In this article
Global prevalence ~2–3%; Taiwan ~0.235% (Chang 2009). Male-to-female ratio approximately 1:1, with two peaks of onset: 20–30 and 50–60 years。Chronic plaque psoriasis accounts for ~90% of all psoriasis。15–30% of psoriasis patients develop psoriatic arthritis, and skin involvement typically precedes joint involvement by 5–10 years — an important early warning sign.
What is psoriasis?
Psoriasis is a chronic, relapsing, immune-mediated systemic inflammatory disease. The skin is the most visible manifestation, but it is not just a skin disease. Pathogenesis centers on the IL-23/Th17/IL-17 axis: dendritic cells release IL-23, driving Th17, Tc17, and γδ T cells to produce IL-17A, IL-17F, and IL-22, which cause keratinocyte hyperproliferation and neutrophil accumulation (Munro microabscess). Modern biologics target this axis: anti-IL-23 (guselkumab, risankizumab), anti-IL-17 (secukinumab, ixekizumab, bimekizumab), anti-TNFα (adalimumab, etanercept).
Six clinical subtypes
- Chronic plaque psoriasis (~90%) — sharply demarcated erythematous plaques with silvery scale on scalp, elbows, knees, lower back, umbilicus.
- Guttate psoriasis — multiple small drop-like plaques on trunk/limbs, often 1-2 weeks after streptococcal pharyngitis. Common in children and adolescents.
- Inverse / flexural psoriasis — smooth, sharply demarcated erythema in skin folds (axilla, groin, inframammary). Scale is sparse due to maceration.
- Pustular psoriasis — sterile pustules; may be generalized (GPP, with fever and leukocytosis, life-threatening) or palmoplantar (PPP).
- Erythrodermic psoriasis — > 90% BSA diffuse erythema with scale; thermoregulation failure, hypoalbuminemia, infection risk; requires admission.
- Nail psoriasis — pitting, oil-drop sign, subungual hyperkeratosis, onycholysis, splinter hemorrhage. Co-exists with skin/joint disease in ~50%.
Severity assessment
BSA (body surface area, 1 palm ≈ 1%): mild ≤ 3%, moderate 3–10%, severe > 10%. PASI (0–72): < 5 mild, 5–10 moderate, > 10 severe. IGA (0–4) and DLQI (patient-reported QoL) complete the picture. The International Psoriasis Council's 2020 consensus recommends replacing mild/moderate/severe with two categories — candidates for topical vs. systemic therapy; BSA > 10%, special-area involvement, or failed topical therapy each qualifies for systemic therapy. Taiwan NHI biologic threshold (§8.2.4.6.1, 2026/9/22 rules): PASI ≥ 10 (or BSA ≥ 10% for non-PASI-measurable forms like pustular), phototherapy ≥ 2× weekly for 12 weeks, AND failure of at least 2 of MTX / acitretin / cyclosporin / apremilast / deucravacitinib (apremilast listed from 2024/3/1, deucravacitinib from 2025/6/1). The "10/10/10 rule" with DLQI ≥ 10 is a BAD/AAD clinical shorthand, not the NHI legal requirement.
Triggers
Streptococcal pharyngitis (guttate), drugs (β-blockers, lithium, antimalarials, IFN, abrupt steroid taper, terbinafine), Köbner phenomenon (trauma, scratching, tattoos, surgical scars), obesity, smoking (dose-dependent), alcohol, stress, sleep deprivation. Winter worsening is typical; UV exposure improves disease.
Diagnosis
Most psoriasis is diagnosed clinically. Skin biopsy is reserved for atypical cases — to differentiate from eczema, tinea corporis, secondary syphilis, mycosis fungoides (CTCL), SCLE, and pityriasis rubra pilaris. Mandatory comorbidity screening (AAD-NPF 2019): annual joint symptom inquiry for PsA (morning stiffness > 30 min, dactylitis, enthesitis, inflammatory back pain), cardiovascular and metabolic risk factors, mood screening (PHQ-2/9), and DLQI.
Bottom line
Psoriasis is an immune-driven chronic inflammation, not a fungal infection, not contagious, and treatable. Correct subtyping, severity quantification, trigger identification, and comorbidity screening (PsA, metabolic syndrome, depression) are foundations of care. With anti-IL-17 and anti-IL-23 biologics, PASI 90–100 clearance is achievable.