latest research on psoriasis

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Psoriasis articles from across Nature Portfolio

Psoriasis is an autoimmune disease in which the skin becomes inflamed, producing red, flaky areas. It affects 1-2% of the population and is thought to be caused by misguided T cell attacks on the skin.

Latest Research and Reviews

Single-cell RNA-seq reveals keratinocyte and fibroblast heterogeneity and their crosstalk via epithelial-mesenchymal transition in psoriasis

• Dianhao Guo
• Xiaokang Li
• Ningning Dang

Gasdermin E promotes translocation of p65 and c-jun into nucleus in keratinocytes for progression of psoriatic skin inflammation

• Fangyuan Long

Identifying the genetic associations among the psoriasis patients in eastern India

• Shantanab Das
• Aditi Chandra
• Raghunath Chatterjee

Saracatinib inhibits necroptosis and ameliorates psoriatic inflammation by targeting MLKL

• Xingfeng Liu

Assessment of safety profile of secukinumab in real-world scenario using United States food and drug administration adverse event reporting system database

• Vishnu Eshwar
• Ashwin Kamath

Effects of psoriasis and psoralen exposure on the somatic mutation landscape of the skin

Analysis of the somatic mutations landscape of 111 patients with psoriasis vulgaris shows that the disease is unlikely to be driven by clonal expansions caused by somatic mutations in keratinocytes. A mutational footprint associated with psoralen treatment was observed and characterized.

• Sigurgeir Olafsson
• Elke Rodriguez
• Carl A. Anderson

News and Comment

High-fat diet depletes skin t reg cells.

A study in Immunity reports that a high-fat diet in mice leads to the loss of PPARγ + T reg cells in the skin, which exacerbates psoriasis mediated by IL-17-producing γδ T cells.

• Kirsty Minton

A protective role for epidermal S100A9 in PsA

A new study uncovers a protective role for epidermal S100A9 in psoriasis and psoriatic arthritis, and highlights this alarmin as a potential biomarker of disease progression.

• Jessica McHugh

Does psoriasis treatment affect PsA development?

The results of several retrospective studies have reported that systemic treatment in patients with psoriasis reduces the risk of incident psoriatic arthritis (PsA). Although encouraging from a prevention perspective, such studies are limited in their ability to provide a conclusive understanding of PsA risk, preventing a clear picture from emerging.

• Joseph F. Merola
• Alexis Ogdie

Targeting metabolism to treat psoriasis

A crucial role for glucose metabolism has been identified in wound repair and in the pathogenesis of chronic inflammatory skin diseases, indicating that targeting metabolism is an approach for treating psoriasis.

• Paul Hiebert
• Sabine Werner

Itaconate charges down inflammation

The metabolite itaconate induces electrophilic stress that induces an antioxidant response and regulates secondary TLR transcriptional responses and IL-17-driven pathology.

• Yvonne Bordon

Old drug, new trick

The immunomodulatory drug dimethyl fumarate blocks GAPDH and aerobic glycolysis in activated immune cells.

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Clinical Trials

Displaying 9 studies

The purpose of this study is to compare the effectiveness, safety (tolerability), and duration of treatment response at 12 weeks of home versus office-based narrowband ultraviolet B phototherapy for the treatment of psoriasis.

The purpose of this study is to assess the long-term safety, tolerability, and effectiveness of secukinumab over ustekinumab for the treatment of patients who have moderate to severe plaque psoriasis.

The primary purpose of this study is to evaluate the clinical effectiveness of apremilast compared with placebo in children and adolescents (ages 6 through 17 years) with moderate-to-severe plaque psoriasis.

The purpose of this study is to survey parents or caregivers of children with psoriasis regarding their quality of life with the newly-developed Psoriasis Caregiver Impact Scale (PsoriaCIS).

This research study is being done to find out whether autoimmune mechanisms are associated with the development of atrial fibrillation.

The purpose of this study is to identify the incidence and prevalence of inflammatory arthritis in patients with Hidradenitis Suppurativa (HS) and compare them with those in patients with psoriasis through implementing a routine screening. Identifying the incidence and prevalence of this comorbidity has the potential to increase awareness across the specialties of rheumatology and comorbid diseases.

The aims of this study are to determine the frequency, severity, and duration of symptoms of arthritis in patients with HS and compare them with those in patients with psoriasis, to determine the association between inflammatory arthritis and disease flare-ups/severity ...

The purpose of this study is to develop a psoriasis-specific tool to assess the quality of life of the parents and caregivers of children with psoriasis.

The purpose of this study is to promote patient-centered care by efficiently determining the presence of quality of life issues and their relation to depression and psoriatic arthritis in psoriasis patients. Screening for quality of life, depression, and psoriatic arthritis is a standard of care for psoriasis patients.   

The purpose of this study is to identify the long-term occurrence of non-melanoma skin cancers in patients who had ultraviolet light therapy as a child in the years 1970 to 2000.

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Home / Living Well / More than skin deep with Dr. V.: Flake-free living with psoriasis

More than skin deep with Dr. V.: Flake-free living with psoriasis

Psoriasis is one of the most common skin conditions in the world.

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“I hate how my scalp psoriasis causes flaking; it looks like I have dandruff all the time. It is so itchy!” said my friend Jasmine. Topical medicines had been challenging for her to consistently use, which made her scalp and body psoriasis difficult to treat.

But now medications known as biologics are revolutionizing the treatment of psoriasis by modulating the immune system. And they are giving people like Jasmine new options for living flake-free.

What is psoriasis?

Psoriasis is one of the most common skin conditions in the world, affecting an estimated 2% to 3% of the United States population. It is a chronic and inflammatory condition that primarily affects the skin but can be associated with manifestations in other parts of the body, including the joints. This condition has a preference for the skin on the front of the knees, back of the elbows, scalp and cleft at the top of the buttocks but can occur anywhere.

Psoriasis most commonly develops in adulthood, often between ages 30 and 39 or between ages 50 and 69. Psoriasis tends to affect men and women equally. Healthcare professionals often diagnose psoriasis by a physical exam, but a biopsy of the skin may be needed.

What causes psoriasis?

Psoriasis is an autoimmune disorder. Its cause is not completely understood. The mechanism is due, at least in part, to an issue with the immune system. The hallmark of psoriasis is inflammation that drives uncontrolled production and aging of skin cells that build up into thick plaques on the skin.

Factors that play a role in an individual’s risk for developing psoriasis or worsening severity of their psoriasis include:

• Genetic predisposition.
• Alcohol use.
• Infections — Infections can rev up the immune system, which can trigger a psoriasis flare.

It is estimated that 35% of individuals who develop psoriasis have a family history of the condition. One study of twins found that in 80% of cases, if one twin had psoriasis, both did.

What does psoriasis look like?

There are multiple forms of psoriasis: plaque, erythrodermic, guttate, pustular, inverse and nail psoriasis.

Lesions develop in response to trauma at the site where the trauma occurred. This is known as the Koebner phenomenon. For this reason, psoriatic lesions can be found at the belt line, where clothing rubs or at places that are commonly bumped during daily activities.

What is plaque psoriasis? What causes scalp psoriasis?

