Psoriasis and Eczema

Psoriasis — non-modifiable

• Polygenic susceptibility: PSORS1 locus on chromosome 6p, with HLA-Cw6 the strongest allele; early-onset (type I) disease and guttate variants cluster in HLA-Cw6 carriers. A first-degree relative with psoriasis is the single most common historical clue in a stem.
• Immune wiring: constitutive IL-23/Th17 signaling is the mechanistic substrate on which every trigger acts — triggers do not create the disease, they unmask a primed axis.

Psoriasis — modifiable / provoked

• Infection: group A streptococcal pharyngitis precedes guttate psoriasis by 1–3 weeks (molecular mimicry between streptococcal M protein and keratin); HIV paradoxically worsens psoriasis despite CD4 depletion.
• Drugs: beta blockers, lithium, antimalarials, NSAIDs, and interferons provoke or flare disease; abrupt withdrawal of systemic corticosteroids is the classic precipitant of generalized pustular psoriasis.
• Trauma: Koebner phenomenon — plaques arise in surgical scars, scratches, tattoos, sunburn.
• Lifestyle: smoking (especially palmoplantar pustulosis), obesity, alcohol, and psychological stress worsen severity and blunt treatment response; the AAD/National Psoriasis Foundation comorbidity guideline frames weight loss and smoking cessation as disease-modifying.

Atopic dermatitis — non-modifiable

• Filaggrin loss-of-function mutations: the strongest genetic risk factor; also cause ichthyosis vulgaris, explaining palmar hyperlinearity and xerosis in affected families.
• Family/personal atopy: maternal atopy carries the greatest weight; onset is usually in infancy.
• Skin of color and lower socioeconomic status are associated with greater severity and undertreatment.

Atopic dermatitis — modifiable

• Barrier insults: harsh surfactant soaps, hot prolonged bathing, wool, low ambient humidity and winter heating increase transepidermal water loss.
• Microbial: Staphylococcus aureus colonization with superantigen-driven T-cell activation drives flares.
• Aeroallergens and, in a minority of infants, food allergens can flare disease; the AAD cautions against broad elimination diets, which risk nutritional harm and true IgE-mediated sensitization.

PSORIASIS

• Th1/Th17 immune dysregulation: Abnormal T-cell activation leads to excessive production of pro-inflammatory cytokines (TNF-α, IL-17, IL-23, IFN-γ) that drive keratinocyte proliferation and differentiation
• Genetic predisposition with environmental triggers: HLA-Cw6 association; triggered by streptococcal infection (guttate variant), stress, NSAIDs, beta-blockers, lithium, and withdrawal of systemic corticosteroids
• Abnormal keratinocyte cycling: Psoriatic lesions show dramatically increased epidermal cell turnover (4-5 days vs. normal 28 days), resulting in thickened stratum corneum and characteristic scale
• Angiogenesis and vasodilation: Increased dermal vascularity and elongated dermal papillae contribute to erythema and bleeding when scale is removed (Auspitz sign)
• Defective skin barrier: Despite appearing to be a surface disease, psoriasis involves dysregulation of tight junctions and increased transepidermal water loss (TEWL)

ATOPIC DERMATITIS (ECZEMA)

• Impaired epidermal barrier function: Loss-of-function mutations in filaggrin gene (FLG) and other structural proteins (claudins, desmoglein-1) reduce skin barrier integrity; mutation carriers show 3-4 fold increased AD risk
• Dysbiosis and antimicrobial dysfunction: Reduced expression of antimicrobial peptides (including β-defensins) and altered microbiome composition predispose to Staphylococcus aureus colonization and superinfection
• Th2-predominant immune response: IL-4, IL-13, and IL-31 drive eosinophilic inflammation, mast cell activation, and intense pruritus; IgE levels are elevated in ~80% of moderate-to-severe cases
• Pruritus-scratch cycle: IL-31 from activated T cells and mast cells acts on nociceptors; scratching causes microtrauma, barrier dysfunction, and further inflammation in self-perpetuating cycle
• Allergen sensitization: Impaired barrier allows epicutaneous allergen penetration, leading to heightened allergic responses and association with "atopic triad" (eczema, allergic rhinitis, asthma)

PSORIASIS

• Well-demarcated erythematous plaques with silvery-white scale: Most common presentation; classic lesions have sharply defined borders distinguishing them from other dermatologic conditions
• Symmetric distribution on extensor surfaces: Characteristic involvement of elbows, knees, scalp, and lower back (sacral region); can become generalized in severe cases
• Auspitz sign (pinpoint bleeding) and Koebner phenomenon (lesions appearing at sites of trauma): Key clinical signs; Koebner effect occurs in ~25% of patients and guides counseling
• Variants with distinct presentations:
• Guttate psoriasis: Abrupt onset of small (1-10mm) papules, often post-streptococcal; good initial prognosis but can progress to chronic plaque type
• Inverse/intertriginous psoriasis: Presents in skin folds (axillae, groin, inframammary) with erythema and minimal scale; often misdiagnosed as fungal infection
• Pustular psoriasis: Localized (palms/soles) or generalized; generalized pustular psoriasis is rare but serious
• Erythrodermic psoriasis: Rare (<3% of cases) but life-threatening; >90% body surface area involvement with systemic symptoms
• Nail involvement (psoriatic onychopathy): Pitting (most specific finding), nail bed discoloration ("oil drop sign"), subungual hyperkeratosis, and onycholysis; present in ~50% of patients
• Minimal to moderate pruritus: Unlike eczema, psoriasis is often less intensely pruritic, though this varies; some patients report significant itch
• Psoriatic arthritis: Occurs in 10-30% of psoriasis patients; asymmetric oligoarthritis most common pattern; may precede skin disease

