Sections

Treatment

Approach Considerations

Plaque psoriasis is a chronic skin condition. Any approach to the treatment of this disease must be considered for the long term. Treatment regimens must be individualized according to age, sex, occupation, personal motivation, other health conditions, and available resources.

Disease severity is defined not only by the number and extent of plaques present but also by the patient's perception and acceptance of the disease. Treatment, therefore, must be designed with the patient's specific expectations in mind rather than the extent of the body surface area involved.^[14]

Many treatments exist for psoriasis; however, the construction of an effective therapeutic regimen is not necessarily complicated. Three basic treatment modalities are available for the overall management of psoriasis: topical agents; phototherapy; and systemic agents, including biologic therapies. All of these treatments may be used alone or in combination.

Topical Therapy

Outpatient topical therapy is the first-line treatment of plaque psoriasis. A number of topical treatments are available (eg, corticosteroids, coal tar, anthralin, calcipotriene, tapinarof, tazarotene, roflumilast topical).^[14]

No single topical agent is ideal for plaque psoriasis, and many are often used concurrently in a combined approach. With the different adverse effect profiles for the various agents, using a rotational therapeutic approach in which different topical agents are used sequentially over time in the same patient is common.

In general, the effects of topical therapy should become evident within the first 2-3 weeks of use. Clearing of scale is usually observed first, followed by flattening of the treated plaques. Resolution of erythema may take 6-8 weeks.

Auxiliary agents such as keratolytics can often be added to these preparations. However, some auxiliary agents are incompatible with the active ingredients of these preparations. For example, salicylic acid inactivates calcipotriene. On the other hand, agents such as anthralin require the auxiliary agent salicylic acid for chemical stability.

Phototherapy

Initiate phototherapy only in the presence of extensive and widespread disease (generally practically defined as more lesions than can be easily counted). Resistance to topical treatment is another indication for phototherapy.

The 2 main forms of phototherapy are ultraviolet B (UVB) irradiation and psoralen plus ultraviolet A irradiation (PUVA). Proper facilities are required for both UVB irradiation and PUVA photochemotherapy.

UVB irradiation uses light with wavelengths of 290-320 nm (in comparison, the visible light range is 400-700 nm). Narrow-band UVB phototherapy uses a fluorescent bulb with a narrow emission spectrum that peaks at 311 nm. This selective and relatively longer wavelength is more effective than broadband UVB for the treatment of plaque-type psoriasis, and poses less risk of burning.^[15]Excimer laser UVB therapy can deliver high-dose light to limited plaques.

UVB therapy is usually combined with one or more topical treatments. The Goeckerman regimen uses coal tar followed by UVB exposure and has been shown to induce disease remission in more than 80% of patients. The Ingram method comprises anthralin application following a tar bath and UVB treatment. At present, UVB is more commonly combined with topical corticosteroids, calcipotriene, tazarotene, or simply bland emollients. Etanercept and narrow-band UVB combination therapy reportedly was successful.^[16]

UVB phototherapy is extremely effective for treating moderate-to-severe plaque psoriasis. The major drawback of this therapy is the time commitment required for treatments and the accessibility of the UVB equipment. Patients may dislike the unpleasant odor when coal tar is added.

Home ultraviolet therapy can overcome some of the logistical problems associated with phototherapy. Because of the expense of the home units, it is most suitable for patients who require long-term maintenance therapy.

PUVA photochemotherapy, also known as PUVA, uses the photosensitizing drug methoxsalen (8-methoxypsoralen) in combination with UVA irradiation to treat patients with more extensive disease. UVA irradiation uses light with wavelengths of 320-400 nm. PUVA interferes with DNA synthesis, decreases cellular proliferation, and induces apoptosis of cutaneous lymphocytes, leading to a localized immunosuppression.

More than 85% of patients report relief of disease symptoms with 20-30 treatments. Therapy is usually administered 2-3 times per week in an outpatient setting, with maintenance treatments every 2-4 weeks until remission.

Adverse effects of PUVA therapy include nausea, pruritus, and a burning sensation. Long-term complications include increased risks of photo damage to the skin and (more importantly) skin cancer. PUVA has been combined with oral retinoid derivatives to decrease the cumulative dose of UVA radiation to the skin.

