Dermatology
AKT · Dermatology/Inflammatory & papulosquamous

Psoriasis

Immune-mediated (IL-17/23, T-cell) epidermal hyperproliferation

Overview

A chronic, immune-mediated papulosquamous disease in which IL-17/23-driven T-cell inflammation accelerates keratinocyte turnover. The exam picture is well-demarcated salmon-pink plaques with silvery scale on extensor surfaces; the discriminators against eczema are sharp demarcation, extensor (not flexural) distribution and the Auspitz sign.

Recognise

  • Well-demarcated salmon-pink plaques with thick silvery-white scale, symmetrically on EXTENSOR surfaces (elbows, knees), scalp and sacrum
  • Auspitz sign (pinpoint bleeding when scale is lifted); Koebner phenomenon (lesions at sites of trauma); nail pitting and onycholysis
  • Variants: guttate (raindrop papules on trunk, post-streptococcal, young patient), flexural/inverse, pustular, erythrodermic; up to ~1 in 5 develop psoriatic arthritis

Red flags

  • Erythrodermic or generalised pustular psoriasis = dermatological emergency (same-day referral, fluid/temperature compromise); new psoriatic arthritis (joint pain/swelling)

Differentials & how to tell them apart

Atopic dermatitis/eczemaill-defined, intensely itchy, FLEXURAL; psoriasis is sharply demarcated and extensor with silvery scale
Seborrhoeic dermatitisgreasy yellow scale in nasolabial folds/scalp, less well-defined
Tinea corporisasymmetrical, annular with an active scaly edge and central clearing, KOH/scrape positive
Lichen planusviolaceous flat-topped polygonal papules with Wickham striae, flexor wrists
Mycosis fungoidespersistent atypical patches/plaques unresponsive to treatment — biopsy

Clinical image

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Investigations

Clinical diagnosis. Assess severity (body surface area / PASI) and impact (DLQI); screen for psoriatic arthritis (PEST questionnaire) and cardiometabolic risk (it is a systemic inflammatory disease).

Management

Potent topical corticosteroid once daily + vitamin D analogue once daily (or a combined product) for up to 4 weeks

  1. 1Emollients + a potent topical corticosteroid (OD) with a vitamin D analogue (OD), or a combined product, for up to 4 weeks for trunk/limb plaques.Gate: Do NOT use potent/very-potent topical corticosteroids continuously for more than 8 weeks at one site — schedule treatment breaks to avoid skin atrophy and rebound; abrupt withdrawal of systemic steroids can precipitate pustular psoriasis
  2. 2If steroid stopped, continue vitamin D analogue alone (can be used twice daily). Scalp = potent corticosteroid; face/flexures = mild corticosteroid or a calcineurin inhibitor.
  3. 3Inadequate response → phototherapy (narrowband UVB); then systemic therapy (methotrexate is usual first systemic), then biologics, under dermatology.
Emollientsreduce scale and itch in all patients — the constant background
Potent topical corticosteroid + vitamin D analogue (calcipotriol)first-line for trunk/limb plaques; often a combined product (e.g. calcipotriol/betamethasone)
Coal tar, dithranololder topicals; tar useful for scalp
Topical calcineurin inhibitor (tacrolimus)face and flexures (steroid-sparing, avoids atrophy)
Methotrexate / ciclosporin / acitretin; biologics (anti-TNF, IL-17, IL-23)systemic options when topical + phototherapy fail

Key points

Guttate psoriasis often follows a streptococcal throat infection and may settle spontaneously. Triggers/aggravators to know: beta-blockers, lithium, antimalarials, NSAIDs, and withdrawal of systemic corticosteroids. Avoid systemic steroids (rebound pustular flare).

Monitor & prognosis

Plaque response and DLQI; methotrexate needs FBC/U&E/LFT monitoring; address cardiovascular risk.

Chronic relapsing-remitting; well controlled with treatment but not cured.

Source: NICE CKS Psoriasis; NICE CG153