Chronic plaque psoriasis

There are numerous psoriasis subtypes, such as plaque psoriasis, flexural (otherwise known as inverse) psoriasis, scalp psoriasis, sebopsoriasis, pustular psoriasis, guttate psoriasis, nail psoriasis, and erythrodermic psoriasis; chronic plaque psoriasis is most pertinent to the periocular region and to this review.

Etiology

• Genetically mediated immune dysfunction leading to an inappropriate, dysregulated inflammatory response (mainly involving the skin).
  • There is a strong genetic component mediating psoriasis.
  • Twin studies which have demonstrated a 2 to 3.5-fold higher concordance of psoriasis in monozygotic twins than in dizygotic twins (Greb, 2016).
  • The mutated genes associated with psoriasis are largely part of the psoriasis susceptibility locus 1 (PSORS1).
    • PSORS1 consists of the human leukocyte antigen (HLA) complex.
      • The HLA complex has long been implicated in autoimmune disease as it encodes for the major histocompatibility complex proteins, a critical feature of antigen recognition and, thus, human immunity. 
      • Psoriasis is strongly associated with HLA-C*06 in Caucasian and Chinese populations.
        • Notably, HLA-C*06 is not associated with nail dystrophy or psoriatic arthritis.
  • Genetic mutations lead to an inappropriate interaction of immune cells with resident cells of the skin.
    • Both the innate and adaptive immune system are dysfunctional in psoriasis.
    • A large number of immune system abnormalities have been described, including excess secretion of pro-inflammatory transcription factors, cytokines, and chemokines. The most pertinent for current treatment regimens are:
      • Transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)
      • T-helper cell 17 (TH17)
      • Cytokines: Interlukin-12 (IL-12), IL-23, IL-17, Tumor Necrosis Factor alpha (TNFα)
    • The identification of specific immune abnormalities has led to the formation of targeted, biologic treatments (see management).
• Triggers
  • Koebner phenomenon due to skin injury (i.e. abrasions, cuts, sunburn)
  • Infection
  • Psychological stress
  • Smoking or excessive alcohol intake
  • Obesity
  • Systemic drugs (i.e. nonsteroidal anti-inflammatories, beta-blockers, antimalarial agents)
  • Use of potent topical corticosteroids or cessation of oral corticosteroids

Epidemiology

• Prevalence of chronic plaque psoriasis in Europe and North America is estimated at 2% (Boehncke, 2015). Chronic plaque psoriasis is by far the most common subtype of psoriasis.
  • Equal prevalence in men and women.
  • A population-based cohort study using the Psoriasis Area and Severity Index demonstrated that men experience more severe disease than women and are more likely to need biologic treatments (Hägg, 2013).
• Onset occurs in a bimodal distribution with individuals commonly affected between 18-39 years old (early-onset psoriasis) and 50-69 years old (late-onset psoriasis).
• 75% of cases occur before age 35.
• The prevalence of psoriasis in the pediatric population is approximately 0.7%. Prevalence increases linearly with age (Boehncke, 2015).

Clinical features

• Chronic plaque psoriasis
  • Round, well-demarcated, erythematous plaques with overlying silvery scale. Differentiated from small plaque psoriasis by the presence of plaques larger than 3 cm.
  • Severe disease leads to lichenification and fissures.
  • Classically located on the extensor surfaces but may occur on the face.
    • Children and adolescents are more likely to develop disease on the eyebrows or periocular skin than adults (Figure 1).
  • Auspitz sign: pinpoint bleeding when psoriasis scales flake off.
  • Koebner phenomenon: a new area of psoriasis development at a site of cutaneous trauma that was not previously involved in disease.
  • Psoriatic arthritis complicates psoriasis in up to 30% of cases and nail changes (i.e. nail pitting or onycholysis) are present in 50% of cases (Greb, 2016).
  • Disease is classified as unstable plaque psoriasis if there is rapid onset of new plaques or aggressive extension of existing plaques. Koebner phenomenon is often present in unstable disease.

