11. Sivanesan SP, Gattu S, Hong J, et al. Randomized, doubleblind, placebo-controlled evaluation of the efficacy of oral psoralen plus ultraviolet A for the treatment of plaque-type psoriasis using the Psoriasis Area Severity Index score (improvement of 75% or greater) at 12 weeks. J Am Acad Dermatol. 2009;61(5):793-798. doi: 10.1016/j.jaad.2009.04.053.
12. Soriano ER. Management of psoriatic arthritis: traditional disease-modifying rheumatic agents and targeted small molecules. Rheum Dis Clin North Am. 2015;41(4):711-722. doi: 10.1016/j.rdc.2015.07.012.
13. Carrascosa JM, de la Cueva P, Ara M, et al. Methotrexate in moderate to severe psoriasis: review of the literature and expert recommendations. Actas Dermosifiliogr. 2016;107(3):194-206. doi: 10.1016/
14. Ryan C, Korman NJ, Gelfand JM, et al. Research gaps in psoriasis: opportunities for future studies. J Am Acad Dermatol. 2014;70(1):146-167. doi: 10.1016/j.jaad.2013.08.042.
15. Mease PJ. Biologic therapy for psoriatic arthritis. Rheum Dis Clin North Am. 2015;41(4):723-738. doi: 10.1016/j.rdc.2015.07.010.
16. Kelly JB III, Foley P, Strober BE. Current and future oral systemic therapies for psoriasis. Dermatol Clin. 2015;33(1):91-109. doi: 10.1016/j.det.2014.09.008.
17. Stelara (ustekinumab) [prescribing information]. Horsham, PA: Janssen Biotech, Inc; 2014.
18. Cosentyx (secukinumab) [prescribing information]. East Hanover, NJ: Novartis Pharmaceuticals Corp; 2016.
19. Cimzia (certolizumab pegol) [prescribing information].Smyrna, GA: UCB, Inc; 2016.
20. Humira (adalimumab) [prescribing information]. North Chicago, IL: AbbVie Inc; 2016.
21. Enbrel (etanercept) [prescribing information]. Thousand Oaks, CA: Immunex Corp; 2013.
22. Otezla (apremilast) [prescribing information]. Summit, NJ: Celgene Corp; 2015.
23. Remicade (infliximab) [prescribing information]. Horsham, PA: Janssen Biotech, Inc; 2015.
24. Simponi (golimumab) [prescribing information]. Horsham, PA: Janssen Biotech, Inc; 2013.
25. Taltz (ixekizumab) [prescribing information]. Indianapolis, IN: Eli Lilly and Company; 2016.
26. Koutnik-Fotopoulos E. The biologic revolution in treatment of psoriasis and PsA. The Dermatologist. 2015;23(12):10-16.
27. Iannone F, Lopriore S, Bucci R, et al. Longterm clinical outcomes in 420 patients with psoriatic arthritis taking anti-tumor necrosis factor drugs in real-world settings. J Rheumatol. 2016;43(5):911-917. doi: 10.3899/jrheum.151042.
28. Menter A, Thaçi D, Papp KA, et al. Five-year analysis from the ESPRIT 10-year postmarketing surveillance registry of adalimumab treatment for moderate to severe psoriasis. J Am Acad Dermatol. 2015;73(3):410-419.e6. doi: 10.1016/j.jaad.2015.06.038.
29. Kimball AB, Rothman KJ, Kricorian G, et al. OBSERVE-5: observational postmarketing safety surveillance registry of etanercept for the treatment of psoriasis final 5-year results. J Am Acad Dermatol. 2015;72(1):115-122. doi: 10.1016/j.jaad.2014.08.050.
30. Leonardi CL, Kimball AB, Papp KA, et al; PHOENIX 1 study investigators. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 76-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 1). Lancet. 2008;371(9625):1665-1674. doi:10.1016/S0140-6736(08)60725-4.
31. Papp KA, Langley RG, Lebwohl M, et al; PHOENIX 2 study investigators. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 52-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 2). Lancet. 2008;371(9625):1675-1684. doi:10.1016/S0140-6736(08)60726-6.
32. Wang TC, Chiu HY, Wang TS, Tsa TF. Practical experience of ustekinumab in patients with moderate-to-severe psoriasis who had inadequate therapeutic response to previous tumor necrosis
factor blockers. Dermatologica Sinica. 2015;33(1):5-10.
33. 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, multicenter,
double-blind, placebo-controlled PSUMMIT I trial. Lancet. 2013;382(9894):780-789. doi: 10.1016/S0140-6736(13)60594-2.