Plaque psoriasis is the most common type of psoriasis, representing over 90% of cases of psoriasis. This type of psoriasis is characterized by well-defined raised, red lesions that are rough to the touch and topped with a fine silvery-white scale. In darker skin tones, psoriatic plaques tend to appear more brown or violet in color and are topped with gray scale. It tends to present equally on both sides of the body on the scalp, knees, elbows and between the buttocks.

Scalp psoriasis can be confused with dandruff (seborrheic dermatitis). However, there is a form of plaque psoriasis that affects individuals’ scalps. The most common complaints of scalp psoriasis include itching and flaking. Psoriasis also can cause areas of hair loss.

How do you treat psoriasis?

There is no cure for psoriasis. Therapies are individualized based on the severity of the disease, patient preferences and other concurrent conditions such as psoriatic arthritis. Treatment can be applied to the affected area (topical) or throughout the whole body (systemic). For limited or mild disease, topical therapies are used. For moderate-to-severe disease, systemic agents are more common.

 Topical therapies include:

• Moisturizers.
• Vitamin D analogs.
• Immunosuppressants.

Systemic therapies can include:

• Phototherapy (a fancy term for exposure to light).
• Oral immunosuppressants.
• Oral, infused or injected immunomodulating agents often called biologics.

Lifestyle changes also could help with scalp psoriasis. You can try:

• Washing hair more frequently.
• Frequently brushing hair to remove scale.
• Using special topical oils and ointments that contain salicylic acid to help break down built-up scale.

How are psoriasis and mood related?

The association between psoriasis and mood is startling, and reflective of the toll skin disease can take on quality of life. People with psoriasis have higher rates of anxiety and depression than those without psoriasis. Social stigmatization is commonly reported. Further, psoriasis can be severe and disabling for some individuals, even impacting their financial security. If you or a loved one are affected, connect with peers affected by psoriasis through the National Psoriasis Foundation for support.

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The Best Drugs for Psoriasis

– cochrane review synopsis ids the four most effective agents.

With so many effective biologics on the market for psoriasis and related conditions, it can be challenging to identify the best ones. A new clinical evidence synopsis covering 18 different psoriasis therapies and based on extensive data from Cochrane Reviews helps clinicians sort out the best options for their patients.

According to the synopsis, which appeared in JAMA Dermatology , the most effective drugs for psoriasis were infliximab, bimekizumab, ixekizumab, and risankizumab. No statistically significant differences in serious adverse events were identified in any of the drugs compared with placebo.

Andrew Blauvelt, MD, MBA, dermatologist and scientific consultant with Blauvelt Consulting, LLC, served as a co-author of the analysis. His exchange with the Reading Room has been edited for length and clarity.

What was the context for setting out on this analysis and what was the key question or knowledge gap it was designed to address?

Blauvelt: Cochrane Reviews are major systematic reviews that are done periodically on a given topic. They are usually massive -- in this case hundreds of pages long. I was asked to summarize the Cochrane Review, basically to make it more digestible. So it's a review of a review. The goal was to summarize and provide highlights.

Would you summarize those highlights in terms of effectiveness, adverse events, or other factors?

Blauvelt: There are 12 different biologics for psoriasis -- and that's a lot. There are a lot of data. And there are a number of different oral meds for psoriasis ... upwards of about six now, depending on if you go to Europe or the U.S. Currently, 18 medicines are available for treatment of moderate-to-severe psoriasis.

We looked at different classes as part of our review. Infliximab was considered the best TNF blocker. Bimekizumab (the newest biologic) and ixekizumab were considered the best IL-17 blockers. Risankizumab was considered the best IL-23 blocker.

Dermatologists usually pick a class of drug for their patient based on not just efficacy, but whether the treatment works in, for example, psoriatic arthritis. It's not just as simple as using the best drugs. As a clinician I want to also make sure I provide the best drug for my patient.

That's why I'm emphasizing that those are the four drugs that emerged as best in class. If you're going to use a certain class of drug because of a comorbidity, like psoriatic arthritis, one would choose an IL-17 blocker. And of course, this doesn't mean that all the other drugs are bad, because the other drugs are good too. But the title of the article is "The Best Medications Emerge," so we highlighted the top performing drugs in each class.

Did anything strike you as a surprise at all as you conducted the review?

Blauvelt: There were a couple of surprises. One was that the Cochrane authors thought that the drugs were all equally safe. And I think, in general, we do not think of them as equally safe.

For example, we consider the TNF blockers -- the older biologics -- to be generally less safe than the newer IL-17 and IL-23 blockers. But that was not the conclusion of the Cochrane Review.

There also was no consideration for comorbidities. You choose a drug not just by skin efficacy, but also by what's happening with joint efficacy, depending on each individual patient.

Further, the authors only looked at data out to one year. But we know that certain drugs show a lack of clinical effectiveness beyond 52 weeks or over years of use. So that was another drawback. For example, guselkumab did not come out as one of the top four drugs, but it has been shown to be an outstanding drug in terms of durability in real-world settings. Durability is a surrogate marker for effectiveness in real-world settings. So the drug that has been shown to have the best durability beyond one year did not come out on top in this analysis.

What are your key take-away messages for dermatologists?

Blauvelt: One of the bottom-line messages is that we have an embarrassment of riches in terms of highly effective and highly safe treatments for psoriasis. One of the things that I emphasize strongly when I'm teaching dermatologists is that there are still dermatologists practicing in the community who do not use biologics. And I think that's a travesty. How much more evidence do we need of safety and efficacy for people to finally start using biologics in their practice?

One of my theories is that there was an imprinting 20 years ago when TNF blockers came out and there were safety warnings and issues. I think some clinicians decided they were not going to use these drugs at that point and have not been paying attention to all the advancements and improvements with the IL-23 and IL-17 blockers, which have reached new heights in terms of efficacy and safety.

So I think some messages for the clinician would be that you shouldn't have any fear of using biologics for patients with psoriasis. The benefits far outweigh the risks.

Also, you should probably pick one top drug in each class if you're worried about learning about all of them. My main message is: you don't have to learn all the drugs; you don't have to learn all the data. You can look to reviews like this and then just select the best-in-class for your use in your office, so no one gets overwhelmed. Rather than get paralyzed and use nothing, practitioners can look to reviews like this to select the best-in-class drugs that have already been identified for them.

Blauvelt disclosed relationships with numerous pharmaceutical companies.

Primary Source

JAMA Dermatology

Source Reference: Blauvelt A, et al "The best psoriasis medications emerge" JAMA Dermatol 2024; DOI: 10.1001/jamadermatol.2023.4445.

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Long-term Outcomes and Prognosis in New-Onset Psoriasis

Axel svedbom.

1 Division of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

2 ICON Clinical Research, Stockholm, Sweden

Lotus Mallbris

3 Eli Lilly, Indianapolis, Indiana

Per Larsson

4 Division of Rheumatology, Department of Medicine Karolinska Institutet, Stockholm, Sweden

Pernilla Nikamo

Katarina wolk.

5 Optimuskliniken, Stockholm, Sweden

Petra Kjellman

6 Diagnostiskt Centrum Hud, Stockholm, Sweden

Enikö Sonkoly

7 Dermatology and Venereology Clinic, Karolinska University Hospital, Stockholm, Sweden

Ulla Lindqvist

8 Department of Medical Sciences, Rheumatology, Uppsala University, Sweden

Mona Ståhle

Accepted for Publication: February 23, 2021.

