INFLAMMATORY AND IMMUNE-MEDIATED SKIN DISORDERS

Psoriasis

Etiology and risk factors

• Genetic susceptibility and family history contribute to psoriasis, with immune and epidermal factors interacting in disease expression (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Triggers and exacerbating factors include streptococcal infection, skin trauma, stress, smoking, alcohol, obesity, and selected medications. Withdrawal of systemic corticosteroids can provoke severe rebound disease (Gohara et al., 2012; Pincus & McCalmont, 2019).

Pathophysiology

• Dendritic-cell and T-cell activation drives TNF, IL-23, and IL-17 signaling. Keratinocyte proliferation accelerates and differentiation becomes incomplete (Norris, 2020; Pincus & McCalmont, 2019).
• Epidermal thickening, elongated rete ridges, parakeratosis, neutrophils in stratum corneum, dilated dermal capillaries, and inflammation produce scale, plaque thickness, and Auspitz bleeding (Norris, 2020; Pincus & McCalmont, 2019).
• Systemic immune activation contributes to psoriatic arthritis and cardiometabolic comorbidity (Norris, 2020; Pincus & McCalmont, 2019).

Clinical manifestations

• Well-demarcated erythematous plaques with adherent silvery scale, commonly on elbows, knees, scalp, lumbosacral area, and umbilicus. Inverse disease affects folds with less scale (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Nail pitting, onycholysis, oil-drop change, or subungual hyperkeratosis. Guttate lesions may follow streptococcal infection. Pustular and erythrodermic forms can be systemic emergencies (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Inflammatory joint pain, stiffness, dactylitis, enthesitis, or asymmetric oligoarthritis suggests psoriatic arthritis (Gohara et al., 2012; Pincus & McCalmont, 2019).

Findings that argue against or redirect

• Transient lesions that resolve within 24 hours favor urticaria. Annular plaques with an active border and fungal evidence favor tinea (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Greasy yellow scale in sebaceous areas favors seborrheic dermatitis. Flexural eczematous disease with intense pruritus favors atopic dermatitis (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Mucosal involvement is uncommon in psoriasis; painful mucosal erosions and skin detachment require evaluation for another disorder (Gohara et al., 2012; Pincus & McCalmont, 2019).

Diagnostic evaluation

• Diagnose psoriasis clinically after examination of the skin, scalp, nails, and joints. Document body-surface area, physician global assessment or another validated severity measure, high-impact sites, symptoms, and quality-of-life burden (American Academy of Dermatology, n.d.; Pincus & McCalmont, 2019).
• Biopsy atypical lesions and perform fungal testing when tinea is plausible. Screen for psoriatic arthritis and associated cardiometabolic disease, inflammatory bowel disease, smoking and alcohol use, and psychiatric comorbidity (American Academy of Dermatology, n.d.; Pincus & McCalmont, 2019).

Expected diagnostic and laboratory findings

• Biopsy: regular psoriasiform epidermal hyperplasia, parakeratosis, reduced/absent granular layer, neutrophils in stratum corneum, and dilated papillary dermal capillaries (Gohara et al., 2012; Pincus & McCalmont, 2019).
• No blood test confirms psoriasis. Inflammatory markers may rise with extensive disease or arthritis but are nonspecific (Gohara et al., 2012; Pincus & McCalmont, 2019).

Differential diagnosis

• Tinea corporis/capitis: annular advancing border, fungal elements on KOH/culture (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Seborrheic dermatitis: greasy scale in scalp, nasolabial, eyebrow, or presternal areas; borders usually less sharp (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Atopic/contact dermatitis: exposure/flexural pattern, vesiculation or lichenification, and less classic silvery extensor scale (Gohara et al., 2012; Pincus & McCalmont, 2019).
• Secondary syphilis: systemic exposure/history, palm/sole involvement, and positive serology (Gohara et al., 2012; Pincus & McCalmont, 2019).

Treatment and management

• For limited plaque psoriasis outside intertriginous areas, topical corticosteroids are first-line. Vitamin D analogs, tazarotene, and calcineurin inhibitors can reduce corticosteroid exposure or treat selected sites (American Academy of Dermatology, n.d.; Pincus & McCalmont, 2019).
• Use phototherapy or systemic therapy for moderate to severe, functionally important, refractory, pustular, erythrodermic, or arthritic disease. Options include methotrexate, apremilast, cyclosporine, acitretin, and biologic therapy selected according to phenotype, comorbidity, pregnancy, infection risk, and monitoring needs (American Academy of Dermatology, n.d.; Pincus & McCalmont, 2019).
• Avoid routine systemic corticosteroids because withdrawal can destabilize disease. Coordinate dermatology and rheumatology care when psoriatic arthritis is present or suspected (American Academy of Dermatology, n.d.; Pincus & McCalmont, 2019).

Additional complications and red flags

• Do not overlook psoriatic arthritis, which can produce irreversible joint damage (American Academy of Dermatology, n.d.; Pincus & McCalmont, 2019).

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References

American Academy of Dermatology. (n.d.). Psoriasis clinical guideline. Retrieved September 9, 2026, from https://www.aad.org/member/clinical-quality/guidelines/psoriasis

Gohara, M. A., Schaffer, J. V., Abbasi, N. R., Kingsley, M. M., Sheehan, J. M., & Arndt, K. A. (2012). Inflammatory dermatoses (rashes). In M. C. Henderson, L. M. Tierney, Jr., & G. W. Smetana (Eds.), The patient history: An evidence-based approach to differential diagnosis (2nd ed.). McGraw-Hill.

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Pincus, L. B., & McCalmont, T. H. (2019). Diseases of the skin. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed.). McGraw-Hill Education.