34. Ritchlin C, Rahman P, Kavanaugh A, et al; PSUMMIT 1 Study Group. Efficacy and safety of the anti-IL-12/23 p40 monoclonal antibody, ustekinumab, in patients with active psoriatic arthritis
despite conventional non-biological and biological anti-tumour necrosis factor therapy: 6-month and 1-year results of the phase 3, multicentre, double-blind, placebo-controlled, randomised PSUMMIT 2 trial. Ann Rheum Dis. 2014;73(6):990-999. doi: 10.1136/annrheumdis-2013-204655
35. Hueber W, Patel DD, Dryja T, et al. Effects of AIN457, a fully human antibody to interleukin-17A, on psoriasis, rheumatoid arthritis, and uveitis. Sci Transl Med. 2010;2(52):52ra72. doi: 10.1126/scitranslmed.3001107.
36. Langley RG, Elewski BE, Lebwohl M, et al; ERASURE Study Group; FIXTURE Study Group. Secukinumab in plaque psoriasis--results of two phase 3 trials. N Engl J Med. 2014;371(4):326-338.
doi: 10.1056/NEJMoa1314258.
37. Mease PJ, McInnes IB, Kirkham B, et al; FUTURE 1 Study Group. Secukinumab inhibition of interleukin-17A in patients with psoriatic arthritis. N Engl J Med. 2015;373(14):1329-1339. doi: 10.1056/NEJMoa1412679.
38. van der Heijde D, Landewé RB, Mease PJ, et al. Secukinumab provides significant and sustained inhibition of joint structural damage in a phase III study of active psoriatic arthritis [Epub ahead of print]. Arthritis Rheumatol. 2016. doi: 10.1002/art.39685.
39. McInnes IB, 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. doi: 10.1016/S0140-6736(15)61134-5.
40. Krueger JG, Fretzin S, Suárez-Fariñas M, et al. IL-17A is essential for cell activation and inflammatory gene circuits in subjects with psoriasis. J Allergy Clin Immunol. 2012;130(1):145-154.e9.
doi: 10.1016/j.jaci.2012.04.024.
41. Griffiths CE, Reich K, Lebwohl M, et al; UNCOVER-2 and UNCOVER-3 investigators. Comparison of ixekizumab with etanercept or placebo in moderate-to-severe psoriasis (UNCOVER-2
and UNCOVER-3): results from two phase 3 randomised trials. Lancet. 2015;386(9993):541-551. doi: 10.1016/S0140-6736(15)60125-8.
42. Armstrong AW, Lynde CW, McBride SR, et al. Effect of ixekizumab treatment on work productivity for patients with moderateto-severe plaque psoriasis: analysis of results from 3 randomized phase 3 clinical trials [Epub ahead of print]. JAMA Dermatol. 2016. doi: 10.1001/jamadermatol.2016.0269.
43. Farahnik B, Beroukhim K, Zhu TH, et al. Ixekizumab for the treatment of psoriasis: a review of phase III trials. Dermatol Ther (Heidelb). 2016;6(1):25-37. doi: 10.1007/s13555-016-0102-0.
44. Mease PJ, van der Heijde D, Ritchlin CT, et al. A randomized, double-blind, active- and placebo-controlled phase 3 study of efficacy and safety of ixekizumab, adalimumab, and placebo therapy
in patients naïve to biologic disease modifying anti-rheumatoid drugs with active psoriatic arthritis. Presented at: the American College of Rheumatology 2015 Annual Meeting. November 7-11, 2015; San Francisco, CA. Abstract 977.
45. Martin DA, Towne JE, Kricorian G, et al. The emerging role of IL-17 in the pathogenesis of psoriasis: preclinical and clinical findings. J Invest Dermatol. 2013;133(1):17-26. doi: 10.1038/jid.2012.194.
46. 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. doi: 10.1056/NEJMoa1315231.
47. Papp K, Leonardi C, Menter A, et al. Safety and efficacy of brodalumab for psoriasis after 120 weeks of treatment. J Am Acad Dermatol. 2014;71(6):1183-1190.e3. doi: 10.1016/j.jaad.2014.08.039.
48. Papp K, Menter A, Strober B, et al. Efficacy and safety of brodalumab in subpopulations of patients with difficult-to-treat moderate-to-severe plaque psoriasis. J Am Acad Dermatol. 2015;72(3):436-439. doi: 10.1016/j.jaad.2014.10.026.