Published Online: April 14, 2021. doi:10.1001/jamadermatol.2021.0734

Author Contributions: Mr Svedbom and Dr Ståhle had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Larsson, Lindqvist, Ståhle.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Svedbom, Ståhle.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Svedbom.

Obtained funding: Ståhle.

Administrative, technical, or material support: Nikamo, Wolk, Kjellman, Eidsmo, Lindqvist, Ståhle.

Supervision: Lindqvist, Ståhle.

Conflict of Interest Disclosures: Mr Svedbom is an employee of ICON Clinical Research, a contract research organization. Dr Mallbris is an employee of Eli Lilly and Company. Dr Ståhle has consulting agreements involving financial compensation with Eli Lilly and Company, AbbVie, Janssen, Leo Pharma, BMS, and Novartis. No other disclosures were reported.

Funding/Support: This study was funded by the Stockholm County Council, the Swedish Medical Research Council, Hudfonden, and the Swedish Psoriasis Association.

Role of the Funder/Sponsor: The funding organizations had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Additional Contributions: We thank the pictured patients for granting permission to publish this information. We are also grateful to the patients for participating, Eva Vingård, PhD (Department of Medical Science, Uppsala University), for input on the clinical research forms, and Maria Lundqvist, BS, and Susanne Bergqvist, BS (Department of Dermatology Karolinska University Hospital), for supporting study operations.

Associated Data

eMethods. Detailed Methods

eTable 1. Treatments and Corresponding ATC Codes Used to Define Severe Psoriasis

eTable 2. PsA Status at Enrollment and Follow-up by Examination Method

eTable 3. Marker Information and Association Analyzed in Patients With a Guttate Onset vs Plaque Onset

eTable 4. Prognostic Factors for the Clinical Remission at Ten Years, Severe Psoriasis and Psoriatic Arthritis (PsA)

eTable 5. Marker Information and Association With Remission at Ten Years and Severe Disease During Follow-up Analyzed in Patients With a Plaque Onset

eTable 6. Marker Information and Association With Remission at Ten Years and Severe Disease During Follow-up Analyzed in Patients With a Guttate Onset

eTable 7. Prognostic Factors for the Development of Mild Psoriasis, Moderate to Severe Psoriasis and Psoriatic Arthritis (PsA) in Complete Case Analysis and Multiple Imputation Analysis

eFigure. Classification Trees

eReferences

What are the prognostic factors for the clinical course of psoriasis?

In this 10-year cohort study of 721 patients with recent-onset psoriasis, 52% of the patients with plaque phenotype, high disease activity, and scalp lesions developed severe disease, compared with 11% of patients with low disease activity at inclusion.

Patient characteristics at onset can help to estimate the long-term course of psoriasis with good discriminatory power.

Psoriasis is a heterogeneous disease. Improved understanding of prognosis and long-term outcomes in new-onset psoriasis may improve care.

To describe the clinical course of psoriasis and identify possible indicators of long-term outcomes.

Design, Setting, and Participants

The Stockholm Psoriasis Cohort was a noninterventional inception cohort study enrolling patients between 2001 and 2005. The present study was conducted from January 15, 2019, to February 5, 2021. At enrollment and 10 years, patients were examined by dermatologists and rheumatologists. Data from examinations were complemented by questionnaires, medical records, and registers. A total of 721 patients with recent-onset psoriasis (<12 months duration), 15 years or older were recruited using advertising and referrals from a broad range of health care settings.

Main Outcomes and Measures

Disease severity and psoriatic arthritis (PsA). Recursive partitioning and regression models were implemented to identify probable indicators of long-term outcomes.

A total of 721 patients (median [interquartile range] age, 39 [27-55] years; 405 [56%] women), including 542 (75%) with plaque-onset and 174 (24%) with guttate-onset psoriasis, were enrolled. The median follow-up was 9.6 years (interquartile range, 8.8-10.4 years). The cumulative incidence of severe psoriasis at 12 years from enrollment was 21%. Among 509 patients examined clinically after 10 years, 77 of 389 patients (20%) with plaque onset and 56 of 116 (48%) with guttate onset had minimal disease activity without treatment, and 120 of 509 (24%) had PsA. Recursive partitioning identified strata with distinct risks for severe skin disease and PsA: the cumulative incidence of severe disease in patients with plaque phenotype, above-median disease activity, and scalp lesions was 52% (95% CI, 41%-64%), compared with 11% (95% CI, 8%-14%) in patients with below-median disease activity at inclusion; and 48 of 82 patients (59%) with peripheral enthesitis had PsA after 10 years compared with 37 of 304 patients (12%) without initial joint pain ( P  < .001). Smoking (hazard ratio, 1.70; 95% CI, 1.10-2.63) and activating genes in the interleukin-23 (IL-23) pathway (odds ratio, 1.55; 95% CI, 1.14-2.11) were also significantly associated with a severe disease course. Systemic therapy at or before enrollment was associated with a lower risk for severe disease at 10 years compared with later initiation of systemic therapy (odds ratio, 0.24; 95% CI, 0.06-0.90).

Conclusions and Relevance

The findings of this cohort study suggest that combinations of clinical characteristics at onset and activating genes in the IL-23 pathway are significantly associated with the clinical course of psoriasis, whereas joint pain and peripheral enthesitis may indicate the probability of PsA. Patients within those categories merit specialist referral and closer follow-up. The possibility of modifying the disease course with early systemic intervention should be tested.

This cohort study examines the disease course in patients with psoriasis over a 10-year follow-up period to identify factors that may be used in prognosis.

Introduction

Psoriasis is a serious immune-mediated skin disease with estimated prevalence ranging from 0.1% to 11.4% worldwide. 1 Psoriasis is clinically heterogeneous, with the main phenotypes at onset being plaque psoriasis and guttate psoriasis, the latter with a more acute onset and often associated with infection. 2 , 3 , 4 The disease substantially affects both the body and psyche, and is associated with comorbidities including psoriatic arthritis (PsA), cardiovascular disease, and depression. 5

Although considerable progress has been made on the knowledge of the pathogenesis and treatment of psoriasis, our understanding of its clinical course is limited and stems from retrospective studies. 6 Therefore, prospective observational inception cohort studies that describe the clinical course of psoriasis, identify prognostic factors for disease severity, and investigate the use of early systemic treatment have repeatedly been deemed key research priorities. 6 , 7 , 8 Such data would help reduce prognostic uncertainty, facilitate identification of patients who merit closer follow-up or specialist referrals, and give insight into the possibility of disease course modification. Therefore, we set up the Stockholm Psoriasis Cohort, a 10-year prospective, inception cohort study to describe the clinical course of psoriasis, identify prognostic factors for the disease course, and explore the use of early systemic treatment on long-term outcomes.

Study Design and Oversight

The Stockholm Psoriasis Cohort was a prospective observational study of patients with recent-onset psoriasis and population-matched controls. Herein, we present findings from the analyses on the clinical course of the disease. The study was approved by the Stockholm Ethics Committee, and all patients provided written informed consent; participants did not receive financial compensation. This study followed the Strengthening the Reporting of Observational Studies in Epidemiology ( STROBE ) reporting guideline for cohort studies.

