Psoriasis

• chronic, immune mediated skin disorder affecting 2-4% of the population. 
• strong family history, if 1 parent affected 25% chance of developing
• Can start at any age, including childhood.
  • Onset peaks:
    • 15–25 years
    • 50–60 years.
• Common in Caucasians, but can affect any ethnicity

Types of psoriasis	Differential diagnosis
Infantile	Seborrhoeic dermatitis, atopic dermatitis
Plaque (commonest)	Seborrhoeic dermatitis, discoid eczema, solar keratoses, Bowen disease
Guttate	Pityriasis rosea, secondary syphilis, drug eruption
Flexural	Tinea, candida intertrigo, seborrhoeic dermatitis
Scalp (sebopsoriasis)	Seborrhoeic dermatitis, tinea capitis
Nail	Tinea, idiopathic onycholysis
Pustular (palmoplantar)	Tinea, infected eczema
Exfoliative	Severe seborrhoeic dermatitis

pathophysiology: 

• disorder causing activation of t cells 🡪 cytokines released & skin cells multiple leading to thickening of the skin & overscaling. New ‘biological agents’ intervene w this

precipitating factors: 

• sunburn
• drugs (NSAIDS, OCP, bBlcokers, antimalarials)
• Infections: Certain infections, particularly streptococcal throat infections, can trigger psoriasis in some people.
• Stress: High stress levels can initiate or worsen psoriasis outbreaks due to its impact on the immune system.
• Weather: Cold, dry weather can worsen symptoms, while warm, sunny climates may improve them.
• Obesity: Excess weight increases the risk of psoriasis and may make the treatment less effective. Fat cells (especially in abdominal fat) can produce inflammatory substances that might affect the skin.
• Physical trauma to the skin, known as the Koebner phenomenon, including cuts, bruises, burns, or insect bites, can trigger psoriasis at the site of the injury.
• Smoking and Alcohol: Tobacco and heavy alcohol use have been linked to the onset and exacerbation of psoriasis.
• Hormonal Changes: Changes in hormone levels, particularly during puberty and menopause, can trigger or impact the severity of psoriasis.
• Certain medications (e.g., lithium, beta-blockers).

Clinical features

• Symmetrical, red, scaly plaques with well-defined edges.
• Silvery white scale, shiny/moist peeling in skin folds.
• Widespread 
• Sharply demarcated
• Overlying loose, white to silvery scale
• Location
  • Symmetrical
  • Over joints and extensor surfaces of extremities
  • On trunk, especially lower back and buttocks
  • Palms and soles/Scalp/Umbilicus
• Pruritus is present in >80% of psoriasis – Psora is greek for itching

Classification

• Early (<35 years) vs late onset (>50 years).
• Acute (guttate) vs chronic plaque psoriasis.
• Localized (scalp, palmoplantar) vs generalized.
• Small (<3 cm) vs large plaques (>3 cm).
• Thin vs thick plaques.
• Nail involvement vs no nail involvement.

Onset follow

• stress or injury
• rash may appear on areas of trauma (koebner phenomenon)
• worse in winter, itch not a feature, better with sun but not sunburn

Systemic Signs

• Psoriatic Arthritis – 5% dev painful arthropathy or spondyloarthropathy (sacroilitis)
  • Distal Interphalangeal Arthritis (Classic, 5% of cases)
    • Adjacent nails may show psoriatic change
    • Progressive bony erosions occur
    • Phalanges/Metatarsals/Metacarpals
  • Symmetric Polyarthritis (15-25%) – Rheumatoid Arthritis similarities
    • Prominent Metacarpal disease
    • Prominent proximal interphalangeal joint disease
  • Rheumatoid Arthritis differences
    • Milder course than Rheumatoid Arthritis
    • No Extra-articular Rheumatoid Arthritis signs
    • No Subcutaneous Nodules
    • No Vasculitis
    • No pulmonary involvement
    • Rheumatoid Factor Seronegative
  • Oligoarthritis (>50-70% of cases)
    • Asymmetric joint involvement (<4 joints)
    • Often presents as Arthritis in one knee
  • Psoriatic Spondylitis
    • Ankylosing Spondylitis type spine involvement
    • Less associated with HLA-B27
    • Atypical axial skeleton involvement
    • Lumbar Spine most commonly affected
  • Sacroiliitis (30%)
  • Uveitis (up to 20% of Psoriatic Arthritis cases)

