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Dermatology›Condition·Updated Jul 11, 2026·v1

Psoriasis

Psoriasis is a common immune-mediated skin disease with significant systemic comorbidities. Diagnosis is clinical with dermoscopic confirmation. Management ranges from topical therapy to biologics, with IL-23 and IL-17 inhibitors offering the highest efficacy. Early intervention may improve long-term outcomes.

High Evidence660 references·10,625 words·43 min read·v1
psoriasisdermatologyinflammatory skin diseaseIL-23IL-17biologicspsoriatic arthritisautoimmune

Quick Reference

RxDrug of choiceGuselkumab 100 mg subcutaneously at weeks 0, 4, then every 8 weeks (IL-23 inhibitor) for moderate-to-severe plaque psoriasis; spesolimab 900 mg IV single dose for generalized pustular psoriasis flares.
AltAlternativesRisankizumab, secukinumab, ixekizumab, bimekizumab, adalimumab, ustekinumab, deucravacitinib, apremilast, methotrexate, cyclosporine, acitretin, NB-UVB phototherapy.
⊘AvoidSystemic corticosteroids (risk of rebound pustulation), methotrexate in pregnancy, acitretin in pregnancy, cyclosporine in renal impairment, TNF inhibitors in NYHA class III-IV heart failure.
DxTest of choiceClinical diagnosis with dermoscopy (regularly distributed dotted vessels on bright-red background with silvery scale); skin biopsy for atypical cases.
ScKey scorePsoriasis Area and Severity Index (PASI), standard endpoint in trials; PASI 75/90/100 used to define response.
→When to referSuspected psoriatic arthritis (joint pain, swelling, dactylitis), severe disease requiring systemic therapy, treatment failure on biologics, pregnancy planning, or significant psychiatric comorbidity.
Psoriasis is a chronic immune-mediated skin disease managed with a stepwise approach; biologics targeting IL-23/IL-17 offer high clearance rates; screen for comorbidities including psoriatic arthritis, cardiovascular disease, and metabolic syndrome.
Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting approximately 2% of the population worldwide, characterized by well-demarcated erythematous plaques with silvery scale. It is associated with significant comorbidities including psoriatic arthritis, cardiovascular disease, and metabolic syndrome. Management follows a stepwise ladder from topical therapy to phototherapy, oral systemic agents, and biologics targeting the IL-23/Th17 axis. Early intervention with effective therapy may modify disease course and improve long-term outcomes.

Overview and Recommendations

Background

  • •Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting approximately 2% of the global population, with a prevalence of 3.0% in US adults (7.55 million people). It is characterized by well-demarcated, erythematous plaques with silvery scale, most commonly on extensor surfaces, scalp, and nails.
  • •The disease is driven by the : dendritic cells produce IL-23, which stabilizes Th17 cells that secrete IL-17A, IL-17F, and IL-22, leading to keratinocyte hyperproliferation and a self-amplifying inflammatory loop. Genetic susceptibility is dominated by .
  • •Plaque psoriasis (psoriasis vulgaris) accounts for ~90% of cases. Other subtypes include guttate (often post-streptococcal), inverse (flexural), pustular (generalized and localized), erythrodermic (dermatologic emergency), nail psoriasis, and (affects 20-30% of patients).
  • •Psoriasis is associated with significant systemic comorbidities: (~20%), cardiovascular disease (HR 1.2-1.5 for MI), metabolic syndrome (~40%), non-alcoholic fatty liver disease (OR 2.16), and increased cancer risk (RR 1.21, especially keratinocyte cancer and lymphoma). Smoking is the strongest modifiable risk factor (OR 1.78).
  • •The disease has a relapsing-remitting course; spontaneous remission is rare. Early intervention with biologics may induce drug-free remission in a subset of patients, supporting a 'window of opportunity' in early disease.