Study Population and Data Collection

Patients aged 15 years or older with their first onset of psoriasis lesions on nonhairy skin within the past 12 months were eligible. Patients were mainly recruited from the Stockholm area, Sweden, between 2000 and 2005 from dermatology clinics, general practitioners, school nurses, sexual health centers, and youth clinics. The study was also advertised in daily newspapers and in the magazine and website of the Swedish Psoriasis Association. The present study was conducted from January 15, 2019, to February 5, 2021.

Individuals were screened via a telephone interview conducted by a dermatologist or a study nurse. Patients who were deemed to fulfill the study inclusion criteria were examined by 2 dermatologists (L.M. and M.S.) and patients with a clinically convincing diagnosis were included. Because the study was limited to new-onset psoriasis, individuals with a history of skin lesions compatible with psoriasis were excluded.

Clinical examinations were performed using standardized forms at enrollment and at 10 years. Patients with subjective joint problems were seen by a rheumatologist (P.L.) for comprehensive joint examination. Relevant patients were also seen by another rheumatologist (U.L.) at 10 years for a similar joint examination. Information from the examinations was combined with medical records, data on outpatient and inpatient care from the National Patient Register, 9 prescriptions from the Prescribed Drug Register, 10 and death and emigration from the Total Population Register. 11

The data collected have been described in detail. 12 In brief, psoriasis phenotypes and clinical manifestations were classified according to established terminology. 13 Plaque psoriasis comprised nummular and large plaque types and guttate psoriasis was defined as acute onset of small, coin-like lesions. Family history of psoriasis and potential precipitating factors, including infection, defined as acute symptoms requiring anti-infective treatment within 10 days of onset of psoriasis, and stressful life events, defined as events with a profound effect on the patients within 2 months of disease onset, were elicited. The rheumatologic examinations included evaluation of the presence of arthrosynovitis, tenosynovitis, axial enthesitis, peripheral enthesitis, dactylitis, and tender and swollen joint counts.

Outcomes and Covariates

Skin disease severity was measured using the Psoriasis Area Severity Index (PASI) and the static Physician’s Global Assessment (s-PGA). 14 , 15 The PASI evaluates 4 body regions (head, trunk, upper extremities, and lower extremities) for erythema, induration, and scaling. Scores range between 0 and 72, with higher scores denoting more severe disease. The s-PGA describes severity on a 7-point scale, ranging from 1 (clear) to 7 (severe). 15

Disease severity at clinical examinations was defined using combinations of current treatment and the PASI score: complete remission (free of lesions and no treatment for 2 years), minimal disease activity (0 ≤ PASI < 1 without treatment), mild disease (1 ≤ PASI < 5 or topical treatment), moderate disease (5 ≤ PASI < 10 or phototherapy), or severe disease (PASI ≥ 10 or systemic treatment). Given that treatment with systemic agents is a valid marker for psoriasis disease severity in observational research, 16 the first instance of severe disease was defined as the first event consistent with severe psoriasis: a filled prescription of systemic treatment for psoriasis (from the Prescribed Drug Register, eTable 1 in the Supplement ) or a PASI score exceeding 10 at clinical examination.

In patients examined rheumatologically, the presence of inflammatory joint disease was assessed according to criteria of the Swedish Psoriatic Arthritis Register. 17 Patients with inflammatory joint disease were classified as having PsA if they fulfilled the CASPAR criteria 18 unless the joint symptoms had another apparent cause. No radiographs were available; therefore, evidence of juxta-articular new bone formation was excluded from the assessment of CASPAR in this study, albeit patients still had to have a score of 3 on the CASPAR tool to be classified as having PsA. Because CASPAR was not available at the time of enrollment examinations, data from enrollment were re-evaluated for conformity in classification between the examinations. Patients who reported joint pain but elected not to see the study rheumatologist were assessed for the presence of PsA using an algorithm combining information from the dermatologic examination, medical records, and the National Patient Register (eMethods and eTable 2 in the Supplement ).

Indicators of severe disease, minimal disease activity, and PsA included the following variables measured at enrollment: sex, age, smoking (current vs never or former smoker), body mass index, nail involvement, scalp lesions, joint pain, infection precipitation, s-PGA level, and peripheral enthesitis. Furthermore, 21 genetic variants were included in analysis of skin disease severity and phenotype based on their potential role in the disease or its treatment as described. 19

Early systemic treatment was defined as systemic treatment at or before enrollment. Later systemic treatment comprised systemic agents initiated thereafter until the 10-year examination. Time to initiation of systemic therapy was stratified into quartiles: initiation before or at enrollment and initiation in the first, second, or third tertiles of follow-up.

All enrolled patients (cohort A) were included in analyses of baseline characteristics and development of severe psoriasis. All other analyses were conducted on patients who participated in the 10-year examination (cohort B).

Statistical Analysis

Comparisons among groups were conducted using χ 2 tests for categorical variables. Relative risks (RRs) were derived using binomial generalized linear models with a log link function. Time-to-event analysis was implemented to estimate the cumulative incidence of severe disease.

To identify subgroups with distinct risks for developing mild disease, severe disease, and PsA, recursive partitioning analyses were implemented using hypothesized clinical predictors and baseline phenotype as covariates (eMethods in the Supplement ). The resulting models were internally validated with C-indices excluding ties on predictor groups. To further explore clinical factors that indicate the probable disease course, univariate and multivariable models stratified by onset phenotype were implemented. Cox proportional hazard regression models were fitted to assess predictors of severe disease and logistic regression models were fitted to assess predictors of minimal disease activity and PsA at 10 years. For the genetic markers, we tested for allele frequency differences for all single nucleotide variants using logistic regression, with sex and age as covariates and without adjustments for multiple testing.

The proportions of patients with severe disease at the 10-year clinical examination stratified by early and late systemic treatment were compared using a χ 2 test and logistic regression controlling for the variables that were found to be significantly associated with development of severe psoriasis in the multivariable analysis described above. Sensitivity analyses using multiple imputation of missing data, including end points were performed to explore the potential impact of loss to follow-up and missing predictors (eMethods in the Supplement ).

Analyses were implemented in R, version 3.4.2 (R Foundation for Statistical Computing) for recursive partitioning analyses, Stata, version 14.2 (StataCorp LLC) for multiple imputation, and SAS, version 9.2 (SAS Institute Inc) for all other analyses.

In total, 765 individuals were examined clinically. Forty-three patients were excluded owing to uncertain diagnosis or erroneous personal identification numbers. Hence, 721 participants were included in the study (cohort A); of these, 405 patients (56%) were women and 316 (44%) were men; median age was 39 years (interquartile range [IQR], 27-55 years). All patients in cohort A were followed up using administrative registers and electronic medical records. During follow-up, 35 participants died. Among the 686 patients alive at 10 years, 177 (26%) did not participate in the follow-up; 509 (74%) were interviewed and examined clinically (cohort B). Median time from onset to enrollment was 6 months (IQR, 3-10 months) and median time from enrollment to the 10-year examination was 9.6 years (IQR, 8.8-10.4 years).

