Psoriasis

Global prevalence ~2–3%; 7.5 million US adults. Bimodal onset: early (20s–30s) and late (50s–60s). Apparent prevalence is lower in East Asian and African populations in epidemiologic studies — but under-recognition in darker skin (violaceous rather than red erythema) likely contributes to under-reporting. ~20–30% of psoriasis patients develop psoriatic arthritis (PsA); skin typically precedes joints by ~10 years.

Associated comorbidities (elevated risk): cardiovascular disease, type 2 diabetes, metabolic syndrome, NAFLD, IBD (especially Crohn), uveitis, depression/anxiety.

Th17/IL-23 axis is central. Activated dendritic cells produce IL-23 → Th17 polarization → IL-17A, IL-17F, IL-22 → keratinocyte hyperproliferation (epidermal turnover 4–7 days vs. normal 28) and inflammation. TNF-α amplifies.

Genetics: strong heritability; HLA-C\*06:02 most associated. Over 60 psoriasis susceptibility loci (PSORS1–PSORS9 and more).

Triggers:

• Infection — β-hemolytic strep → guttate psoriasis (post-pharyngitis, especially children).
• Medications — beta-blockers, lithium, antimalarials, IFN-α, rapid corticosteroid taper, paradoxical with TNF-α inhibitors.
• Trauma — Koebner phenomenon.
• Stress, smoking, obesity, alcohol — all worsen.

Classic plaque psoriasis: well-demarcated, salmon-pink to red erythematous plaques with loosely adherent silvery-white scale. Bilateral, symmetric. Favored sites: elbows, knees, extensor surfaces, scalp, lumbosacral area, umbilicus, intergluteal cleft, nails. Variably pruritic (~60–70%); not always.

Auspitz sign: removing scale reveals pinpoint bleeding from dilated papillary vessels.

Koebner phenomenon: new plaques at sites of skin injury (tattoo, scar, sunburn).

Morphology differs substantially and is routinely under-recognized:

• Color: plaques appear violaceous, grey-brown, hyperpigmented, or dusky — not salmon-pink. 'Erythema' in Fitzpatrick V–VI is not red; describe what you actually see.
• Scale: often thicker, more silver-grey or even dull grey. Dry scale over dark background can look less inflammatory than it is.
• Post-inflammatory hyper- and hypopigmentation: prominent, long-lasting (months to years), and frequently the patient's dominant concern. This is part of the disease, not a cosmetic side issue — counsel on it at every visit.
• Scalp psoriasis in textured hair: often misdiagnosed as seborrheic dermatitis or 'dandruff.' Scale is typically thicker, more demarcated, and can extend onto the forehead (frontal hairline band). Look between braids/locs carefully.
• Palmoplantar psoriasis is common in SoC and is both disabling and frequently confused with eczema or tinea.
• Nail psoriasis (pitting, oil drops, onycholysis, subungual hyperkeratosis) occurs across skin tones but is under-recognized because nails are not always examined.
• Misdiagnosis as eczema, tinea, or seborrheic dermatitis is common; biopsy if uncertain — histology is tone-independent.

• Plaque — 80–90% of cases; as described.
• Guttate — 1–10 mm 'droplet' papules/small plaques on trunk/extremities; frequently post-streptococcal; younger patients; may resolve or progress to plaque.
• Inverse (intertriginous) — intertriginous regions (axillae, inframammary, inguinal, intergluteal); lack scale (friction/moisture); smooth, well-demarcated erythema.
• Pustular — generalized (von Zumbusch — emergency, fever, sheets of sterile pustules), localized palmoplantar pustulosis, acrodermatitis continua of Hallopeau (distal digit).
• Erythrodermic — >90% BSA erythema; fluid/electrolyte/thermoregulation emergency.
• Nail — pitting (most common), onycholysis, subungual hyperkeratosis, oil drop sign, splinter hemorrhages.
• Palmoplantar — hyperkeratotic, painful, disabling.
• Scalp — plaques with adherent scale, may extend onto forehead/nape.
• Psoriatic arthritis (PsA) — see below.