Associated Conditions (related to psoriatic medications)

• Inflammatory Bowel Disease (Crohns’ Disease or Ulcerative Colitis)
  • Risk increased 3.8 to 7.5x
• Psoriatic arthritis and spondyloarthropathy
• Uveitis
• Coeliac disease.
• Non-alcoholic fatty liver disease.
• Metabolic syndrome (obesity, hypertension, dyslipidaemia, insulin resistance).

dx: 

• clinical but biopsy may be needed to confirm

differentials

• Lichen Simplex Chronicus 
• Nummular Eczema
• Seborrheic Dermatitis 
• Tinea Corporis 
• Group A Beta Hemolytic Streptococcus
  • May present as Guttate Psoriasis in children
  • Obtain ASO Titer and Throat Culture

Management

• General:
  • Provide education, reassurance and support.
  • Rest
  • holidays in sun
  • avoid skin damage / stress
  • Avoid irritants and use a soap substitute
  • Smoking cessation.
  • Limit alcohol consumption.
  • Maintain optimal weight
• Referral to specialist if beyond mild or your comfort level

• Topical regimens: 
  • Salicylic acid  2 –10% w emulsifying ointment or white paraffin ointment. Soften & lift scale, commonly used. Apply overnight & persist for 3/52.
  • Tar (lpc 2 – 10%) cream.
    • Anti-inflam + anti-pruritic effect but less commonly used due to limited pt acceptability (smell, colour) but still important in children. Apply overnight & persist for 3/52
  • Dithranol 0.1% with salicylic acid 2 – 5%
    • anti-proliferative effect & very good but not for face, flexures or genitals as will burn. It stains clothes permanently & skin transiently. Apply overnight & persist for 3/52

Nb: after all of these treatments shower in the morning & apply a topical corticosteroid

Topical Steroid

• most common treatment for psoriasis
• anti-inflammatory, reduces rate of skin turnover
• useful for flares; add tar or calcipotriol if ineffective or step down to tar alone once controlled

• Consider limiting potent steroids to 2-4 weeks at a time
  • Then rotate to lower potency steroids or decrease application frequency (e.g. twice weekly)
  • Consider Emollient only periods until reexacerbation
• High Potency Topical Steroids (Class 2 to 5, usually indicated)
  • Very high potency: e.g. Clobetasol (Temovate)
  • High potency: e.g. Fluocinonide (Lidex)
• Low Potency Topical Steroids (e.g. Hydrocortisone 2.5%)
  • Face
  • Genitalia
  • Forearms
  • Intertriginous regions
• Maintenance Therapy

• Phototherapy: can be used in combo with topical or systemic therapy
• Systemic therapy: consultant led, when severe, widespread or causing disfigurement. Options =
  • Vitamin D based topicals (Calcipotriene, Calcitriol)
  • Immunosuppression
    • Tacrolimus
    • Methotrexate w folic acid – risk nausea, pancyotpaenia & deranged lfts (folic acid  this risk)
    • Cyclosporin
  • Biological therapies – target tnf-α (ie: infliximab, etanercept, adalimumab)

RECOMMENDED TOPICAL REGIMENS

Chronic stable plaque psoriasis

For trunk and limb psoriasis, apply:

• coal tar prepared 1% emulsion or gel, once or twice daily, for 1 month or
• LPC 6% + salicylic acid 3% cream or ointment, twice daily for 1 month
• if insufficient or flare, add
  • moderately potent to potent topical corticosteroid ointment, daily until skin is clear (usually 2 to 6 weeks)
• or if inadequate response
  • calcipotriol + betamethasone dipropionate
  • 50 + 500 mcg/g ointment, daily until skin is clear (usually about 6 weeks)

Once psoriasis controlled, reduce the potency of steroid and withdraw if possible. Continue tar as maintenance therapy.