Disease Onset and Course

The number of patients with plaque phenotypes at onset was 542 (75%); guttate, 174 (24%); and other phenotypes, 5 (1%). Baseline characteristics for patients with plaque and guttate onset are presented in the Table . We found 4 genetic variants associated with guttate onset, IL13 (rs20541), IL12B (rs3212227), HLA-C*06 , and NFKBIL1 (rs2255798) (eTable 3 in the Supplement ).

Abbreviations: BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); IQR, interquartile range; PASI, Psoriasis Area Severity and Severity Index; s-PGA, static Physician Global Assessment Index.

Among the 389 patients with plaque onset who were examined clinically at 10 years (cohort B), 346 (89%) retained plaque phenotype, 13 (3%) had nonplaque phenotypes, and 30 (8%) were in complete remission. Among the 116 patients with guttate onset in cohort B, 75 (65%) had plaque phenotype at 10 years, 4 (3%) had nonplaque phenotypes, and 37 (32%) were in complete remission.

Disease severity at onset and 10 years in cohort B are presented in Figure 1 . In 389 patients with plaque onset, the proportion of patients with severe disease increased from 7% (n = 27) at onset to 12% (n = 45) at 10 years ( P  = .02) ( Figure 1 A). Conversely, in 116 patients with guttate onset, the proportion of patients with severe disease decreased from 19% (n = 22) at onset to 4% n = 5) at 10 years ( P  < .001) ( Figure 1 B). Among the 50 patients with severe disease at the 10-year clinical examination, 22 had a PASI score greater than or equal to 10, and 10 of those did not receive previous systemic treatment for moderate to severe psoriasis. At the 10-year clinical examination 77 of 389 patients (20%) with plaque onset and 56 of 116 patients (48%) with guttate onset had minimal disease activity; 120 of 509 patients (24%) had developed PsA.

Distribution of disease severity at enrollment and at 10 years in patients with plaque-onset (A) and guttate-onset (B) psoriasis. The transparent fields between the bars illustrate the flow of patients between disease severity categories at enrollment and the 10-year clinical examination.

Among patients with plaque onset, 11 of 27 (41%) individuals with severe disease at onset had severe disease at 10 years compared with 34 of 362 (9%) patients with mild or moderate disease at onset (RR, 4.3; P  < .001). Conversely, 59 of 253 (23%) patients with mild disease at onset had minimal disease activity at 10 years compared with 18 of 136 (13%) patients with moderate or severe disease at onset (RR, 1.8; P  < .001). Among patients with guttate onset, 4 of 22 (18%) of those with severe disease at onset had severe disease at 10 years compared with 1 of 94 (1%) patients with mild or moderate disease at onset ( P  = .001). There was no significant association between disease severity at onset and minimal disease activity at 10 years in patients with guttate onset. Among the 721 patients enrolled in the study, the estimated cumulative incidence of severe psoriasis at 12 years from enrollment was 21% in all patients, 23% in patients with plaque phenotype, and 13% in patients with guttate phenotype at onset. The prevalence of PsA increased from 18% (69 of 389) to 26% (102 of 389) in patients with plaque onset ( P  < .001) and from 4% (5 of 116) to 14% (16 of 116) in those with guttate onset ( P  = .02).

Prognostic Factors and Outcomes

Examples of the benign and severe disease course are presented in Figure 2 . In patients with plaque onset, male sex, high s-PGA score, scalp lesions, smoking, and an IL23R genotype increased the risk of severe disease (eTable 4 and eTable 5 in the Supplement ). The same factors decreased the probability of minimal disease activity at 10 years, whereas previous infection and an NKBIA genotype increased the probability of minimal disease activity (eTable 4 and eTable 6 in the Supplement ). In patients with guttate onset, older age, high s-PGA score, an IL12B genotype, and lack of the HLA-C*06 genotype increased the risk of severe disease (eTables 4 and 5 in the Supplement ), whereas previous infection, no scalp lesions, and an LCE genotype increased the probability of minimal disease activity at 10 years (eTables 4 and 6 in the Supplement ). Joint pain and peripheral enthesitis at enrollment increased the risk of PsA at 10 years in both plaque and guttate onset. Coefficients from models based on multiple imputation data did not differ substantially from the main analyses (eTable 7 in the Supplement ).

A patient with mild plaque psoriasis at onset (A) and severe disease at follow-up (B). A patient with severe guttate psoriasis at onset (C) and minimal disease activity (D) at follow-up.

Recursive partitioning analyses identified 3 subgroups with distinct risks for development of severe psoriasis, mild disease, and PsA ( Figure 3 and eFigure in the Supplement ). For severe disease, patients with an s-PGA score exceeding 3 at enrollment with nonguttate phenotypes and scalp lesions had the highest risk of severe disease, with an estimated 12-year cumulative incidence of 52% (95% CI, 41%-64%), compared with 11% (95% CI, 8%-14%) for patients with an s-PGA score of 3 or below at enrollment. Patients with guttate onset had the highest probability of having minimal disease activity at 10 years: 49% (57 of 116) compared with 33% (59 of 177) in patients with nonguttate onset without scalp lesions, and 11% (23 of 216) among those with nonguttate onset and scalp lesions. Patients with peripheral enthesitis at enrollment were more likely to have PsA at 10 years: 59% (48 of 82) compared with 25% (24 of 97) of those with self-reported joint problems but no enthesitis, and 12% (37 of 304) of those patients without self-reported joint pain. The C-indices for the models were 0.794 for severe disease, 0.821 for mild disease, and 0.794 for PsA.

Cumulative incidence of severe disease beyond 10 years (A), proportion of patients with minimal disease activity at 10 years (B), and proportion of patients with psoriatic arthritis at 10 years. For panel A, group 1, the static Physician Global Assessment Index (s-PGA) was ≤3; for group 2, s-PGA was >3 in guttate onset or s-PGA was >3 in nonguutate onset without scalp lesions; for group 3, s-PGA was >3 in nonguttate onset with scalp lesions. For panel B, group 1 was the guttate onset; group 2 was nonguttate onset without scalp lesions; and group 3 was nonguttate onset with scalp lesions. For panel C, group 1 was no joint pain; group 2 was joint pain but no enthesitis; and group 3 was enthesitis. eTable 5 in the Supplement presents further details.

In total, 66 patients initiated systemic treatment before the 10-year examination. Patients who initiated systemic therapy at enrollment or before were less likely to have severe disease at the 10-year clinical examination (6 of 16 [38%]) compared with patients who initiated systemic treatment thereafter (33 of 50 [65%]) ( P  = .04). The differences remained significant after adjustments for s-PGA score, smoking, PsA, and scalp lesions at enrollment (odds ratio, 0.24; 95% CI, 0.06-0.90). The proportions of patients with severe disease at the 10-year examination stratified by timing of the systemic therapy initiation are presented in Figure 4 .

Error bars indicate exact binomial 95% confidence limits.

This inception cohort study of 721 participants with recent onset psoriasis found that plaque psoriasis exhibited a notable persistence in its overall disease course from onset. Forty-eight percent of the participants with severe disease at onset had severe disease at the 10-year clinical examination compared with 14% of participants with mild or moderate disease at onset (RR, 4.3; P  < .001). Guttate-onset psoriasis had a favorable prognosis, with 48% of the patients having minimal disease activity at 10 years. In addition, 20% of participants with plaque-onset psoriasis had minimal disease activity without treatment at 10 years. The prevalence of PsA increased from 18% to 26% in participants with plaque onset and from 4% to 14% in participants with guttate onset.

