Dermatology · PANCE / PANRE

Psoriasis

Chronic immune-mediated inflammatory disorder with well-demarcated erythematous plaques and silvery scale; systemic comorbidities.

Also known as: psoriasis, plaque psoriasis, psoriasis vulgaris, guttate psoriasis, inverse psoriasis, pustular psoriasis

Overview

A chronic immune-mediated inflammatory skin disease driven by IL-23/Th17 axis activation, characterized by well-demarcated erythematous plaques with silvery-white scale and frequent involvement of scalp, extensor surfaces, and nails. Systemic disease with cardiometabolic and joint comorbidities.

Epidemiology

Prevalence 2-3% in the US; bimodal onset (16-22 and 57-60 years). Equal sex distribution. ~30% develop psoriatic arthritis (PsA). Strong genetic component — HLA-Cw6 association.

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Question 1DermatologyMedium
A 35-year-old woman has a several-month history of itchy, well-demarcated erythematous plaques topped with thick silvery scale on the extensor surfaces of her elbows and knees and on her scalp. Several fingernails show pitting, and the eruption reliably worsens during the winter months. Which of the following is the most likely diagnosis?
  • ALichen planus
  • BSeborrheic dermatitis
  • CTinea corporis
  • DPsoriasis vulgaris
Reveal answer & full explanation
Correct answer: D — Psoriasis vulgaris
  • ALichen planus
  • BSeborrheic dermatitis
  • CTinea corporis
  • DPsoriasis vulgaris

Why Psoriasis vulgaris is correct

  • Well-demarcated erythematous plaques with silvery scale on extensor surfaces (elbows, knees) and the scalp are the classic distribution of chronic plaque psoriasis
  • Nail pitting is a characteristic associated finding, along with distal onycholysis and oil-drop spots
  • Winter worsening reflects reduced ultraviolet exposure and drier skin, a typical seasonal pattern
  • The chronic, sharply marginated, scaly extensor plaques integrate into one coherent diagnosis

Why the others are wrong

  • Lichen planus — presents with purple, polygonal, flat-topped papules and lacy Wickham striae on flexural surfaces, not silvery extensor plaques (confused-with another papulosquamous disorder)
  • Seborrheic dermatitis — causes greasy, yellowish scale on the scalp, nasolabial folds, and chest rather than thick silvery plaques on elbows and knees (buzzword-matching scalp scaling)
  • Tinea corporis — a dermatophyte infection forming annular plaques with central clearing and a scaly advancing border; it does not cause nail pitting or this symmetric extensor pattern (premature closure on a "scaly rash")
Question 2DermatologyMedium
A 45-year-old man with moderate-to-severe plaque psoriasis (PASI 22) and a longstanding history of Crohn disease presents for treatment. He has previously failed methotrexate and adalimumab. His dermatologist wants a biologic that will treat his skin disease without flaring his inflammatory bowel disease. Which of the following biologics is the most appropriate choice for this patient?
  • ARisankizumab
  • BSecukinumab
  • CInfliximab
  • DBrodalumab
Reveal answer & full explanation
Correct answer: A — Risankizumab
  • ARisankizumab
  • BSecukinumab
  • CInfliximab
  • DBrodalumab

Why Risankizumab is correct

  • PASI 22 plaque psoriasis with comorbid Crohn disease requires an agent effective for both conditions, and prior failure of methotrexate plus the anti-TNF adalimumab narrows the options
  • Risankizumab is a selective interleukin-23 (IL-23 p19) inhibitor FDA-approved for both moderate-to-severe plaque psoriasis and Crohn disease (ADVANCE and MOTIVATE trials)
  • It delivers high skin clearance while inducing and maintaining remission in Crohn disease, so it treats the bowel rather than flaring it
  • AAD-NPF and gastroenterology (ECCO/AGA) guidance favor IL-23 inhibitors or ustekinumab in psoriasis with coexisting IBD

Why the others are wrong

  • Secukinumab — an IL-17A inhibitor; IL-17 blockade can precipitate or worsen inflammatory bowel disease, so it is avoided in Crohn disease (right-disease-wrong-pathway)
  • Infliximab — an anti-TNF agent, but this patient already failed adalimumab, so switching within the same class has lower yield than changing mechanism (confused-with class switch)
  • Brodalumab — blocks the IL-17 receptor and carries the same IBD-flare risk plus a boxed warning for suicidal ideation (anchoring on psoriasis efficacy)

Additional high-yield points

  • In psoriasis with IBD, IL-23 inhibitors (risankizumab, guselkumab) and ustekinumab are preferred because they treat both diseases, whereas IL-17 pathway agents should be avoided
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Risk factors

