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Psoriasis Academy
Declaration of sponsorship Almirall S.A

Psoriasis Treatment

Declaration of sponsorship Almirall S.A
Read time: 210 mins
Last updated:26th May 2022

Learn about the inflammatory pathways involved in disease initiation and progression and the latest updates on treatments for moderate-to-severe psoriasis, including:

  • Psoriasis pathophysiology in our expert interview with Professor Stefano Piaserico
  • Key clinical trial results of available systemic and biologic treatments
  • Recent long-term efficacy and safety data with Professor Diamant Thaçi
In This Section

Treatment goals for psoriasis

How important is maintenance of response to patients with psoriasis?


Psoriasis is a chronic systemic inflammatory condition, with long-term systemic maintenance therapy recognised as the preferred method of clinical management. Greater understanding of the inflammatory and immunological pathways involved in psoriasis has led to the development of many targeted psoriasis treatments1–8.

Many people with psoriasis express frustration and dissatisfaction with their treatment because of a failure to achieve their treatment goals and long-term control9

This is especially true for people with moderate-to-severe psoriasis who experience a high impact on quality of life, long absences from work, and require frequent inpatient care9. In cases of high disease activity, continual treatment is the preferred option over switching of therapies9. Data from long-term clinical studies could therefore be a valuable guide for determining treatment goals.

Clinically meaningful goals for psoriasis

Several factors should be taken into account when establishing treatment goals for systemic therapy in people with moderate-to-severe psoriasis, including disease severity, the coexistence of psoriatic arthritis (PsA) or other comorbidities, physical impact, psychological and social well-being, and the risk–benefit ratio of continuous systemic treatment1–8.

A person-centred approach to care requires therapeutic decisions to align with patients’ needs and goals for treatment. In people with moderate-to-severe psoriasis, the desired treatment goals can be wide-ranging and go beyond merely achieving skin clearance10.

An analysis of the German Psoriasis Registry (PsoBest), that aimed to establish important treatment goals for patients receiving systemic treatment, found that, in addition to symptom reduction, patients desired a normal everyday life and treatment that did not constitute an additional burden (N=3,066)10.

Greater clearance also translates to greater patient satisfaction; however, effective treatment of psoriasis may lead to a lower level of disease that can be tolerated11. As a consequence, discontinuation of treatment following an initial success can also lead to a worsening of quality of life11.

How important is maintenance of response to people with psoriasis?

Learn about the importance of maintaining treatment response for improving the social, environmental, and occupational quality of life of patients.

Even small recurrences of psoriasis can have a disproportionately large impact on quality of life in patients with psoriasis12. This may also be true of drug dose reduction following initial treatment success13.

This highlights the importance of avoiding unnecessary switching and recognising patient expectations for long-term control and improved quality of life in order to develop and reach achievable clinical goals. Failure to do so could also be a contributing factor to the lower adherence to treatment in psoriasis compared to other chronic conditions11.

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Inflammatory pathways in psoriasis

Psoriasis is more than a dermatological disorder. It is a chronic immune-mediated disease in which genetically susceptible individuals develop cutaneous inflammation and keratinocyte hyperproliferation13,14.

Psoriasis is associated with epidermal thickening and keratinocyte hyperproliferation. As a result, the skin becomes inflamed and has raised plaques with silvery scales, which can cover large areas of the body13,14,15.

Clinical course

The clinical course of psoriasis can be divided into two stages: an initiation phase and a maintenance phase that perpetuates the inflammatory state16. This separation may be helpful when considering treatments that act in the trigger phase and those that block the self-perpetuating cycle of inflammation17. 

The histological features of psoriasis include epidermal (keratinocyte) hyperplasia, leukocyte infiltrates and an increased number of leaky vessels in the dermis of the skin. Notably, lymphoid-like tissues have also been identified in the psoriatic plaques17.

Psoriasis pathophysiology

Figure 3. Psoriasis pathophysiology (Adapted from Palfreeman et al15).