Based on disease characteristics at onset, the study identified subgroups with an elevated risk of developing severe psoriasis or PsA. Participants with greater than mild symptoms (s-PGA score >3), plaque phenotype, and scalp lesions were almost 5 times more likely to develop severe psoriasis than participants with mild symptoms or less (s-PGA score ≤3) at enrollment (52% vs 11%; P  < .001). Similarly, participants with peripheral enthesitis were more than 4 times more likely to have PsA at 10 years compared with participants without self-reported joint pain (59% vs 12%; P  < .001).

The study also found that participants who initiated systemic therapy at or before enrollment were less likely to have severe disease at the 10-year clinical examination (6 of 16 [38%]) compared with participants who initiated systemic treatment thereafter (33 of 50 [65%]) ( P  = .04).

To our knowledge, this is the first study that has enrolled participants with recent-onset psoriasis and followed them prospectively over an extended period; therefore, comparable studies may not exist. However, the study supports the notion that guttate psoriasis has a fairly favorable prognosis. 20 The factors for the probability of severe disease for participants with plaque-onset psoriasis in this study included scalp psoriasis, smoking, sex, and an IL23R single nucleotide variant and partially corroborates previous cross-sectional and retrospective studies. 19 , 21 , 22 The finding that the same factors decrease the probability of minimal disease activity at 10 years strengthens the notion that these factors are important for the disease course. In line with previous research, subjective joint pain and peripheral enthesitis were associated with the development of PsA. 23 , 24 However, in contrast to previous findings 25 nail manifestations were not statistically significant indicators for probable development of PsA.

Strengths and Limitations

The study was designed to describe the clinical course of psoriasis and identify prognostic factors; it was therefore suited to address these objectives. The inception cohort design removed recall and survivorship biases, enabling accurate description of the disease course and the prognosis at onset. The comprehensive recruitment strategy should render the study participants broadly representative of the population with recent-onset psoriasis. Clinical examination of all participants by a specialist dermatologist ensures diagnostic accuracy and minimizes misclassification bias. Low attrition rates and data linkage to population-based registers facilitate accurate estimates of the long-term outcomes.

The study has limitations. As with all non–population-based observational research with less than complete follow-up, there may be selection and attrition bias. There is a risk of chance findings given that we explored multiple outcomes, especially in the analysis of genetic variants. Radiographs were not available for the assessment of PsA, resulting in a potential underestimation of PsA prevalence. However, any underestimation would be limited given that CASPAR requires only 1 criterion (ie, negative rheumatoid factor, nail lesions, or dactylitis) to classify individuals with psoriasis and inflammatory joint pain as having PsA. Even though patients were recruited within 1 year of the first onset of psoriasis, several patients were treated before enrollment, influencing the measure of baseline disease severity. The Prescribed Drug Register only contains data on dispensed prescriptions; therefore, a prescription for a systemic agent for treatment of psoriasis that was never filled would not be included in the definition of severe disease, resulting in a potential underestimation of the cumulative incidence of severe disease. Furthermore, the Swedish population is mostly of White race, potentially affecting generalizability.

Conclusions

The findings from this study contribute to the knowledge about the disease course of psoriasis, reducing prognostic uncertainty. In the light of the persistent nontreatment and undertreatment of both psoriasis and PsA, 26 the identified subgroups with elevated risk for severe skin disease and PsA merit close follow-up or specialist referrals to facilitate timely and appropriate intervention. Our study also suggests that early systemic intervention may be beneficial for the long-term prognosis of psoriasis, supporting a long-standing notion in dermatology practice. 27 However, the number of individuals in the analyses was limited and treatment was not randomized. Therefore, causality cannot be determined and this finding should be tested in randomized clinical trials.

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Accelerometry in Follow up of Arthritis - a Pilot Study

This is a proof-of-concept study. The main goal is to evaluate if the accelerometry signal recorded from patients with arthritis in different disease activity stages, allows for assessment of the activity status. It will also be analysed if the accelerometry signal can be classified as registered in arthritis patients vs. registered in healthy control. Arthritis subjects will be recruited from the outpatients' clinic of the Rheumatology Department Helse Førde, Førde, Norway. Healthy control subjects will be recruited from the same administrative area as the patients and will be invited to participate via announcement on the Helse...

A Clinical Study of ICP-488 in Healthy Subjects and Patients With Psoriasis

This is a Randomized, Double-Blind, Placebo-Controlled, Parallel Group, Single and Multiple AscendingDose Phase I Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of ICP-488 in Healthy Subjects and Patients With Psoriasis

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This project is divided into a single dose escalation and a multiple dose escalation phase Ia clinical study. This is a single-center, randomized, double-blind, placebo-controlled study to evaluate the safety, tolerability, and pharmacokinetic characteristics of TQH2929 injection in healthy adults.

A Clinical Study to Compare the Safety and Pharmacokinetics of SHR-1314 Injection in Healthy Subjects at Different Specifications Devices

The purpose of this study is to evaluate the safety and pharmacokinetics of SHR-1314 injection in healthy subjects at different specifications devices.

A Clinical Study to Evaluate the Efficacy and Safety of Subcutaneous JS005 Injection in the Treatment of Adults With Moderate to Severe Chronic Plaque Psoriasis

This is a multicenter, randomized, double-blind, parallel, placebo-controlled Phase III clinical study to evaluate the efficacy and safety of JS005 in 702 adult patients with moderate-to-severe chronic plaque psoriasis

A Clinical Trial of TQH3906 Capsules in Healthy Volunteers

This study was divided into three parts: single and multiple dosing and food effect study, which were designed to evaluate the safety and tolerability of TQH3906 capsules administered in single or multiple dose escalation in healthy adult subjects.

Adjusted Brodalumab Dose Compared With Standard Brodalumab Dose in Subjects With Moderate-to-severe Plaque Psoriasis and ≥120 kg Body Weight

This study investigates if an adjusted brodalumab dosage regimen will give improved efficacy in psoriasis in patients with a body weight of over 120 kg. The increased dosage regimen will be compared to the standard brodalumab treatment plus placebo.

A First in Human Study of AX-202 in Healthy Subjects and Patients With Psoriasis.

The first-in-human study will be performed in healthy volunteers and patients with a chronic inflammatory skin disease. The primary objective is to evaluate the safety, tolerability and pharmacokinetics of increasing doses of AX-202 infusion.

A Longitudinal Observational Study of Patients Undergoing Therapy for IMISC

TARGET-DERM is a longitudinal, observational study of adult and pediatric patients being managed for Atopic Dermatitis and other Immune-Mediated Inflammatory Skin Conditions (IMISC) in usual clinical practice. TARGET-DERM will create a research registry of patients with IMISC within academic and community real-world practices in order to assess the safety and effectiveness of current and future therapies.

A Long-term Extension Study of Ustekinumab in Pediatric Participants

The purpose of this study is to collect long-term safety data of subcutaneous (SC) ustekinumab

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Psoriasis Therapies in 2024 and Beyond

This article will highlight recently approved psoriasis therapies that will shape the 2024 treatment landscape and provide some exciting updates in the psoriasis management market this coming year and beyond.