  • Family history (40% of patients)
  • HLA-Cw6 and other PSORS susceptibility loci
  • Smoking, obesity, alcohol
  • Streptococcal pharyngitis (triggers guttate psoriasis)
  • HIV (may unmask or worsen disease)
  • Medications: beta-blockers, lithium, antimalarials, IFN-α, abrupt systemic steroid withdrawal, ACEi
  • Koebner phenomenon: trauma, sunburn, tattoo trigger plaques at injured sites
  • Stress, cold weather

Pathophysiology

Dendritic cell activation → IL-23 production → Th17 polarization → IL-17A, IL-17F, IL-22, TNF-α release → keratinocyte hyperproliferation (turnover accelerated from 28 to 3-5 days), incomplete differentiation (parakeratosis), neutrophil microabscesses (Munro), and dilated dermal vessels (Auspitz sign — pinpoint bleeding when scale removed).

Clinical presentation

Symptoms

  • Pruritus (often less intense than eczema), burning, soreness
  • Joint pain, stiffness (PsA) — morning stiffness, dactylitis, enthesitis
  • Psychosocial impact, depression, sexual dysfunction

Signs / physical exam

  • Plaque psoriasis (90%): well-demarcated erythematous plaques with adherent silvery scale on extensor elbows, knees, scalp, lumbosacral area, umbilicus
  • Guttate psoriasis: sudden eruption of small (<1 cm) drop-shaped plaques on trunk and proximal extremities, 1-3 weeks after streptococcal infection; often in children/young adults
  • Inverse (intertriginous) psoriasis: smooth, glossy, erythematous, scale-poor plaques in axillae, inguinal folds, inframammary, intergluteal
  • Pustular psoriasis: generalized (von Zumbusch) — sheets of sterile pustules on erythroderma, fever, leukocytosis, life-threatening; palmoplantar — chronic pustules on palms/soles
  • Erythrodermic psoriasis: >90% BSA erythema and scaling, thermoregulatory failure, high-output cardiac failure — emergency
  • Nail psoriasis: pitting, oil drop sign, onycholysis, subungual hyperkeratosis, splinter hemorrhages, leukonychia
  • Scalp psoriasis: thick adherent scale extending beyond hairline

Classic findings

Auspitz sign (pinpoint bleeding after scale removal); Koebner phenomenon (plaques at sites of trauma); silvery micaceous scale.

Differential diagnosis

  • Seborrheic dermatitis (sebopsoriasis) — Greasy yellow scale in seborrheic distribution; less sharply demarcated; nasolabial folds, eyebrows
  • Atopic dermatitis — Pruritus prominent, flexural, atopy history, less defined borders
  • Tinea corporis — Annular with central clearing, raised scaly border; KOH positive
  • Cutaneous T-cell lymphoma (mycosis fungoides) — Patches/plaques in sun-protected sites in adults; refractory to topical steroids; biopsy
  • Pityriasis rubra pilaris — Salmon-colored plaques with islands of sparing, follicular hyperkeratosis, waxy palmoplantar keratoderma
  • Secondary syphilis — Palmoplantar copper-colored macules, condyloma lata, lymphadenopathy; RPR positive
  • Lichen planus — Purple polygonal pruritic papules with Wickham striae; mucosal involvement
  • Subacute cutaneous lupus — Photo-distributed annular/psoriasiform plaques; SSA positive

Diagnostic workup

Diagnostic criteria

Clinical diagnosis based on lesion morphology and distribution; severity by BSA, PASI, and impact (DLQI). Mild: BSA <3%; moderate: 3-10%; severe: >10% OR involvement of face, palms/soles, genitals, or nails with disability.

Labs

  • Clinical diagnosis
  • Skin biopsy if diagnosis uncertain: parakeratosis, Munro microabscesses, regular acanthosis, thinned suprapapillary plates, dilated tortuous capillaries
  • Pre-biologic workup: CBC, CMP, hepatitis B/C, TB testing (IGRA or PPD), HIV, pregnancy test; chest X-ray if indicated
  • PsA screening: PEST or PsAID questionnaire, joint exam at each visit

Imaging

  • Not routinely indicated for skin disease
  • Joint X-rays/MRI for suspected PsA: 'pencil-in-cup' deformity, periostitis, ankylosis

Diagnostic algorithm

SubtypeHallmarkPreferred First-Line
Plaque (vulgaris)Silvery scale on extensor surfaces, scalp, lumbosacralTopical steroid + vitamin D analogue; NBUVB or biologic if extensive
GuttateDrop-shaped lesions post-strepTreat strep; NBUVB; topical steroid
InverseGlossy red plaques in foldsLow-potency steroid, TCI, calcipotriene
Pustular (generalized)Sheets of sterile pustules, feverHospitalize; cyclosporine, infliximab, spesolimab
Erythrodermic>90% BSA erythema/scaleHospitalize; cyclosporine, infliximab
NailPitting, oil drop, onycholysisIntralesional triamcinolone; systemic if associated PsA
Psoriasis subtypes and preferred first-line therapy.