Also see Clinical Practice Guidelines.

Systemic Agents

Initiate systemic treatment only after both topical treatments and phototherapy have proved unsuccessful. Consider systemic therapy for patients with very active psoriatic arthritis. Patients who have disease that is physically, psychologically, socially, or economically disabling are also considered candidates for systemic treatment. All patients must be informed of the risks and adverse effects of systemic therapy before treatment is initiated.^{[2, 3, 4]}

Plaque psoriasis appears to respond better to combination topical/systemic therapy than to systemic treatment alone. In a randomized study, adding a topical corticosteroid to etanercept therapy in patients with moderate to severe plaque psoriasis proved to be a more effective treatment than etanercept alone.^[17]In the study, which involved 592 adult patients with a Psoriasis Area and Severity Index (PASI) score of 10 or higher and with 10% or more of their body surface area affected by psoriasis, treatment consisted of either etanercept alone or etanercept plus topical clobetasol propionate foam. Significant differences favoring combination therapy were seen at week 12, including percentage of improvement in the PASI score (76.5% for combination therapy vs 68.2% for etanercept alone).^[17]

Two clinical studies, ESTEEM 1 and ESTEEM 2, showed that patients treated with apremilast experienced significant, clinically meaningful improvement in plaque psoriasis at week 16 as measured by the PASI score. Apremilast, a phosphodiesterase (PDE)-4 inhibitor, was approved by the FDA for the treatment of plaque psoriasis in September 2014.^[1] A topical PDE-4 inhibitor, roflumilast cream, was approved for plaque psoriasis in 2022.

Tyrosine kinase 2 inhibitors

Deucravacitinib is an oral tyrosine kinase 2 (TYK2) inhibitor. TYK2 pairs with JAK1 to mediate multiple cytokine pathways and pairs with JAK2 to transmit signals as shown in cell-based assays. The precise mechanism linking inhibition of TYK2 enzyme to therapeutic effectiveness is unknown. It is indicated for moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy.

Approval was supported with results from the POETYK PSO-1 trial. At week 16, the Psoriasis Area and Severity Index showing at least 75% reduction of symptoms from baseline (PASI 75) response rates were significantly higher with deucravacitinib versus placebo or apremilast (58.4% vs 12.7% vs 35.1%; P < 0.0001). The static physician’s global assessment score 0/1 (sPGA 0/1) also favored deucravacitinib (53.6% vs 7.2% vs 32.1%; P < 0.0001). Efficacy improved beyond week 16 and was maintained through week 52.^[18]

Biologic Therapies

These relatively new systemic therapies provide selective, immunologically directed intervention at key steps in the pathogenesis of the disease.^[5]These steps include the following:

Inhibiting the initial cytokine release and Langerhans cell migration
Targeting activated T cells, preventing further T-cell activation, and eliminating pathologic T cells
Blocking the interactions that lead to T-cell activation or migration into tissue
Altering the balance of T-cell types
Inhibiting proinflammatory cytokines such as tumor necrosis factor (TNF),^[6]IL-12, IL-17, and IL-23^{[7, 19, 20]}

As with the systemic agents, biologic therapies are typically reserved for more severe and recalcitrant cases.^{[21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32]}Patients with active psoriatic arthritis in addition to their skin disease should also be considered.

In a study completed by the Psoriatic Arthritis Study Group, beneficial effects were observed for patients with psoriasis and psoriatic arthritis on stable doses of methotrexate when one or more courses of intramuscular alefacept were added. Further benefit in psoriatic arthritis was apparent after a second course of alefacept, and no additional toxicity was observed.^[33]

Also see Clinical Practice Guidelines.

TNF inhibitors

Psoriasis of the palms and soles is more difficult to treat than psoriasis on other body sites. Adalimumab is effective, but only 31% of patients treated with adalimumab for hand or foot psoriasis in a placebo-controlled trial achieved clear or almost clear.^[34]

In 2017, the US Food and Drug Administration (FDA) approved the addition of moderate-to-severe fingernail psoriasis data to the adalimumab (Humira) prescribing information, based on results from a phase 3, multicenter, randomized, double-blind, parallel-arm, placebo-controlled clinical trial.^[35] It is indicated for moderate-to-severe chronic plaque psoriasis in patients who are candidates for systemic therapy or phototherapy and for whom other systemic therapies are inappropriate. Several adalimumab biosimilar products are also approved for plaque psoriasis.