Decades ago, psoriasis was still primarily considered a problem with hyperproliferation of the epidermis. Given the antiquated understanding of this disease pathophysiology, traditional oral immunosuppressive agents were used for moderate to severe presentations. Recent research into the pathophysiology of psoriasis has highlighted the importance of the immune-mediated nature of this very common inflammatory skin disease. There now exists a clear mechanism down to the molecular level regarding which cytokines are implicated in the pathophysiology of psoriatic disease. When considering these different molecular signaling pathways, IL-23–mediated activation of the Th17 pathway is hypothesized to be the main contributor to the inflammation seen in psoriasis. 1 Due to its important role in the pathophysiology of psoriasis, IL-23 has been referred to as the master cytokine in psoriatic disease by many clinicians and researchers. Other important cytokines include TNF-α and IL-17. The fact that biologic agents interact with a specific cytokine (such as TNF-α, IL-17, or IL-23) in a targeted manner has revolutionized the capacity to manage psoriasis compared with the era of a more generalized immunosuppression reflected by the traditional oral medications (eg, methotrexate, cyclosporine, and acitretin). This represents an improved treatment paradigm where targeted immunomodulation has resulted in a great enhancement in both safety and efficacy for the biologic agents.

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There are now more than 13 FDA-approved biologic options for moderate to severe psoriasis. Additionally, there have been new approvals for oral and topical therapies for psoriasis, including a topical first-in-class mechanism of action for psoriatic skin lesions. Given that psoriasis affects more than 7 million adults in the US, the therapeutic landscape is constantly evolving. 2 It is estimated that the psoriasis management market will be worth nearly $121 billion by the end of 2024. 3 This article will highlight recently approved psoriasis therapies that will shape the 2024 treatment landscape and provide some exciting updates in the psoriasis management market this coming year and beyond. It will also highlight how biosimilar medications will affect the field for years to come and cover new updates in the management of pediatric psoriasis.

The newest biologic agent for psoriasis, bimekizumab (Bimzelx), was approved by the FDA on October 18, 2023, for the management of moderate to severe psoriasis. Bimekizumab is unique in that it blocks both the IL-17A and IL-17F cytokines. The other IL-17 antagonists approved to manage psoriasis either only block IL-17A (ixekizumab and secukinumab) or block the IL-17 receptor (brodalumab). In findings from the phase 3 BE READY trial (NCT03410992), which studied bimekizumab in the management of moderate to severe psoriasis, 91% of 349 patients receiving this medication at 320 mg every 4 weeks achieved a Psoriasis Area and Severity Index (PASI) score of 90 compared with 1% of 86 patients receiving placebo. 4 In findings from the phase 3 BE OPTIMAL trial (NCT03895203), which studied bimekizumab in the management of psoriatic arthritis (for biologic-naive patients), significantly more patients receiving bimekizumab (44%) reached American College of Rheumatology 50% response vs those receiving placebo (10%). 5 “Head-to-head studies with bimekizumab vs currently FDA-approved biologic agents, including adalimumab, secukinumab, and ustekinumab, have highlighted the rapid onset of action of this new biologic medication. Even before the second dose, this is a significant PASI response, making this a great option for a patient whose main concern is rapid improvement with infrequent dosing compared with some competitors. Bimekizumab’s unique mechanism of action [IL-17A/F] is a novel and exciting addition to the current biologic landscape for psoriasis,” G. Michael Lewitt, MD, FAAD, a board-certified dermatologist at Rosealind Franklin-Chicago Medical School in Chicago, Illinois, said.

Pooled safety analysis from phase 2 and phase 3 showed that nasopharyngitis, oral candidiasis, and upper respiratory tract infection were the most common treatment-emergent adverse events reported with bimekizumab. IL-17 is involved in mucosal host defenses against fungal infections; therefore, anti–IL-17 biologics can be associated with an increased risk of oral mucocutaneous candidiasis. 6 Of the patients in the phase 2/3 trials, 15.4% reported an oral candidiasis event in the first year and 9.1% reported it during the second year. These rates are higher when compared with the other IL-17 antagonists.

Although not considered a new biologic, adalimumab will greatly affect the 2024 psoriasis treatment landscape because generic versions are approved for the management of adult plaque psoriasis. These include the 9 following FDA-approved agents: adalimumab-aacf (Idacio), adalimumab-fkjp (Hulio), adalimumab-adbm (Cyltezo), adalimumab-bwwd (Hadlima), adalimumab-adaz (Hyrimoz), adalimumab-aaty (Yuflyma), adalimumab-aqvh (Yusimry), adalimumab-afzb (Abrilada), and adalimumab-atto (Amjevita). 7 According to the FDA, biosimilars must prove bioequivalence and be tested by way of clinical trials to ensure they will exhibit no significant differences to their parent product. 8

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Suffering from psoriasis? Blame this trio of proteins

New study shows there may be a way to help even more psoriasis patients.

About 7.5 million Americans suffer from psoriasis, an autoimmune disease that shows up as patches of red, inflamed skin and painful, scaly rashes. Although there are effective treatments for psoriasis, not everyone responds to these therapies -- and for many, the relief is temporary.

"These therapies don't reduce disease by 100 percent, and they don't cure the disease" says La Jolla Institute for Immunology (LJI) Professor Michael Croft, Ph.D. "And if you take patients off those drugs, the disease almost always comes back."

Now Croft and his team in LJI's Center for Autoimmunity and Inflammation have discovered how a key protein called TWEAK damages skin cells in psoriasis patients. Their findings, in mice and with human skin cells, suggest targeting TWEAK may help control the disease

"We think TWEAK might be considered a potential target for the treatment of psoriasis," says Rinkesh Gupta, Ph.D., a postdoctoral fellow at LJI and first author of the new Science Immunology study. "It's good to have this chance to develop a new therapeutic option."

The findings build on the Croft Lab's previous work showing that TWEAK can interact with the most common type of skin cell, called a keratinocyte. By investigating TWEAK-deficient mice, the researchers found that TWEAK is a driver of inflammation in a model of psoriasis.

The new study shows that TWEAK does not work alone. By studying human keratinocytes, the researchers discovered that TWEAK teams up with two other proteins, called tumor necrosis factor (TNF) and interleukin-17 (IL-17), to trigger inflammation. This trio appears to control the production of inflammatory molecules and the expression of additional inflammation-associated proteins in patients with psoriasis.

"The fact that they work together suggests the disease is essentially driven by all three of those particular proteins at the same time," says Croft. "The primary implication is that TWEAK will also be a good drug target. as has already been proven for TNF and IL-17."

To test this, the researchers used a mouse model of psoriasis to compare how well a TWEAK-inhibitor measured up to therapies inhibiting IL-17 or TNF.

The results suggest the team is on the right track. "If you inhibit TWEAK from working on its receptor on keratinocytes, you get the same therapeutic effect as when you inhibit TNF or IL-17," says Gupta. This finding is especially encouraging because TNF and IL-17 are both FDA-approved drug targets for psoriasis.

Although human clinical trials remain to be done, Croft sees a future for TWEAK inhibitors as therapies for many types of skin diseases. "We think TWEAK is involved in skin inflammation in general," says Croft.