Initiation phase

An interplay between environmental and genetic factors facilitates disease-initiating events and the initiation of the complex and dynamic psoriatic cascade within skin and immune cells13. 

Introduction to Psoriasis Pathophysiology – Professor Stefano Piaserico

Find out more about the basics of psoriasis pathophysiology in this brief, yet highly informative introductory video from Professor Stefano Piaserico.

The histological features of cutaneous psoriasis are due to the interactions between T cells, dendritic cells and keratinocytes, giving rise to sustained inflammation in the skin (Figure 4)17,18. It is now well accepted that T cells, particularly T helper (Th) 17 lymphocytes, play an important role as effector cells in the pathogenesis of psoriasis16,19.

Early events in psoriasis involve the following steps18:

  • Skin insults activate dendritic cells (DCs) through pattern recognition receptors (PRRs) or cytokines interleukin 1 (IL-1), TNFα and IL-36. Meanwhile, a subset of DCs called plasmacytoid dendritic cells (pDCs) that typically mount a type 1 interferon (IFN) response to viral/microbial DNA have also been implicated in psoriasis
    • Research has suggested that combination of self-DNA with an antimicrobial peptide called LL37 (also called CAMP) can lead to a pDC-mediated immune response against self-DNA and subsequent activation of T cells. Infiltration of psoriatic skin has been observed for pDCs and it has been hypothesised that skin damage and subsequent release of self-DNA can lead to local pDC activation and drive autoimmunity and inflammation in psoriasis20
  • Activated DCs produce IL-23, which activates T cells and innate lymphoid cells (ILCs) to produce TNFα, IL-17 and IL-22
    • IL-22 induces keratinocyte hyperproliferation
    • TNFα and IL-17 activate DCs and keratinocytes, leading to up-regulation of adhesion molecules by the skin epithelium, angiogenesis and chemokine production
    • IL-17–induced chemokines CXCL1 and CXCL8 which recruit neutrophils
  • IL-17R engagement by keratinocytes leads to production of CCL20, which attracts more circulating CCR6+ γδ T cells and ILCs. This escalates into a self-amplifying inflammatory loop that can also be mediated by the adaptive immune system18

Initiation of psoriasis

Figure 4. Initiation of psoriasis (Adapted from Becher et al18).
CCL20, chemokine ligand 20; CCR6, chemokine receptor 6; CLA, cutaneous lymphocyte antigen; CXCL, chemokine (C-X-C motif) ligand; IFN-γ, interferon-gamma; IL, interleukin; ILC, innate lymphoid cells; PRRs, pattern recognition receptors; RORγt, retinoid-related orphan receptor γt; TH, T helper cell; TNF-α, tumour necrosis factor-alpha.

Maintenance phase

Key processes during disease maintenance involve ‘cross talk’ between epithelial and immune cells and the transition from innate to adaptive immunity as described in Figure 513. 

Maintaining psoriasis – transition from adaptive to innate immunity

Figure 5. Maintaining psoriasis – transition from adaptive to innate immunity (Adapted from Nestle et al13).
CCL, chemokine ligand; CXCL, chemokine (C-X-C motif) ligand; IFN-α, interferon-alpha; IFN-γ, interferon-gamma; IL, interleukin; TH, T helper cell; TNF-α, tumour necrosis factor-alpha.

Targeting inflammatory pathways in psoriasis has been a common strategy; the cells and cytokines involved in the perpetuation/maintenance of psoriasis represent key therapeutic targets13,14,17,21-23:

  • Secretion of IL-23 and IL-12 by DCs within the lymph nodes induces naïve T cells to differentiate into Th17 or Th1 cells, respectively
  • T cells migrate to skin and produce further cytokines (IFNγ, IL-17 and IL-22) which drive epidermal cell proliferation

These cytokines lead to over-activity of keratinocytes and this leads to the release of cytokines and chemokines that continue to recruit and activate inflammatory cells. The balance between regulatory and effector functions is lost and regulatory T cells (Tregs) are unable to control ongoing inflammation.