Certolizumab pegol (Cimzia) was approved by the FDA in May 2018 for use in moderate-to-severe plaque psoriasis. Approval was based on data from the CIMPASI-1, CIMPASI-2, and CIMPACT phase 3 clinical trials (n >1000). Nearly one third of participants had prior biologic exposure. The trials included an assessment of patients who achieved at least 75% and 90% improvement from baseline as measured by the Psoriasis Area and Severity Index (PASI) compared with placebo (CIMPASI-1 and CIMPASI-2) and/or etanercept (CIMPACT). Significant improvement was observed by week 16 and meaningful improvements were maintained through 48 weeks.^{[36, 37]}

Interleukin inhibitors

Risankizumab (Skyrizi) is a humanized immunoglobulin G1 (IgG1) monoclonal antibody that selectively binds to the p19 subunit of human interleukin 23 (IL-23) cytokine and inhibits its interaction with the IL-23 receptor. It was approved in April 2019 for treatment of moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy.

Approval was based on the UltlMMa-1 and UltlMMa-2 replicate phase 3, randomized, double-blind, placebo-controlled and active comparator-controlled international trials (N=997).^[20]Coprimary endpoints were proportions of patients achieving a 90% improvement in the PASI 90 and a static Physician's Global Assessment (sPGA) score of 0 or 1 at week 16 (nonresponder imputation). Risankizumab showed superior efficacy to both placebo and ustekinumab in the treatment of moderate-to-severe plaque psoriasis.

At week 16 of each study, PASI 90 was achieved by 74.8-75.3% patients receiving risankizumab compared with 2-4.9% receiving placebo and 42-47.5% receiving ustekinumab (P< .0001 vs placebo and ustekinumab). Results from each trial for sPGA 0 or 1 at week 16 was achieved by 83.7-87.8% patients receiving risankizumab compared with 5.1-7.8% receiving placebo and 61.6-63% receiving ustekinumab (P< .0001 vs placebo and ustekinumab).^[20]

Ustekinumab (Stelara), a fully human IL-12 and IL-23 antagonist, is FDA approved to treat adults with moderate or severe psoriasis who may benefit from systemic or phototherapy. Approval was based on data from the phase 3 ACCEPT trial that revealed ustekinumab (administered as 2 subcutaneous injections at weeks 0 and 4) was significantly more effective than etanercept (50 mg injected subcutaneous twice weekly for 12 weeks) for achieving a 75% or greater reduction in psoriasis at week 12, as measured by the PASI 75. At week 12, 68% and 74% of patients receiving ustekinumab 45 mg and 90 mg, respectively, achieved a PASI 75 compared with 57% of patients receiving etanercept.^[38]

In October 2017, the FDA expanded its approval to include patients aged 12 years or older. Approval of ustekinumab for adolescents aged 12-17 years with moderate-to-severe plague psoriasis was based on the phase 3, double-blind, placebo-controlled, multicenter CADMUS trial (n=110). Patients were randomly assigned to receive ustekinumab standard dosing (SD) or half-standard dosing (HSD) at weeks 0 and 4 and every 12 weeks thereafter or placebo at weeks 0 and 4 with crossover to either SD or HSD at week 12 and 16 and then every 12 weeks. At week 12, 67.7% and 69.4% of patients receiving ustekinumab HSD and SD achieved Physician’s Global Assessment (PGA) of cleared/minimal psoriasis (PGA 0/1) compared with 5.4% for placebo (P< .001). PASI 75 was 78.4% and 80.6% in HSD and SD, respectively, compared with 10.8% for placebo; PASI 90 was 54.1% and 61.1% in HSD and SD, respectively, compared with 5.4% for placebo.^[39]

Guselkumab (Tremfya) was approved by the FDA in July 2017 for adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy. It is a human monoclonal IgG1-lambda antibody that selectively binds to the p19 subunit of interleukin (IL)–23. IL-23 is a natural cytokine associated with inflammatory and immune responses. Guselkumab inhibits the proinflammatory actions of IL-23, thereby decreasing cytokine and chemokine release.