His lab is now investigating the role of TWEAK in atopic dermatitis, also called eczema, a very common type of skin inflammation, especially in babies and young children. Croft says while psoriasis and atopic dermatitis are distinct diseases, they do have a few things in common -- and there are not as many good treatments for atopic dermatitis.

"There's certainly a lot of room for improvement in treatment of atopic dermatitis patients," he says.

The study, "TWEAK functions with TNF and IL-17 on keratinocytes and is a potential target for psoriasis therapy," was supported by the National Institutes of Health (grant AR072640).

Additional study authors include Donald T. Gracias, Daniela Salgado Figueroa, Haruka Miki, Jacqueline Miller, Kai Fung, Ferhat Ay and Linda Burkly.

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Story Source:

Materials provided by La Jolla Institute for Immunology . Original written by Madeline McCurry-Schmidt. Note: Content may be edited for style and length.

Journal Reference :

• Rinkesh K. Gupta, Donald T. Gracias, Daniela Salgado Figueroa, Haruka Miki, Jacqueline Miller, Kai Fung, Ferhat Ay, Linda Burkly, Michael Croft. TWEAK functions with TNF and IL-17 on keratinocytes and is a potential target for psoriasis therapy . Science Immunology , 2021; 6 (65) DOI: 10.1126/sciimmunol.abi8823

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Strange & offbeat.

Plaque psoriasis plagues Marietta man for over 30 years until new treatment

A breakthrough in plaque psoriasis.

It causes itchy, raised patches of skin that look and feel uncomfortable, but a Cobb County man believes he may have found a breakthrough.

MARIETTA, Ga. - Greg Morrison of Marietta has been living with plaque psoriasis for more than 30 years.

"The rash, it itches constantly," Morrison says. "It flakes. It kind of pinches you, and then your skin feels too tight. It's not, like, super intense pain, but it's just irritating. It's hard to sleep."

Dr. Jamie Weisman of Medical Dermatology Specialists is Morrison's dermatologist.

"He's a person who had a really high amount of psoriasis," Weisman says. "Almost half of his body was covered, and it was thick, and it was angry, and you can't hide it."

Dr. Weisman says plaque psoriasis is an autoinflammatory skin disease that tends to hit people in adulthood, but can affect just about anyone.

What is psoriasis?

"So, classically, psoriasis has these red scaly plaques, and they're really well-defined," she says.  "You can see where they begin and end. It likes the scalp. It likes the elbows, it likes the knees."

About 30% of people also develop psoriatic arthritis.

"And it doesn't have to correlate with the severity of the rash," Dr. Weisman says. "You can have very mild skin disease and really crippling psoriatic arthritis, and you can be covered head to toe with psoriasis and have no joint pain at all."  

Morrison had both the skin rash and joint pain.

"We would find prescriptions that were great for my skin or great for my arthritis, but we couldn't find one that was doing really good things for both," he says.

Plaque psoriasis treatment shows promise

But about four months ago, he had a breakthrough. Morrison started receiving injections of a newly FDA-approved monoclonal antibody, Bimzelx, which Weisman helped study in clinical trials.

It is designed to block two naturally occurring proteins in the body thought to trigger the inflammation and swelling driving psoriasis.

"So, targeting both interleukin 17A and interleukin 17F really saturates that pathway both in the bloodstream and in the skin," Weisman explains.

The safety and efficacy of Bimzelx were evaluated in two clinical trials involving 839 adult patients with moderate to severe plaque psoriasis.

The manufacturer, UCB, says in combined clinical studies, nearly 90% of people saw 90% clearer skin 16 weeks into treatment.

And, Weisman says, the treatment works quickly, sometimes after the first injection.

"For patients, it's so reassuring when they see the response to know that they've chosen correctly, chosen the right medicine: 'Right, This is working. My psoriasis is going away after just that first injection,'" she says.

Greg Morrison says this is the first treatment that seems to be helping both his skin and his joint pain.

This is the first time since I developed the arthritis that I've been good with both," he says. "So, she was kind of like, 'This drug may be actually made just for you!"

Bimzelx impacts the immune system and can reduce the body's ability to fight off infection.

Side effects of the treatment can include upper respiratory tract infections, headache, herpes simplex infections (cold sores in or around the mouth), small red bumps on the skin feeling tired, fungal infections (oral thrush or infections in the mouth, throat, skin, nails, feet, or genitals), pain, redness, or swelling at the injection site, stomach flu (gastroenteritis), and acne, according to the Food and Drug Administration

The agency says Bimzelx has also been associated with suicidal thoughts and behavior, infections, liver laboratory abnormalities, and inflammatory bowel disease.

The FDA notes patients on Bimzelx should not receive live vaccines.

NPF Selects Three Youth Ambassador Scholarship Recipients

April 11, 2024 – Alexandria, VA

Three dedicated National Psoriasis Foundation (NPF) Youth Ambassadors have been selected to receive scholarships to support their post-secondary education. Each scholar will receive $1,000 as a result of an application and evaluation process that included an essay and a review of their participation in the NPF Youth Ambassador program.

The NPF Youth Ambassadors program was launched in 2016. It fosters opportunities for youth to engage with others who have psoriatic disease and serve as leaders in the community. NPF Youth Ambassadors act as role models to help peers manage and take control of their disease and inspire others with psoriatic disease to lead confident and fulfilling lives.

The 2024 Youth Ambassador Scholarship Recipients

• Zoe Roman is a junior at Boston University in Boston, Massachusetts. She is from Boca Raton, Florida. Zoe is an international relations major with a focus on regional politics and cultural anthropology. After graduation, she plans to participate in international patient advocacy to give patients like her a voice. Eventually, her goal is to work for the United Nations in issues of health and health care.
• Lena Oslund is a junior at Michigan State University in East Lansing, Michigan. She is from Lansing, Michigan. Lena is majoring in molecular genetics and genomics. She anticipates a gap year after graduation when she will focus on clinical hours as she applies to physician’s assistant programs.
• Emme Rooney is a sophomore at DePauw University in Greencastle, Indiana. She is from Sellersburg, Indiana. Emme currently plays on the women's basketball team at DePauw University, where she majors in global health on the pre-law pathway. 

“The Youth Ambassador program empowers youth living with psoriatic disease by joining them with peers, offering guidance and education around community engagement, and providing leadership opportunities,” said Audrey Riggs, NPF Volunteer Services Manager, who manages the program. “These three youths embody the ideals of the program. NPF is proud to support them in their next steps.”

“Psoriasis and NPF have had a major impact on my decision to go into medicine,” says Lena Oslund. “When I was younger and first diagnosed, I didn't feel very supported by my medical providers since we got a lot of ‘I don't really know’ from them, but NPF was there with answers. I want to go into medicine to bridge that gap and support young patients the way that I wanted to be.” 

The National Psoriasis Foundation congratulates these three worthy scholarship recipients on their selection as the 2024 awardees.

Learn more about the NPF Youth Ambassador program .

About the National Psoriasis Foundation

Serving the community of people impacted by psoriatic disease for more than 55 years with patient support, advocacy, research, and education, the National Psoriasis Foundation is the leading nonprofit representing individuals with psoriasis and psoriatic arthritis. The mission of NPF is to drive efforts to cure psoriatic disease and improve the lives of more than 8 million individuals in the United States affected by this chronic immune-mediated disease. Learn more at psoriasis.org.

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