Onset frequently in late childhood/adolescence. Guttate common after streptococcal pharyngitis. Differentiate from atopic dermatitis (more pruritic, flexural, less demarcated) and tinea (KOH). Scalp involvement may precede plaques. Topical therapy is first-line; use lower-potency steroids on face/intertriginous; vitamin D analogs well-tolerated. Systemic options expanded — MTX, cyclosporine, and several biologics approved in pediatrics (etanercept, adalimumab, ustekinumab, ixekizumab, secukinumab depending on age). Screen for PsA in juvenile-onset psoriasis.

• Atopic dermatitis — ill-defined, more pruritic, flexural, weepier; often personal/family atopy.
• Seborrheic dermatitis — greasy yellowish scale, nasolabial/scalp/chest distribution.
• Tinea corporis/capitis — annular with central clearing; KOH positive.
• Nummular eczema — round, often oozing, less scale.
• Lichen planus — violaceous polygonal papules, Wickham striae, mucosal involvement.
• Pityriasis rubra pilaris — salmon plaques with islands of sparing, palmoplantar keratoderma; rare.
• Mycosis fungoides (CTCL) — adult-onset 'eczema' or 'psoriasis' unresponsive to therapy; biopsy.
• Cutaneous lupus erythematosus (DLE, SCLE) — photodistributed, atrophy (DLE), ANA.
• Secondary syphilis — palmoplantar copper-colored plaques, palmar and generalized; RPR.

Clinical diagnosis in most cases. Biopsy if atypical.

Screen every patient for:

• PsA — joint pain, morning stiffness, dactylitis, enthesitis. Tools: PEST, GEPARD questionnaires. Early rheumatology referral for suspicious findings.
• Cardiovascular/metabolic risk — BP, lipids, HbA1c, BMI.
• Depression — PHQ-9 if clinical concern.
• IBD — ask about GI symptoms; affects biologic choice.

Pre-biologic workup:

• Tuberculosis — IGRA (QuantiFERON or T-SPOT) at baseline and annually.
• Hepatitis B and C — HBsAg, HBcAb, HCV Ab.
• HIV — where clinically appropriate.
• CBC, LFTs — baseline.
• Immunization status — pneumococcal, influenza, shingles (avoid live vaccines with systemic immunosuppressives; RZV/Shingrix is preferred and recombinant).

Classic findings:

• Regular acanthosis with elongated, club-shaped rete ridges.
• Parakeratosis (retained nuclei in stratum corneum).
• Absent or diminished granular layer.
• Munro microabscesses — neutrophils in stratum corneum.
• Spongiform pustules of Kogoj — neutrophils in the upper spinous layer.
• Thinned suprapapillary plates.
• Dilated, tortuous capillaries in dermal papillae (basis of the Auspitz sign).
• Perivascular lymphocytic infiltrate in the papillary dermis.

Guttate — similar but more parakeratotic, less acanthotic; patchy.

Pustular — large subcorneal pustules (macropustules of Kogoj).

Differentiators on histology: spongiform pustules and Munro microabscesses are highly suggestive of psoriasis; eosinophils favor an eczematous process; eczema shows spongiosis (intercellular edema) rather than regular acanthosis.

Localized plaque psoriasis:

• Topical corticosteroids — potency matched to site and severity. Class I (clobetasol 0.05%) for body plaques, short courses; class VI–VII for face/intertriginous. Pulsed dosing to minimize tachyphylaxis and atrophy.
• Vitamin D analogs (calcipotriene, calcitriol) — steroid-sparing, slower onset; combination products (Taclonex, Enstilar foam) are more effective than either alone.
• Tazarotene — topical retinoid; adjunct, irritation limits.
• Topical calcineurin inhibitors (tacrolimus, pimecrolimus) — off-label, useful for face/intertriginous where steroids thin skin.
• Tapinarof (AhR modulator) and roflumilast (PDE4) — newer non-steroid topicals with clean safety profile.

Scalp: clobetasol foam/solution, calcipotriene solution, coal tar shampoo, salicylic acid to lift scale. Textured hair: emulsify with oil/conditioner to reach scalp; overnight oil-based treatments.