Approval was based on three phase 3 studies that included more than 2000 patients. In the VOYAGE 1 trial, guselkumab was compared with adalimumab. At 16 weeks, at least 7 of 10 patients treated with guselkumab achieved at least 90% clearer skin (Psoriasis Area and Severity Index [PASI 90]) and more than 80% demonstrated cleared or almost cleared skin. Patients who achieved PASI 90 at week 28 maintained that response at week 48.^[40]Similar results were shown in the VOYAGE 2 trial that included adalimumab nonresponders.^[41]

Guselkumab also demonstrated effectiveness in patients who had an inadequate response to ustekinumab.^[42]

Tildrakizumab (Ilumya) is a high-affinity, humanized, IgG1/κ, anti–IL-23p19 monoclonal antibody that does not bind human IL-12 or p40. In March 2018, the FDA approved tildrakizumab-asmn for moderate-to-severe plaque psoriasis, which is supported by the two pivotal phase 3 trials (reSURFACE 1 and 2).^[43] The two multicenter, randomized, double-blind, placebo-controlled trials involved 926 adults with moderate-to-severe plaque psoriasis, with 616 treated with tildrakizumab-asmn and 310 receiving placebo. Both studies met the primary efficacy endpoints, demonstrating significant clinical improvement with tildrakizumab-asmn compared with placebo when measured by at least a 75% reduction in PASI 75 and PGA score of "clear" or "minimal" at week 12 after two doses.

In the reSURFACE 1 study, 74% of patients achieved PASI 75 at week 28 after three doses of tildrakizumab-asmn and 84% of patients who continued on the drug maintained PASI 75 at week 64, compared with 22% of patients who were rerandomized to placebo. In reSURFACE 2, 66% of the 200-mg group and 61% of the 100-mg group achieved PASI 75, compared with 6% of the placebo group and 48% of the etanercept group at week 12.

The first IL-17A inhibitor, secukinumab (Cosyntex), was approved by the FDA in January 2015. IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses and plays a key role in the pathogenesis of plaque psoriasis. Approval was based on the efficacy and safety outcomes that included more than 3990 patients.

In two pivotal trials, secukinumab was shown to be superior compared with placebo at week 12 with respect to the proportion of patients who had a reduction of greater than 75% from baseline in the PASI score (PASI 75). The proportion of patients who met the criterion for PASI 75 at week 12 was higher with each secukinumab dose than with placebo or etanercept. In the ERASURE study (Efficacy of Response And Safety of two fixed secUkinumab REgimens in psoriasis), the rates were 81.6% with 300 mg of secukinumab, 71.6% with 150 mg of secukinumab, and 4.5% with placebo. In the FIXTURE study (Full year Investigative eXamination of secukinumab vs. eTanercept Using 2 dosing Regimens to determine Efficacy in psoriasis), the rates were 77.1% with 300 mg of secukinumab, 67% with 150 mg of secukinumab, 44% with etanercept, and 4.9% with placebo (P< .001 for each secukinumab dose vs comparators).^[19]

A second IL-17A inhibitor, ixekizumab (Taltz), was approved in March 2016. Efficacy was observed in two prospective, double-blind, multicenter, phase 3 trials (UNCOVER 2, UNCOVER 3) that compared ixekizumab to placebo and etanercept. Ixekizumab (q2wk or q4wk) showed greater efficacy (measured by PASI 75) compared with placebo or etanercept (P< .0001). Greater proportions of patients given ixekizumab achieved PASI 90 by week 2 compared with etanercept in both studies (UNCOVER 2: P=.0002 [ixekizumab q4wk] and P< .0001 [ixekizumab q2wk]; UNCOVER 3: P < .0001 [ixekizumab q4wk] and P=.0001 [ixekizumab q2wk]).^[8]IL-17 inhibitors may be associated with a small increase in the incidence of Candida infections.^[44] Additionally, ixekizumab’s prescribing information includes data supporting use for genital plaque psoriasis.