Treatment

First-line

  • Mild-moderate (limited BSA): topical corticosteroid potency by site — clobetasol 0.05% (high; trunk/extremities, 2 wks then taper), triamcinolone 0.1% (mid), hydrocortisone 1-2.5% (face/folds)
  • Topical vitamin D analogues — calcipotriene/calcipotriol, calcitriol — often combined with steroid (calcipotriene/betamethasone foam, ointment)
  • Topical retinoid — tazarotene 0.05-0.1%
  • Topical calcineurin inhibitors (tacrolimus, pimecrolimus) for face and intertriginous areas
  • Topical PDE4 inhibitor — roflumilast 0.3% cream daily (FDA-approved, all body areas including folds and face)
  • Topical AhR agonist — tapinarof 1% cream daily
  • Coal tar preparations (older) for scalp and plaque psoriasis

Moderate-severe / extensive plaque

  • Phototherapy: narrowband UVB (first-line for widespread plaque), PUVA (rarely used due to skin cancer risk), targeted excimer laser (308 nm) for localized
  • Oral systemics: methotrexate 7.5-25 mg/week (folate, monitor LFTs, CBC), cyclosporine 2.5-5 mg/kg/day (short-term, monitor BP/Cr), acitretin 10-50 mg/day (teratogenic, avoid pregnancy 3 years post), apremilast 30 mg BID (PDE4 inhibitor; no monitoring needed), deucravacitinib 6 mg daily (TYK2 inhibitor)
  • Biologics: anti-TNF — adalimumab, etanercept, infliximab, certolizumab; anti-IL-17 — secukinumab, ixekizumab, brodalumab, bimekizumab; anti-IL-23 — guselkumab, risankizumab, tildrakizumab; anti-IL-12/23 — ustekinumab
  • Choose biologic by comorbidities: IBD favors anti-IL-23 or anti-TNF (avoid anti-IL-17); PsA favors anti-TNF, anti-IL-17, anti-IL-23, JAK inhibitors

Guttate

  • Treat strep infection if active
  • Narrowband UVB highly effective
  • Topical steroids and vitamin D analogues
  • Many cases resolve spontaneously within months

Generalized pustular / erythrodermic

  • Hospitalize; fluid/electrolyte support, temperature regulation
  • Cyclosporine or infliximab for rapid control
  • Spesolimab (anti-IL-36R) — FDA-approved for generalized pustular psoriasis flares
  • Acitretin once stabilized

Second-line / adjunct

  • Salicylic acid keratolytics (3-6%) to remove scale before topical therapy
  • Intralesional triamcinolone for nail matrix or isolated plaques
  • Avoid systemic corticosteroids — rebound and pustular flare on withdrawal

Complications

  • Psoriatic arthritis — peripheral, axial, dactylitis, enthesitis; permanent joint damage if untreated
  • Cardiovascular disease — accelerated atherosclerosis, MI, stroke (independent of traditional risk factors)
  • Metabolic syndrome, obesity, type 2 diabetes, NAFLD
  • Depression, anxiety, suicidality
  • Inflammatory bowel disease (Crohn > UC)
  • Uveitis
  • Erythroderma and pustular flares — life-threatening
  • Increased risk of lymphoma (modest), nonmelanoma skin cancer with PUVA
  • Biologic adverse effects: infection (TB reactivation, HBV reactivation), injection site reactions, candidiasis (anti-IL-17), demyelination (anti-TNF)

PANCE pearls

  • Never give systemic corticosteroids for psoriasis flare — withdrawal can precipitate pustular or erythrodermic psoriasis.
  • Auspitz sign (pinpoint bleeding after scale removal) and Koebner phenomenon (lesions at sites of trauma) are classic.
  • Nail pitting + onycholysis in a patient with joint pain = think psoriatic arthritis even if skin disease is mild.
  • Anti-IL-17 biologics (secukinumab, ixekizumab) can worsen or precipitate IBD — choose anti-IL-23 or anti-TNF for IBD overlap.
  • Check IGRA/PPD and HBV serologies before starting any biologic — TB and HBV reactivation are well-described.

References

  • AAD-NPF 2020-2021 — AAD-National Psoriasis Foundation Joint Guidelines: Biologics, Phototherapy, Topical Therapy, Pediatric Psoriasis, and Comorbidities (Menter et al., J Am Acad Dermatol)
  • GRAPPA 2021 — GRAPPA Treatment Recommendations for Psoriatic Arthritis (Coates et al., Nat Rev Rheumatol 2022)
  • NPF Treat-to-Target — From the Medical Board of the National Psoriasis Foundation: Treatment Targets for Plaque Psoriasis (Armstrong et al., J Am Acad Dermatol 2017)

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