Palmoplantar psoriasis

Treat as for trunk or limb psoriasis, but higher dose of salicylic acid is required if hyperkeratotic, i.e. LPC 6% + salicylic acid 6%. Also consider earlier use of calcipotriol, given common resistance to topical therapy.

Scalp psoriasis

• potent corticosteroid lotion or shampoo (as for seborrhoeic dermatitis), daily until skin is clear (usually 2 to 6 weeks)
• then
• coal-tar shampoo (over the counter) for maintenance
• or if thickened scale, add
• LPC 6% + salicylic acid 3% in aqueous cream, twice daily
• if inadequate response
• calcipotriol + betamethasone dipropionate
• 50 + 500 mcg/g gel, once daily until skin is clear (expect some response within 2 weeks)

Facial psoriasis

• methylprednisolone aceponate 0.1% ointment or fatty ointment, daily for several weeks (usually 2 to 6 weeks) or 1% hydrocortisone for children once controlled
• LPC 2% + salicylic acid 2% in aqueous cream at night

Flexural (inverse) and genital psoriasis

Note that Assuring (e.g. inframammary, natal cleft) is a feature. There is little or no scale.

• methylprednisolone aceponate 0.1% ointment or fatty ointment, once daily for several weeks (up to 2 weeks in children)
• once controlled
• LPC 2% in emulsifying ointment at night

Nail psoriasis

If patient motivated:

• calcipotriol + betamethasone dipropionate 50 + 500 mcg/g ointment, in proximal nail fold and under nail, at night for up to 3 months

If onycholysis or subungual hyperkeratosis:

• betamethasone dipropionate 0.05% lotion topically, twice daily under nail for up to 3 months

Guttate Psoriasis (drop-like)

Uncommon

• accounting for only 2% of Psoriasis cases
• Typically affects younger patients, under age 30 years
• Trunk lesions are 1-10 mm Papules with fine scale
• Commonly occurs after strep infection
• mx: good chance of spontaneously clearing completely but mx options = rx underlying strep infection, phototherapy + topical solutions (tars, steroids etc) 

Nail (Psoriatic Onychodystrophy) 

• Lifetime Prevalence in up to 90% of Psoriasis patients (esp. Fingernails)
• Findings secondary to abnormal nail plate growth
  • Nail Pitting
  • Subungual hyperkeratosis
  • Onycholysis
    • Separation of distal edge of nail from nail bed
    • Accumulation of crumbly subungual debris

• (A) Structural components of the nail unit.
• (B) The subdivisions of the nail matrix.
• (C) Pit formation in the nail plate arising from the nail matrix.⁵ 
• (D) Anatomical relationship between the nail and distal interphalangeal extensor tendon enthesitis: histology sections showing the superficial lamina and deep lamina from the extensor tendon are associated with the nail root and matrix.¹⁵ 
• (A), (B), and (C) reprinted from Jiaravuthisan MM, Sasseville D, Vender RB, Murphy F, Muhn CY. Psoriasis of the nail: anatomy, pathology, clinical presentation, and a review of the literature on therapy. J Am Acad Dermatol 2007; 57:1-27. Copyright 2007, with permission from Elsevier.
• (D) Reproduced from Tan AL, Benjamin M, Toumi H, Grainger AJ, Tanner SF, Emery P, et al. The relationship between the extensor tendon enthesis and the nail in distal interphalangeal joint disease in psoriatic arthritis—a high-resolution MRI and histological study. Rheumatology 2007;46:253-6. Copyright 2009: the author. Journal compilation copyright 2009: European Academy of Dermatology and Venereology. Adapted from: Tan AL, et al. Rheumatology 2007;46:253-256 by permission of Oxford University Press.