ATOPIC DERMATITIS (ECZEMA)

• Intense pruritus (often worse at night): Hallmark feature often precedes visible lesions ("pruritus precedes rash"); severely impacts sleep and quality of life; pruritus-induced excoriations are common
• Acute phase: Erythema, vesicles, oozing, and crusting: Poorly demarcated erythematous areas with microscopic vesicles that rupture; may appear "weeping" with serous drainage
• Chronic phase: Lichenification, excoriations, and hyperpigmentation/hypopigmentation: Results from chronic scratching and rubbing; thickened skin with exaggerated skin markings pathognomonic for chronic eczema
• Characteristic age-dependent distribution:
• Infants (2-6 months): Face, scalp, extensor surfaces (cheeks, forehead, shins)
• Children (2-12 years): Face, neck, hands, feet, flexural surfaces (antecubital/popliteal fossae)
• Adults: Often flexural; hands frequently affected (occupational irritant dermatitis overlap common)
• Associated features indicating atopic predisposition:
• Xerosis (dry skin) and ichthyosis vulgaris
• Keratosis pilaris (follicular hyperkeratosis on extensor surfaces)
• Palmar hyperlinearity (increased palmar creases)
• Elevated IgE levels and positive allergen-specific IgE testing
• Personal or family history of allergic rhinitis, asthma, or food allergies
• Susceptibility to secondary bacterial infection: Colonization with S. aureus is nearly universal; clinical signs of infection include pustules, purulent drainage, increased oozing, and systemic symptoms (fever, lymphadenopathy)
• Facial dermatitis variant in infants: Can mimic seborrheic dermatitis but typically more pruritic and doesn't spare intertriginous areas

PSORIASIS

• Clinical diagnosis based on morphology and distribution: No single diagnostic test; diagnosis made by characteristic appearance and location of well-demarcated scaly plaques on extensor surfaces
• Dermoscopy findings: Regular dots (stippled vasculature), white lines (fibrin layers), and red globules seen with dermoscopic examination; helpful in atypical presentations
• Skin biopsy (rarely needed): Reserved for atypical cases; shows parakeratosis (nuclei retained in stratum corneum, pathognomonic for psoriasis), regular acanthosis (epidermal thickening), elongated dermal papillae, and dilated vasculature in papillary dermis; absence of spongiosis distinguishes from eczema
• Clinical assessment tools: PASI (Psoriasis Area and Severity Index) quantifies disease burden; BSA (body surface area) estimation guides systemic therapy decisions (systemic agents typically considered for ≥10% BSA involvement)
• Rule out secondary causes or triggers: Careful history for medications (beta-blockers, lithium, NSAIDs), recent streptococcal infection (especially in guttate variant), and triggers (stress, alcohol)
• Metabolic screening in moderate-to-severe disease: Screen for associated metabolic syndrome (obesity, hypertension, dyslipidemia, type 2 diabetes) with weight, BP, lipid panel, and fasting glucose

ATOPIC DERMATITIS

• **Diagnostic criteria (Hanifin &

Psoriasis — first line (AAD/National Psoriasis Foundation)

• Topical corticosteroids: e.g., triamcinolone to the body, low-potency hydrocortisone to face/folds; the backbone for limited plaque disease.
• Vitamin D3 analogs: calcipotriene, usually combined with a steroid (fixed-dose calcipotriene/betamethasone) to normalize keratinocyte differentiation and permit steroid sparing.
• Adjuncts: tazarotene, coal tar, keratolytics (salicylic acid); topical calcineurin inhibitors (tacrolimus) off-label for face and inverse disease to avoid atrophy.

Escalation for extensive (roughly ≥10% BSA), disabling, or joint disease

• Phototherapy: narrowband UVB first, as it lacks systemic toxicity.
• Oral systemics: methotrexate (also treats psoriatic arthritis), apremilast (PDE4), acitretin (best for pustular/erythrodermic), cyclosporine for rapid control only.
• Biologics: TNF-α inhibitors (adalimumab), IL-12/23 (ustekinumab), IL-17 (secukinumab), IL-23 (guselkumab). Screen for latent tuberculosis and hepatitis B before starting.

