Psoriasis guide: causes, types, and the full treatment hierarchy

Psoriasis affects approximately 2–3% of the global population — roughly 125 million people. It is a chronic, immune-mediated inflammatory disease that primarily affects the skin but has systemic manifestations including psoriatic arthritis, increased cardiovascular risk, and metabolic syndrome association. Here is the complete evidence-based guide.

What causes psoriasis

The immune mechanism

Psoriasis is driven by a dysregulated adaptive immune response — not a primary keratinocyte defect. The cascade:

Dendritic cell activation: Unknown trigger (often infection, stress, or drug) activates plasmacytoid dendritic cells → they produce IFN-α and IL-12/IL-23
T-cell polarization: IL-23 drives naïve T cells toward the Th17 pathway → Th17 cells produce IL-17A, IL-17F, IL-22
Keratinocyte hyperproliferation: IL-17A binds keratinocyte receptors → activates NF-κB → releases more cytokines (TNF-α, IL-6, IL-8) and antimicrobial peptides → dramatic acceleration of epidermal turnover (from normal 28 days to 3–5 days)
The plaque: Hyperproliferating keratinocytes cannot mature normally → accumulate as the characteristic silvery-white scale; dermal vasodilation and immune cell infiltrate produce the underlying erythema

TNF-α plays a central amplifying role — produced by macrophages and T cells in psoriatic lesions, it amplifies the IL-17 response and directly drives keratinocyte activation. This is why anti-TNF biologics were the first to demonstrate efficacy in psoriasis.

IL-23 is the master upstream regulator — blocking IL-23 (the p19 subunit) produces sustained remission in many patients because it cuts off the driver of Th17 polarization. The IL-23 inhibitors (risankizumab, guselkumab, tildrakizumab) have emerged as the highest-efficacy biologics in psoriasis.

Genetic basis

Psoriasis has strong genetic heritability — roughly 65–70% concordance in identical twins. The strongest genetic association is HLA-Cw6 (the PSORS1 locus on chromosome 6p), which increases risk 10-fold. HLA-Cw6 positive patients more commonly have guttate-onset disease and a strong response to IL-17 inhibitors.

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Clinical types

Plaque psoriasis (psoriasis vulgaris)

The most common type — ~90% of psoriasis cases. Characterized by:
Well-demarcated, salmon-pink plaques with adherent silvery-white scale
Koebner phenomenon: New plaques form at sites of skin trauma (scratches, surgical incisions, sunburns)
Auspitz sign: Removal of scale reveals pinpoint bleeding (dilated superficial capillaries)
Symmetric distribution on extensor surfaces (elbows, knees), scalp, lumbosacral area, and umbilicus

Guttate psoriasis

Small, drop-shaped plaques (guttate = "drop") scattered over the trunk and extremities. Often triggered by streptococcal pharyngitis (throat swab + ASO titer useful). Most common first presentation in children and young adults. May resolve spontaneously; may evolve to plaque psoriasis.

Inverse psoriasis

Affects skin folds — axillae, inguinal folds, inframammary area, gluteal cleft. Minimal scale (maceration in folds removes it); smooth, glazed erythema. Resembles intertrigo, seborrheic dermatitis, or candidiasis — diagnosis often requires biopsy.

Pustular psoriasis

Sterile pustules on an erythematous base. Can be localized (palmoplantar pustulosis — palms and soles) or generalized (von Zumbusch — rare, acute, potentially life-threatening with fever and systemic involvement). Generalized pustular psoriasis requires emergency management.

Erythrodermic psoriasis

Widespread erythema covering >90% of body surface area — may arise from unstable plaque psoriasis. Potentially life-threatening from thermoregulatory failure and protein loss. Emergency dermatology management required.

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Distinguishing psoriasis

| Feature | Psoriasis | Seborrheic Dermatitis | Atopic Dermatitis |
|---|---|---|---|
| Scale | Thick, silvery-white, adherent | Thin, yellowish, greasy | Fine, dry |
| Borders | Sharp, well-demarcated | Diffuse | Diffuse |
| Distribution | Extensor, scalp, nails | Sebaceous areas (T-zone, scalp) | Flexural |
| Itch | Moderate | Moderate | Severe |
| Nail changes | Yes (pitting, onycholysis) | No | Rarely |
| Koebner | Yes | No | No |

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Treatment hierarchy

Mild psoriasis (BSA &lt;3%, limited body areas)

Emollients: All psoriasis patients need regular emollient application — softens and partially removes scale, reducing the barrier function deficit. Thick creams and ointments preferred.