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Systemic and biologic treatments for psoriasis

Professor Peter van de Kerkhof (Radboud University Nijmegen Medical Centre, Netherlands) discusses treatment options for localised psoriasis and highlights the importance of contraindications and risk factors when considering systemic treatments for psoriasis.

Are treatment options limited for patients with localised psoriasis?

4

What should you consider in managing patients with moderately severe psoriasis?

1
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For people with milder disease, first-line psoriasis treatment often involves topical therapies including corticosteroids, vitamin D3 analogues, and combination products6. However, people with moderate-to-severe and refractory symptoms may be candidates for systemic therapy4,5,53.

In a survey conducted in the United States, Canada, France, Germany, Italy, Spain, and the United Kingdom, dermatologists reported that among people with moderate-to-severe psoriasis, approximately 75% of patients were receiving topical therapy, 20% of patients were receiving conventional oral therapy, and 20% of patients were receiving biologics54

Systemic treatments for psoriasis

Systemic treatments for psoriasis are usually reserved for people with moderate-to-severe forms of the disease (Psoriasis Area Severity Index [PASI] >10, or Body Surface Area [BSA] >10, and Dermatology Life Quality Index [DLQI] >10), or milder forms with a significant impact on quality of life that cannot be controlled by topical treatment2–5,55. Systemic treatments include oral drugs, subcutaneous injections, and intravenous infusions2,4,5,55.

Current treatment guidelines recommend a conventional oral drug as first-line systemic treatment for moderate-to-severe psoriasis, whereas a biologic is applied as second-line treatment in case of treatment failure, intolerance or contra-indication to an oral therapy4,5,55. Options for systemic therapy include immunosuppressive and immunomodulatory drugs such as methotrexate, ciclosporin, acitretin, fumaric acid esters, apremilast and biologic agents4,5,55.

While the trend is for biologics to be prescribed earlier, other systemic options, such as dimethyl fumarate and apremilast offer an alternative in the moderate-to-severe psoriasis population in the goal of achieving long-term control4,5,56,57.

A 2020 Delphi exercise to recategorise psoriasis severity has led to final international consensus stating that psoriasis patients should be classified as candidates for systemic therapy if they meet at least 1 of the following criteria58:

  1. BSA >10%
  2. Disease involving special areas
  3. Failure of topical therapy

Patient quality of life should also be considered in the decision to move to systemic treatment. Professor Peter van de Kerkhof (Department of Dermatology, Radboud University, the Netherlands) describes how even very limited disease can have a dramatic effect on a patient’s quality of life.

There are many current systemic treatments available that differ in terms efficacy and safety, and the two must be balanced when making therapeutic decisions. Treatment with systemics can provide long-term benefit for some patients with psoriasis. 

Professor Peter van de Kerkhof reminds us of the importance of considering contraindications and risk factors in selecting systemic treatments.

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Key research and clinical data

Psoriasis-related publications have grown substantially since 1960, and recent discoveries have paved the way for future research. Although research topics have expanded and diversified, the goal of research has remained to better understand psoriasis and its treatment to benefit people living with the disease176.

In this section, we provide a concise overview of the key results from the most significant clinical trials for each systemic and biologic treatment currently available.

Fumaric acid ester key clinical trials

Dimethyl fumarate

The European Medicines Agency's (EMAs) decision to approve a new formulation dimethyl fumarate (DMF) across Europe in 2017 was based on a Phase III, double-blind, placebo-controlled, non-inferiority trial (BRIDGE), which assessed the efficacy and safety of the new formulation DMF, compared with placebo, and an older DMF72. 

The BRIDGE study72

In the BRIDGE trial, patients were randomised to receive a new formulation DMF, an older formulation DMF, or placebo (2:2:1) for 16 weeks, up-titrating to a maximum daily DMF dose of 720 mg, depending upon individual response72.

At week 16: 

The BRIDGE study at Week 16

LAS410008, a new formulation DMF.

Most treatment‐related adverse events were classed as ‘mild’72.

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Achieving long-term control in moderate-to-severe psoriasis

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