Palmoplantar: class I steroid under occlusion; tazarotene; phototherapy; systemic escalation often required.

Moderate-severe = BSA >10%, involvement of critical sites (face, palms, soles, genital), or significant QoL impact.

Phototherapy:

• Narrowband UVB (nb-UVB) — first-line, durable, steroid-sparing, safe long-term; 2–3x/week.
• Targeted excimer laser — small recalcitrant areas.
• PUVA — largely superseded; skin cancer risk.

Traditional systemics:

• Methotrexate 7.5–25 mg weekly + folate; monitor CBC, LFTs. Effective, widely available.
• Cyclosporine 2.5–5 mg/kg/day — short-term bridge; BP, renal monitoring; limit duration.
• Apremilast (PDE4 inhibitor) — oral, modest efficacy, clean safety, GI side effects common, no labs.
• Acitretin — retinoid, teratogenic (3-yr pregnancy avoidance), good for pustular/erythrodermic.
• Deucravacitinib (TYK2 inhibitor, oral) — newer; mild immunosuppression.

Biologics — now standard of care for moderate-severe:

• IL-17 inhibitors: secukinumab, ixekizumab, brodalumab (anti-IL-17R). Fast onset, high clearance rates. Avoid in inflammatory bowel disease (can worsen). Candida surveillance.
• IL-23 inhibitors: guselkumab, risankizumab, tildrakizumab. Long dosing intervals (every 8–12 weeks maintenance), excellent safety profile, current first-line for many. Work well in IBD overlap.
• IL-12/23 inhibitor: ustekinumab — older, well-tolerated, pediatric approved.
• TNF-α inhibitors: adalimumab, etanercept, infliximab, certolizumab. Historical first-line; still important for PsA/IBD overlap. Watch TB reactivation, heart failure, demyelinating disease.

Choice is guided by comorbidities (PsA → TNF or IL-17 or IL-23; IBD → IL-23 or TNF, avoid IL-17; pregnancy → certolizumab preferred for placental transfer profile), access, and patient preference.

Chronic and relapsing. Modern biologic therapy achieves PASI 90 (90% clearance) in 60–80% of treated patients — complete or near-complete skin clearance is a realistic goal for most. Untreated moderate-severe disease is associated with increased cardiovascular mortality, depression, and disability. Early systemic treatment may reduce progression to PsA (observational evidence).

• Violaceous or grey-brown plaques in darker skin is psoriasis, not eczema, not tinea. Describe what you see.
• PIH is the disease, not a cosmetic issue. Counsel patients that PIH can outlast active disease by months; treatments include gentle care, photoprotection, and time.
• Screen for PsA every visit. Dactylitis, enthesitis, and AM stiffness often precede radiographic changes.
• Undertreatment is the commonest failure. A patient with 15% BSA on topicals is inadequately treated; escalate to phototherapy, systemic, or biologic.
• Biologics are remarkably safe. Don't avoid them out of caution when the disease burden justifies.
• Beta-blockers, lithium, antimalarials, rapid steroid taper, and IFN can all flare psoriasis — check med list before labeling 'treatment-resistant.'
• Auspitz sign and Koebner are classic but not pathognomonic.
• Scalp psoriasis at the frontal hairline in textured hair is often missed; look deliberately.
• Genital and inverse psoriasis cause disproportionate QoL impact — ask about them.

Psoriasis is a chronic autoimmune condition, not an infection and not contagious. It is strongly linked to inflammation throughout the body — heart, joints, liver, mood — so treatment matters beyond the skin. Modern treatment (including biologic injections) can clear most people's skin completely. Trigger reduction helps: don't smoke, moderate alcohol, manage weight, treat strep infections early. Watch for joint symptoms (pain, morning stiffness, swelling) and report them — early joint treatment prevents damage. In darker skin, the plaques may look purplish or grey-brown rather than red, and the color changes left behind after plaques clear will fade but may take months to a year. Vaccinate according to your derm/PCP before starting biologics.