Atopic dermatitis (AAD guidelines)

• Foundation: liberal emollients, short lukewarm baths with immediate moisturizing, trigger avoidance — continued even in remission.
• First line: topical corticosteroids by potency-to-site matching; topical calcineurin inhibitors (tacrolimus, pimecrolimus) or crisaborole for face, eyelids, and folds.
• Escalation: proactive twice-weekly topical therapy, wet-wrap therapy, narrowband UVB, then dupilumab (IL-4Rα blockade) or tralokinumab; oral JAK inhibitors (upadacitinib, abrocitinib) carry a boxed warning for thrombosis, MACE, and malignancy.
• Avoid: chronic systemic corticosteroids (rebound flare) and routine systemic antibiotics without clinical infection. Dilute bleach baths may reduce S. aureus burden in recurrent infection.

Psoriasis — disease

• Psoriatic arthritis: enthesitis and erosive joint destruction from the same IL-23/IL-17 axis; signaled by dactylitis ("sausage digit"), morning stiffness, and nail pitting — nail disease is the strongest cutaneous predictor. Irreversible if untreated, so screen at every visit.
• Erythrodermic psoriasis — emergency: loss of the cutaneous barrier over >90% BSA causes high-output cardiac failure, hypothermia, hypoalbuminemia, and sepsis.
• **Generalized pustular psoriasis (von Zumbusch) — emergency**: sheets of sterile pustules with fever and leukocytosis; classically follows systemic steroid withdrawal.
• Cardiometabolic disease: chronic systemic inflammation accelerates atherosclerosis; the AAD/NPF comorbidity guideline advises screening for hypertension, dyslipidemia, diabetes, and obesity. Also associated with inflammatory bowel disease, uveitis, and depression.

Psoriasis — treatment

• Methotrexate: hepatotoxicity, myelosuppression, pneumonitis; monitor CBC and LFTs, supplement folate.
• Cyclosporine: nephrotoxicity and hypertension — limits use to short courses.
• Biologics: reactivation of latent tuberculosis and hepatitis B; IL-17 blockers cause mucocutaneous candidiasis and may unmask or worsen IBD; TNF inhibitors can produce paradoxical psoriasiform eruptions and demyelination.
• Phototherapy/PUVA: photoaging and nonmelanoma skin cancer.

Atopic dermatitis — disease

• Eczema herpeticum — emergency: HSV disseminating through a defective barrier; monomorphic punched-out erosions with hemorrhagic crust, fever, and pain. Confirm with PCR/Tzanck and start systemic acyclovir immediately; ocular involvement warrants ophthalmology.
• Bacterial superinfection: honey-colored crust, pustules, or worsening exudate from S. aureus.
• Atopic march: progression to food allergy, asthma, allergic rhinitis via epicutaneous sensitization.
• Ocular disease: keratoconjunctivitis, keratoconus, atopic cataract; sleep deprivation and depression are underappreciated morbidities.

Atopic dermatitis — treatment

• Potent topical corticosteroids: atrophy, striae, telangiectasia, periorificial dermatitis, and HPA-axis suppression in infants (high surface-area-to-weight ratio).
• Calcineurin inhibitors: application-site burning; boxed lymphoma warning remains largely theoretical.
• Dupilumab: conjunctivitis and facial erythema.

• Auspitz sign and Koebner phenomenon are psoriasis, not eczema: pinpoint bleeding on scale removal reflects elongated dermal papillae with thinned suprapapillary plates. Eczema's counterpart clue is lichenification from chronic scratching.
• Histology is the cleanest discriminator: psoriasis shows parakeratosis, regular acanthosis, and Munro microabscesses with no spongiosis; eczema shows spongiosis (intercellular epidermal edema) with a perivascular lymphocytic infiltrate.
• Child with abrupt "raindrop" papules on the trunk 2 weeks after sore throat = guttate psoriasis. The best next step is confirming recent streptococcal infection (throat culture/ASO); treat the skin with topicals or narrowband UVB — antibiotics do not reliably clear the eruption.
• Never treat chronic plaque psoriasis with systemic corticosteroids: taper precipitates von Zumbusch pustular psoriasis or erythroderma. This is the most frequently tested management error in the topic.
• The drug triggers to memorize: beta blockers, lithium, antimalarials, NSAIDs, and interferons. A newly worsening psoriatic patient started on a beta blocker for hypertension is a stock stem.
• Nail pitting plus dactylitis predicts psoriatic arthritis; rheumatoid factor is typically negative (seronegative spondyloarthropathy), and radiographs may show the pencil-in-cup deformity.
• Rapidly worsening eczema with monomorphic punched-out erosions, fever, and pain = eczema herpeticum: the single best next step is systemic acyclovir, not a topical steroid or oral antibiotic. Delay risks HSV viremia and ocular involvement.
• Common distractors: inverse psoriasis in the groin is misread as candidal intertrigo (look for satellite pustules and a KOH prep to separate them); seborrheic dermatitis mimics scalp psoriasis but has greasy yellow scale and less sharply demarcated borders; and filaggrin mutation belongs to atopic dermatitis while HLA-Cw6 belongs to psoriasis.