49. Psoriasis trial drug halted due to suicide concerns. National Psoriasis Foundation website. Published January 5,
2016. Accessed April 1, 2016.
50. Valeant announces FDA acceptance of BLA submission for brodalumab in moderate-to-severe plaque psoriasis [press release]. Quebec, Canada. PR Newswire; January 26, 2016. Accessed April 1, 2016.
51. 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. doi:10.1136/annrheumdis-2015-207963.
52. Zerilli T, Ocheretyaner E. Apremilast (Otezla): a new oral treatment for adults with psoriasis and psoriatic arthritis. PT. 2015;40(8):495-500.
53. 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. doi: 10.1136/annrheumdis-2013-205056.
54. Papp K, Reich K, Leonardi CL, et al. Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, in patients with moderate to severe plaque psoriasis: results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis [ESTEEM] 1). J Am Acad Dermatol. 2015;73(1):37-49. doi: 10.1016/j.jaad.2015.03.049.
55. Mamolo C, Harness J, Tan H, Menter A. Tofacitinib (CP-690,550), an oral Janus kinase inhibitor, improves patient-reported outcomes in a phase 2b, randomized, double-blind, placebo-controlled study in patients with moderate-to-severe psoriasis. J Eur Acad Dermtol Venereol. 2014;28(2):192-203. doi: 10.1111/jdv.12081
56. Papp KA, Krueger JG, Feldman SR, et al. Tofacitinib, an oral Janus kinase inhibitor, for the treatment of chronic plaque psoriasis: long-term efficacy and safety results from 2 randomized phase-III studies and 1 open-label long-term extension study. J Am Acad Dermatol. 2016;74(5):841-850. doi: 10.1016/j.jaad.2016.01.013.
57. Bachelez H, van de Kerkhof PC, Strohal R, et al; OPT Compare Investigators. Tofacitinib versus etanercept or placebo in moderate-to-severe chronic plaque psoriasis: a phase 3 randomised
non-inferiority trial. Lancet. 2015;386(9993):552-561. doi: 10.1016/S0140-6736(14)62113-9.
58. Gao W, McGarry T, Orr C, McCormick J, Veale DJ, Fearon U. Tofacitinib regulates synovial inflammation in psoriatic arthritis, inhibiting STAT activation and induction of negative feedback
inhibitors. Ann Rheum Dis. 2016;75(1):311-315. doi: 10.1136/annrheumdis-2014-207201.
59. Asahina A, Etoh T, Igarashi A, et al; study investigators. Oral tofacitinib efficacy, safety and tolerability in Japanese patients with moderate to severe plaque psoriasis and psoriatic arthritis: a
randomized, double-blind, phase 3 study [Epub ahead of print]. J Dermatol. 2016. doi: 10.1111/1346-8138.13258.
60. Ports WC, Khan S, Lan S, et al. A randomized phase 2a efficacy and safety trial of the topical janus kinase inhibitor tofacitinib in the treatment of chronic plaque psoriasis. Br J Dermatol.
2013;169(1):137-145. doi: 10.1111/bjd.12266.
61. Horn EJ, Fox KM, Patel V, Chiou CF, Dann F, Lebwohl M. Are patients with psoriasis undertreated? Results of National Psoriasis Foundation survey. J Am Acad Dermatol. 2007;57(6):957-962.
62. Augustin M, Holland B, Dartsch D, Langenbruch A, Radtke MA. Adherence in the treatment of psoriasis: a systematic review. Dermatology. 2011;222(4):363-374. doi: 10.1159/000329026.
63. Krueger G, Koo J, Lebwohl M, Menter A, Stern RS, Rolstad T. The impact of psoriasis on quality of life: results of a 1998 National Psoriasis Foundation patient-membership survey. Arch
Dermatol. 2001;137(3):280-284.
64. Schmieder A, Schaarschmidt ML, Umar N, et al. Comorbidities significantly impact patients’ preferences for psoriasis treatments. J Am Acad Dermatol. 2012;67(3):363-372. doi: 10.1016/j.
65. Schaarschmidt ML, Umar N, Schmieder A, et al. Patient preferences for psoriasis treatments: impact of treatment experience. J Eur Acad Dermatol Venereol. 2013;27(2):187-198. doi: 10.1111/j.1468-3083.2011.04440.x.

Copyright AJMC 2006-2019 Clinical Care Targeted Communications Group, LLC. All Rights Reserved.
Welcome the the new and improved, the premier managed market network. Tell us about yourself so that we can serve you better.
Sign Up