Evaluation

  • •Suspect psoriasis in any patient with well-demarcated, erythematous plaques covered by silvery micaceous scale, especially on extensor elbows, knees, scalp, lumbosacral area, and nails. Pruritus is present in 80-100% of patients.
  • •Ask about onset and duration, family history of psoriasis, joint pain or stiffness (suggesting ), triggers (stress, infection, medications including beta-blockers, lithium, TNF inhibitors), and impact on quality of life.
  • •Examine for the (pinpoint bleeding upon scale removal) and (lesions at sites of trauma). In skin of color, erythema may appear violaceous or slate-gray.
  • •Assess body surface area (BSA) involvement and use the to quantify severity. Also evaluate special sites: scalp, face, genitals, palms, soles, nails.
  • •Perform dermoscopy: hallmark is regularly distributed dotted vessels (glomerular capillaries) on a bright-red background with diffuse silvery white scale. This is the most reliable noninvasive pattern.
  • •If diagnosis is uncertain (atypical morphology, pustular, erythrodermic, or suspicion of mycosis fungoides), perform a skin biopsy. Histopathology shows psoriasiform hyperplasia, parakeratosis with Munro microabscesses, hypogranulosis, and dilated tortuous capillaries.
  • •No specific laboratory test is diagnostic, but consider screening for (anti-tissue transglutaminase antibodies) in moderate-to-severe disease. Assess for metabolic syndrome: blood pressure, fasting glucose, lipids.
  • •Screen for using the Psoriasis Epidemiology Screening Tool (PEST) or PURE-4 scale (dactylitis, inflammatory heel pain, bilateral buttock pain, peripheral joint pain with swelling in patients <50).
  • •Differential diagnoses include (spongiosis, flexural distribution), (purple, polygonal, Wickham striae), (atypical lymphocytes, epidermotropism), (annular, KOH positive), and (alternating orthokeratosis/parakeratosis).
  • •For generalized pustular psoriasis (GPP), diagnose by macroscopically visible sterile pustules on an erythematous base with systemic symptoms (fever, leukocytosis). Use International Consensus Criteria.
  • •For erythrodermic psoriasis, diagnose by confluent erythema involving >90% BSA with systemic symptoms (tachycardia, hypothermia, high-output heart failure), a dermatologic emergency.
  • •Consider AI-assisted diagnosis using multimodal models (clinical + dermoscopic images) which improve dermatologist accuracy from 77.5% to 89.0% for differentiating psoriasis from other inflammatory diseases.

