Psoriasis
Epidemiology
Etiology
- Trigger factors
- Infectious
- Infections of the upper respiratory tract caused by β-hemolytic streptococci
- A possible explanation is molecular mimicry, as the M protein of streptococci closely resembles the keratin of the skin.
- Infections of the upper respiratory tract caused by β-hemolytic streptococci
- Mechanical irritation
- Drugs (e.g., beta-blockers, chloroquine, lithium, interferon)
- Infectious
Pathophysiology
- Increased proliferation of keratinocytes
- Normally, the epidermis takes about 26–28 days to completely renew itself. This process involves the formation of new keratinocytes and shedding of aged (keratotic) skin cells. In individuals with psoriasis, the proliferation rate increases five-fold to ten-fold.
- Acanthosis: thickening of the epidermis = typical erythematous plaques
- Parakeratosis: retention of nucleated keratinocytes in the stratum corneum = characteristic silvery scales
- T cells secrete cytokines, which mediate an inflammatory response.
Clinical features
Cutaneous lesions
- Well-demarcated, erythematous plaques and/or papules with silver-white scaling
- Located mainly on the scalp, trunk, elbows, and knees (extensor surfaces)
- Pruritus in ∼ 80% of cases
- Characteristic features may be present.
- Auspitz sign
- Small pinpoint bleeding when scales are scraped off
- Removal of the scales exposes the dermal papillae, which leads to bleeding.
- Koebner phenomenon: Physical stimuli or skin injury (e.g., trauma, scratching, irritating clothing) can lead to the appearance of psoriatic skin lesions on previously unaffected skin (isomorphic response).
- Auspitz sign
Nail involvement
- Nail pitting: small, round depressions in the nail
- Brittle nails: nail dystrophy with crumbling of the nail
- Onycholysis: partial and mostly distal separation of the nail plate
Diagnostics
Skin biopsy
- Indications: Consider only if clinical presentation is atypical.
- Supportive findings
- Acanthosis and parakeratosis
- Thickening of the stratum spinosum, thinning of the stratum granulosum
- Acanthosis = typical erythematous plaques
- Parakeratosis = characteristic silvery scales
- Munro microabscesses: accumulation of neutrophils in the stratum corneum surrounded by parakeratosis
Differential diagnostics
Psoriasis vs Lichen planus
- Immune Mechanism:
- Lichen Planus primarily involves CD8+ T cells targeting basal keratinocytes, creating a band-like lymphocytic infiltrate at the dermo-epidermal junction and interface dermatitis
- Psoriasis is driven by Th17/Th1 cells and involves complex cytokine cascades (IL-17, IL-22, TNF-α), affecting the entire epidermis and leading to neutrophil recruitment
- Keratinocyte Response:
- Lichen Planus shows normal to slow keratinocyte turnover, allowing time for proper differentiation, resulting in hypergranulosis (increased keratohyalin granules)
- Because of immune stress?
- Psoriasis exhibits extremely rapid keratinocyte turnover (3-5 days vs normal 28-30 days), preventing proper differentiation, leading to loss of granular layer and parakeratosis
- Lichen Planus shows normal to slow keratinocyte turnover, allowing time for proper differentiation, resulting in hypergranulosis (increased keratohyalin granules)
Treatment
- Topical corticosteroids (first-line)
- Additional therapy: the following agents may be used in combination with topical corticosteroids
- Vitamin D analogues: e.g., calcipotriene/calcipotriol
- Keratolytics: retinoids (e.g., tazarotene), or salicylic acid
- Tar preparations, e.g., 1% coal tar lotion
- Anthralin