Topical corticosteroids: First-line anti-inflammatory. Moderate to potent TCS (triamcinolone 0.1%, betamethasone valerate 0.1%, clobetasol 0.05% for thick plaques). Applied daily to active plaques; taper to 2–3×/week after clearance; not for indefinite daily use (skin atrophy, tachyphylaxis).

Vitamin D analogues (calcipotriol/calcitriol): Inhibit keratinocyte proliferation via VDR (vitamin D receptor); reduce Th17 cytokine signaling. Used alone or in combination with TCS. Dovobet (calcipotriol + betamethasone) — the fixed-dose combination gel — is more effective than either component alone; approved for scalp and body use.

Calcineurin inhibitors: Tacrolimus and pimecrolimus for inverse psoriasis in skin folds — appropriate where TCS atrophy is a concern; less effective than TCS for plaque disease.

Coal tar: Antiproliferative and anti-inflammatory; older agent but effective for scalp and body. Cosmetically less acceptable.

Moderate-severe psoriasis (BSA >10% or significant impact on quality of life)

Phototherapy — narrowband UVB (NBUVB):
Most effective non-systemic treatment; 3 sessions/week for 12–16 weeks
Induces T-cell apoptosis in the skin and reduces IL-17/IL-23 production locally
70–80% achieve PASI 75 (75% reduction in Psoriasis Area and Severity Index) with a full course
Safe in pregnancy; safe long-term (unlike systemic agents)
Requires ongoing maintenance or re-treatment for relapse

Conventional systemics:
Methotrexate: Inhibits dihydrofolate reductase → antiproliferative and anti-inflammatory. Weekly dosing (7.5–25mg). Monitor LFTs and CBC. Effective for both skin and psoriatic arthritis.
Cyclosporine: Calcineurin inhibitor → T-cell suppression. Rapid response (weeks). Reserved for severe/acute disease; not for long-term use (nephrotoxicity, hypertension).
Acitretin: Oral retinoid. Most effective for pustular psoriasis; less effective as monotherapy for plaque. Teratogenic — strict contraception required.

Biologics (moderate-severe, or conventional systemic failure)

Anti-TNF agents: Adalimumab, etanercept, infliximab. First-generation biologics; well-established long-term safety data. PASI 75 rates ~60–70%.

Anti-IL-17 agents: Secukinumab (Cosentyx), ixekizumab (Taltz), bimekizumab (Bimzelx — also blocks IL-17F). Faster onset than anti-TNF; PASI 90 rates ~60–70%; among the highest-efficacy biologics available.

Anti-IL-23 agents (p19): Risankizumab (Skyrizi), guselkumab (Tremfya), tildrakizumab (Ilumya). Every 8–12 week maintenance dosing after induction; PASI 90 rates 70–80%; PASI 100 (complete clearance) in 40–50%. Among the highest single-agent efficacy in psoriasis.

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Psoriatic arthritis

Up to 30% of psoriasis patients develop psoriatic arthritis — inflammatory arthritis that can cause permanent joint damage. Screening questions:
Morning joint stiffness lasting >30 minutes
Joint swelling (particularly fingers/toes — "sausage digit" dactylitis)
Back/sacroiliac pain (axial involvement)

Early diagnosis and treatment with DMARDs or biologics prevents joint damage. Refer to rheumatology if suspected.

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Triggers

Streptococcal infection — guttate flares; treat throat infections promptly
Stress — well-documented trigger; mind-body approaches are adjuncts
Medications: Lithium, beta-blockers, antimalarials, NSAIDs — can trigger or worsen psoriasis
Alcohol — worsens severity and reduces treatment response
Obesity — pro-inflammatory adipokine excess worsens psoriasis; weight loss improves severity
Trauma/Koebner — avoid skin trauma where possible

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