Management

  • •For mild disease (BSA <5%, PASI <10, DLQI <10), initiate topical therapy: potent (e.g., betamethasone dipropionate 0.05% cream once daily) or vitamin D analogues (calcipotriol 0.005% cream). The fixed combination calcipotriol/betamethasone dipropionate is superior to either alone.
  • •Alternative topical options include tapinarof 1% cream (aryl hydrocarbon receptor agonist) achieving PGA success in 35-40% at week 12, and roflumilast 0.3% cream (PDE4 inhibitor) with IGA success in 37-42% at week 8, particularly effective in intertriginous areas.
  • •For moderate-to-severe disease (BSA >10%, PASI >10, DLQI >10, or special-area involvement), escalate to phototherapy or systemic therapy. First-line phototherapy: narrowband UV-B (NB-UVB) 3 times weekly. Home NB-UVB is noninferior to office-based and has higher adherence (51.4% vs 15.9%).
  • •Oral systemic options: 5-7.5 mg weekly, titrated to 25 mg weekly (with folic acid 5 mg weekly); 2.5-3 mg/kg/day, max 5 mg/kg/day (limited to ≤1 year due to nephrotoxicity); acitretin 10-25 mg/day (teratogenic, useful for palmoplantar pustulosis).
  • •Newer oral agents: 6 mg once daily (TYK2 inhibitor) achieved PASI 75 in 58.4% at week 16 vs 12.7% placebo; 30 mg twice daily (PDE4 inhibitor) achieves ~35% PASI 75; 200 mg once daily (oral IL-23 receptor antagonist) achieved PASI 90 in 55-57% at week 16.
  • •For patients requiring biologic therapy, first-line options include IL-23 inhibitors ( 100 mg at weeks 0,4 then every 8 weeks; 150 mg at weeks 0,4 then every 12 weeks) and IL-17 inhibitors ( 300 mg at weeks 0,1,2,3,4 then every 4 weeks; 160 mg week 0 then 80 mg every 2 weeks; 320 mg every 4 weeks).
  • •IL-23 inhibitors have the highest drug survival and long-term efficacy: guselkumab PASI 90 73-85% at week 16, risankizumab PASI 90 75% at week 16. IL-17 inhibitors have faster onset: ixekizumab PASI 90 82-89% at week 12, bimekizumab PASI 90 85-91% at week 16.
  • •For generalized pustular psoriasis (GPP) flares, administer 900 mg IV as a single dose (54% pustule clearance at week 1 vs 6% placebo). If unavailable, use cyclosporine 2.5-5 mg/kg/day or infliximab 5 mg/kg IV.
  • •For erythrodermic psoriasis, hospitalize and initiate cyclosporine 2.5-5 mg/kg/day or infliximab 5 mg/kg IV. Avoid systemic corticosteroids due to risk of rebound pustulation.
  • •Monitor all patients on biologics for tuberculosis (IGRA before initiation), hepatitis B/C, and HIV. For latent TB, complete prophylaxis or start biologic after 1-2 months of treatment if patient is tolerating.
  • •Do NOT use systemic corticosteroids for plaque psoriasis. Do NOT combine multiple immunosuppressive biologics. Do NOT use TNF inhibitors in NYHA class III-IV heart failure. Do NOT continue a biologic beyond 12-16 weeks without evidence of meaningful improvement (PASI <75 or patient dissatisfaction).
  • •For patients with inadequate response to a biologic, confirm adherence, then switch to a different class (e.g., IL-23i to IL-17i or vice versa). Prior biologic exposure reduces response (OR 0.44). Obesity (BMI ≥30) reduces efficacy; adjunctive weight loss improves outcomes (RR 1.6 for PASI75).
  • •In pregnancy, first-line therapies are topical corticosteroids and NB-UVB. is the preferred biologic due to minimal placental transfer. Methotrexate and acitretin are contraindicated. Continue biologics through first two trimesters; pause in third trimester.
  • •In children, approved biologics include etanercept 0.8 mg/kg/week (max 50 mg), adalimumab 0.8 mg/kg every other week, guselkumab weight-based (50 mg for <60 kg, 100 mg for ≥60 kg), and ustekinumab weight-based. Guselkumab achieved PASI 75 in 76% at week 16.
  • •Refer to rheumatology if psoriatic arthritis is suspected (joint pain, swelling, dactylitis, enthesitis). Refer to cardiology for cardiovascular risk management. Refer to mental health if depression or suicidal ideation (PHQ-9 screening).

Board Review — High Yield

  • •Auspitz sign, pinpoint bleeding upon scale removal; classic but not pathognomonic.
  • •Koebner phenomenon, development of psoriatic lesions at sites of trauma; present in 25-50% of patients.
  • •PASI 75, standard efficacy endpoint in clinical trials; modern targets aim for PASI 90 or PASI 100.
  • •IL-23/Th17 axis, central pathogenic pathway; IL-23 stabilizes Th17 cells which produce IL-17, driving keratinocyte proliferation.
  • •HLA-C*06:02, strongest genetic risk allele, particularly for early-onset plaque psoriasis.
  • •Spesolimab, anti-IL-36 receptor antibody; first-line for generalized pustular psoriasis flares (900 mg IV single dose).
  • •Deucravacitinib, oral TYK2 inhibitor; PASI 75 ~58% at week 16, superior to apremilast.
  • •Bimekizumab, dual IL-17A/F inhibitor; highest PASI 100 rates (62% at week 16 vs 49% with secukinumab).
  • •Guselkumab, IL-23p19 inhibitor; superior to adalimumab and secukinumab at week 48 in head-to-head trials.
  • •Certolizumab pegol, PEGylated Fab fragment with minimal placental transfer; preferred biologic in pregnancy.

Deep Dive — Evidence Details

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