Evidence‑Based Guidelines for Psoriasis and Atopic Dermatitis
Pathophysiology & Systemic Associations
- Psoriasis is a genetic, systemic inflammatory disorder driven by tumor‑necrosis factor‑α (TNF‑α) and the IL‑17A axis, with release of antimicrobial peptides from activated keratinocytes. 1
- Psoriasis is linked to several systemic comorbidities: psoriatic arthritis (affects ~25‑30 % of patients), inflammatory bowel disease, cardiovascular disease, metabolic syndrome, and diabetes. 1, 2
Dermatologic Manifestations
Psoriasis – Core Clinical Features
- Well‑demarcated, erythematous plaques with thick silvery‑white scale, often painful or intensely pruritic and markedly impairing quality of life. 1
- Nail involvement occurs in ~50 % of patients, presenting with pitting, onycholysis, subungual hyperkeratosis, and the “oil‑drop” sign. 2
Psoriasis – Major Subtypes
| Subtype | Typical Presentation | Key Points |
|---|---|---|
| Guttate psoriasis | 1–10 mm salmon‑pink papules with fine scale; common in patients < 30 years, frequently follows streptococcal infection. | Post‑streptococcal trigger. [2] |
| Inverse psoriasis | Erythematous plaques with minimal scaling in intertriginous zones (axillae, genital, inframammary). | Affects flexural folds. [4] |
| Erythrodermic psoriasis | Near‑total body erythema with risk of hypothermia, dehydration, fever, and malaise. | Severe, potentially life‑threatening. [4] |
| Pustular psoriasis | Widespread sterile pustules on an erythematous base; von Zumbusch variant may present with fever and systemic toxicity. | Acute systemic involvement. [4] |
Triggers & Disease Course
- Certain medications—beta‑blockers, non‑steroidal anti‑inflammatory drugs, lithium, chloroquine, and mepacrine—can precipitate severe psoriasis flares. 5
- Alcohol consumption is a recognized aggravating factor for psoriasis. 5
- Streptococcal infection is a common trigger for guttate psoriasis. 2
- Psoriasis follows a relapsing‑remitting pattern, with rare spontaneous remission. 1
Severity Assessment
- Disease severity is not defined solely by body‑surface‑area (BSA); involvement of critical sites (hands, feet, scalp, face, genitals) or intractable pruritus denotes severe disease regardless of extent. 7, 6
Management Strategies
Psoriasis
- Mild disease (< 3 % BSA): First‑line topical agents include corticosteroids, vitamin D analogues, coal‑tar preparations, and dithranol. 5, 6
- Moderate‑to‑severe disease (> 10 % BSA or significant QoL impact): Biologic therapies targeting TNF‑α, IL‑17, or IL‑23 are recommended as first‑line systemic options. 7
- Combination therapy: Adding topical corticosteroids to vitamin D analogues can enhance biologic efficacy. 7
- Phototherapy: Narrow‑band UVB may be combined with topical or systemic treatments for additional benefit. 7
- Corticosteroid safety: Limit use of moderately potent topical corticosteroids to ≤ 100 g per month, with regular clinical review and intermittent non‑steroidal alternatives. 5
Atopic Dermatitis (Eczema)
- Topical therapy: Low‑ to medium‑potency corticosteroids and topical calcineurin inhibitors are the mainstay for mild‑to‑moderate disease. 8
- Systemic therapy: Indicated for extensive disease, severe QoL impairment, or failure of optimized topical regimens. 8
- Holistic assessment: Management should integrate disease severity scores with patient‑reported QoL measures. 8
- Monitoring: Serial disease activity assessments are essential due to the characteristic pattern of exacerbations and remissions. 8