Psoriasis !

Psoriasis is a long-term immune skin disease that causes thick, red, scaly plaques, often on elbows, knees and scalp. It is not contagious.

Updated 2026-11-01

Structures involved

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In embryology

In the clinical exam

Why it happens

What it is

A chronic, immune-mediated inflammatory disease in which skin cells multiply too fast, forming well-demarcated red plaques with silvery scale. It can also affect nails and joints and is linked to cardiometabolic disease.

Who gets it

Affects about 2–3% of people worldwide, with lower reported rates in some Latin American and Asian populations. It can start at any age, with peaks in young adulthood and later middle age, and affects men and women about equally.

Causes

Genetic predisposition (e.g. HLA-Cw6)
Dysregulated immunity along the IL-23/Th17 axis
Environmental triggers acting on a susceptible person

Risk factors

Family history of psoriasis
Streptococcal throat infection (trigger of guttate psoriasis)
Skin injury (Koebner phenomenon)
Smoking, alcohol, obesity and psychological stress
Drugs such as lithium, beta-blockers, antimalarials and abrupt withdrawal of systemic corticosteroids
HIV infection (can cause severe flares)

Pathophysiology

Dendritic cells activate T cells that release IL-17, IL-22 and TNF under the drive of IL-23. Keratinocytes respond by proliferating so fast that the epidermis renews in days instead of weeks, retaining nuclei in the scale (parakeratosis), thickening (acanthosis) and forming neutrophil microabscesses. Dilated dermal capillaries explain pinpoint bleeding when scale is removed (Auspitz sign).

Classification

Plaque psoriasis (vulgaris): the most common form; extensor surfaces, scalp and lower back
Guttate: many small drop-like papules, often after streptococcal pharyngitis in young people
Inverse: smooth red patches in skin folds
Pustular (localised palmoplantar or generalised)
Erythrodermic: redness over most of the body, an emergency
Nail psoriasis and psoriatic arthritis as associated forms

Symptoms and signs

Well-defined, red, raised plaques with thick silvery-white scale
Symmetric involvement of elbows, knees, scalp, lower back and gluteal cleft
Itch, sometimes burning or soreness
Nail changes: pitting, onycholysis, oil-drop discoloration and thickening
New plaques at sites of skin injury (Koebner phenomenon)
Joint pain, swelling or a sausage-shaped finger (dactylitis) suggesting psoriatic arthritis

Diagnosis

Clinical: Clinical diagnosis based on typical plaques, distribution and nail findings; severity is scored by body surface area and indices such as PASI. Joint examination screens for psoriatic arthritis.
Tests: Skin biopsy only when the diagnosis is uncertain (parakeratosis, acanthosis, Munro microabscesses). Lipids, glucose, liver tests and screening for tuberculosis and hepatitis before systemic or biologic therapy.
Imaging: Not needed for skin disease; X-ray or ultrasound of joints when psoriatic arthritis is suspected.

Differential diagnosis

Atopic or seborrhoeic dermatitis
Tinea corporis or tinea capitis
Lichen planus
Pityriasis rosea (for guttate forms)
Secondary syphilis
Onychomycosis (for nail disease)

Goal of treatment

Clear or reduce skin lesions, control itch, treat nail and joint disease, and address cardiovascular and metabolic comorbidities and psychological impact.

Treatment

Medical: Topical therapy for limited disease: corticosteroids, vitamin D analogues (calcipotriol), often combined, plus keratolytics and coal tar; emollients for all patients.
Procedure: Phototherapy with narrowband UVB or PUVA for moderate disease or when topicals are not enough.
Medical: Systemic conventional agents for moderate to severe disease: methotrexate, cyclosporine, acitretin and apremilast.
Medical: Biologics targeting TNF, IL-17, IL-23 or IL-12/23 for moderate to severe disease or psoriatic arthritis, after screening for latent tuberculosis.
Lifestyle: Weight loss, stopping smoking, limiting alcohol and managing stress, which reduce flares and cardiometabolic risk.
Follow-up: Blood counts and liver and kidney tests on systemic drugs, blood-pressure and metabolic screening, and assessment of mood and joints.

Drugs for this condition

Complications

Psoriatic arthritis
Cardiovascular disease, metabolic syndrome, obesity and diabetes
Depression, anxiety and social stigma
Erythroderma with fluid and temperature loss
Infections and other adverse effects of systemic therapy
Associated inflammatory bowel disease (Crohn disease)

Prognosis

A lifelong disease with flares and remissions; it is not curable but modern treatments, especially biologics, can achieve near-complete clearance in many patients. Severe disease is linked to higher cardiovascular risk.

Prevention

Avoiding known triggers (smoking, excess alcohol, skin injury) to reduce flares
Prompt treatment of streptococcal infections in people prone to guttate psoriasis

Test yourself

Think of the answer, then tap the question to see it.

What is the classic appearance and location of plaque psoriasis?

Well-demarcated red plaques with silvery scale on extensor surfaces such as elbows and knees, plus scalp and lower back.

What is the Auspitz sign?

Pinpoint bleeding when psoriatic scale is scraped off, from dilated capillaries in the dermal papillae.

Which infection classically triggers guttate psoriasis?

Streptococcal pharyngitis.

Which three nail changes are typical of psoriasis?

Pitting, onycholysis and oil-drop (salmon patch) discoloration; also subungual hyperkeratosis.

Which immune pathway is the main target of modern biologic therapy for psoriasis?

The IL-23/IL-17 axis (along with TNF).

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Psoriasis (MedlinePlus, US National Library of Medicine, 2026); Psoriasis (National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), 2026).

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Representative model, for educational purposes only.

Skin highlighted on the Durgical 3D model