Brodalumab (Siliq), another monoclonal antibody that targets IL-17, was approved in February 2017. Approval was contingent upon including a boxed warning in the prescribing information warning of the risk of suicide and suicidal ideation, particularly in patients with a history of suicidality or depression. Because of the observed suicidal behavior, brodalumab is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS).

Approval of brodalumab was based on data from the AMAGINE phase III pivotal studies. At the 210-mg dose, brodalumab was shown to be effective in total skin clearance of psoriasis compared with placebo and superior to ustekinumab at week 12 in two replicate comparator trials involving over 3500 patients.^[9]

Complications

Overly aggressive use of topical steroids could produce progression from plaque psoriasis to generalized pustular or erythrodermic forms. Topical steroids used with occlusion increase the risk of developing cutaneous atrophy. Potential adverse effects of systemic agents and phototherapy should be monitored on a regular basis and treated as soon as possible.

Consultations

Consider consultation with a rheumatologist for patients who have evidence of psoriatic arthritis. Patients with cardiovascular comorbidities should be considered for referral to a cardiologist. Evidence-based guidelines have been published on the management of cardiovascular morbidities.^[45]

Diet

Alcohol is considered a risk factor for psoriasis in young to middle-aged males. All patients with psoriasis should avoid or minimize alcohol use; patients with dependency states should be appropriately treated. Otherwise, specific dietary restrictions or supplements other than a well-balanced and adequate diet are unimportant in the management of plaque psoriasis.

Prevention

Avoiding specific exacerbating factors (see Etiology for details) may help prevent or minimize flare-ups of psoriasis in some patients, although the cause of disease exacerbation in many patients often is unknown.

Guidelines

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Media Gallery

Plaque psoriasis. Courtesy of University of British Columbia, Department of Dermatology and Skin Science.
Plaque psoriasis. Courtesy of University of British Columbia, Department of Dermatology and Skin Science.
Plaque psoriasis. Photomicrograph of psoriasis. (1) Hyperkeratosis and parakeratosis, (2) neutrophils in the epidermis, (3) thinning of the epidermis overlying the dermal papillae, (4) vessels close to the epidermis, and (5) elongated rete ridges. Courtesy of Richard Crawford, MD, University of British Columbia, Department of Dermatology and Skin Science.

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Author

Harvey Lui, MD, FRCPC Professor and Head, Department of Dermatology and Skin Science, Vancouver General Hospital, University of British Columbia; Medical Director, The Skin Centre, Lions Laser Skin Centre and Psoriasis and Phototherapy Clinic, Vancouver General Hospital

Harvey Lui, MD, FRCPC is a member of the following medical societies: Canadian Medical Association, American Society for Photobiology, Photomedicine Society, European Academy of Dermatology and Venereology, National Psoriasis Foundation, Canadian Dermatology Association, College of Physicians and Surgeons of British Columbia, North American Hair Research Society, Canadian Dermatology Foundation, American Academy of Dermatology, American Society for Laser Medicine and Surgery

Disclosure: Received consulting fee from Astellas for review panel membership; Received consulting fee from Amgen/Wyeth for speaking and teaching; Received honoraria from LEO Pharma for speaking and teaching; Received grant/research funds from LEO Pharma for investigator; Received grant/research funds from Galderma for other.

Coauthor(s)

Adam J Mamelak, MD, FRCPC Attending Physician, Division of Dermatology, The Ottawa Hospital, University of Ottawa

Adam J Mamelak, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery, Canadian Dermatology Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Christen M Mowad, MD Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Mark G Lebwohl, MD Chairman, Department of Dermatology, Mount Sinai School of Medicine

Mark G Lebwohl, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Received none from Amgen for consultant & investigator; Received none from Novartis for consultant & investigator; Received none from Pfizer for consultant & investigator; Received none from Celgene Corporation for consultant & investigator; Received none from Clinuvel for consultant & investigator; Received none from Eli Lilly & Co. for consultant & investigator; Received none from Janssen Ortho Biotech for consultant & investigator; Received none from LEO Pharmaceuticals for consultant & inves.