Other diagnostic tests

• Biopsy can be performed if presentation is atypical.
  • Histopathologic features include perivascular infiltration of lymphocytes, parakeratosis, elongated rete ridges, and epidermal microabscesses.

Severity assessment (Delphi consensus from the International Psoriasis Council, 2019)

• Psoriasis severity has been recategorized from mild, moderate or severe to individuals who are candidates for topical therapy or candidates for phototherapy and/or systemic therapy. Indications for systemic therapy include:
  • Failure of topical therapy
  • Disease involving >10% of body surface area
  • Disease involving “special areas” (i.e. face, scalp, genitalia, palms, soles)
• Numerous validated tools exist to assess the severity of psoriasis using the traditional mild, moderate and severe categories.
  • Psoriasis Area and Severity Index (PASI)
    • A commonly used assessment tool that calculates psoriasis severity based on intensity (defined by the levels of erythema, induration and desquamation) and the percent of body surface area involved.

• Small plaque psoriasis
• Guttate psoriasis
• Sebopsoriasis
• Seborrheic dermatitis
• Nummular dermatitis
• Bowen’s disease
• Pityriasis rubra pilaris
• Atopic dermatitis
• Tinea infection
• Hypertrophic lichen planus

• Medical management of chronic plaque psoriasis: 70-80% of patients have disease adequately controlled with topical agents (Boehncke, 2015). Disease involving the face categorizes an individual as a candidate for systemic therapy and/or phototherapy as first-line treatment (Delphi consensus from the International Psoriasis Council, 2019).
• Topical therapy
• Topical calcineurin inhibitors
• Low potency topical glucocorticoids
• Adverse effects associated with periocular use including dermal atrophy and increase in intraocular pressure.
• Vitamin D derivatives (i.e. calcipotriol)
• Phototherapy
• Narrowband ultraviolet B
• Broadband ultraviolet B
• Targeted phototherapy with an excimer laser
• Psoralen plus ultraviolet A
• Systemic therapy:
• First line non-biologic systemic therapy: methotrexate, cyclosporin, oral retinoids (i.e. acitretin)
• Second line non-biologic systemic therapy (less frequently used): mycophenalate, fumaric acid esters, hydroxyurea, azathioprine, 6-mercaptopurine
  • Apremilast (phosphodiesterase 4 inhibitor)
    • Demonstrated in a 2019 phase-2 open label study to be efficacious in children as well as adults for plaque psoriasis (Paller, 2020).
• Biologic agents with the following targets:
  • Tumor necrosis factor alpha (entanercept, certolizumab, adalimumab, infliximab)
  • IL-17 (secukinumab, brodalumab, ixekizumab)
  • The p40 subunit of IL-12 and 1L-23 (ustekinumab)
  • The p19 subunit of IL-23 (risankizumab, guselkumab, tildrakizumab)
• Natural history and prognosis:
  • Chronic plaque psoriasis
    • Chronic, relapsing, remitting course
    • After plaques clear, they may result in several months of hypopigmentation or hyperpigmentation.

• Both adults and children with psoriasis have increased risk of developing other chronic diseases:
• Psoriatic arthritis and spondyloarthropathy
• Cardiovascular disease
• Metabolic syndrome
• Gout
• Non-alcoholic fatty liver disease
• Inflammatory bowel disease
• Celiac disease
• Uveitis
• Anxiety and/or depression
• Psoriasis has been demonstrated to reduce physical and mental functioning at levels comparable to congestive heart failure, myocardial infarction, and cancer (Rapp, 1999). 


Photograph courtesy of D@nderm Atlas of Clinical Dermatology.

Figure 1. Chronic plaque psoriasis of the face involving the cheeks, bridge of the nose, and the eyebrows. Erythematous patches with silver scale and mild desquamation can be seen.

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