Common. Prevalence of 1-2%. M = F. Characterised by chronic erythematous papules and plaques covered by silvery white scales – severity varies. 10% are associated with a seronegative inflammatory arthritis.
Basic pathophysiology is a greater population of epidermal cells that divide too rapidly. Hereditary component is important. Higher frequency of some of the HLA antigens has been noted (HLA-B27, -Cw2, -Cw6, B13, B17. Exacerbated by physiological and psychological stress.
Wide variety of patterns and distribution of lesions:
1) Plaque psoriasis:
• most common pattern
• typically dark red papules with silvery white scales coalesce into plaques which generally are sharply marginated. Classically occur of ‘extensor’ areas – the elbows, knees and back.
2) Pustular psoriasis:
• severe and progressive, but less common variant
• inflammatory red patches with irregular bordered, studded with small pustules – pustules are sterile, but may get secondary infection
• skin is sore; also have fever, malaise, leucocytosis
• many are drug induced
debated if this is actually a form of psoriasis or a closely related disorder
onset usually > 50 yrs; F>M; strong association with cigarette smoking; 20-30% also have plaque psoriasis
differential diagnosis – tinea pedis
3) Erthrodermic and exfoliative psoriasis:
4) Guttate psoriasis
• variant usually seen in adolescents and young adults
• characterised by small ‘drop’ like papules and plaques
• often associated with streptococcal pharyngitis
Commonly involved. Pitting (small ‘dents’) are most common (from psoriasis of the proximal matrix), ‘oil spots’ (from psoriasis of distal matrix), discolouration and onycholysis – affects up to 50%. Also can get leukonychia, crumbling of nail plate (from psoriasis of entire nail plate) and subungual hyperkeratosis (from involvement of nail bed).
The pits result from psoriatic foci in the nail matrix produce abnormal keratin in superficial nail plate sloughs as nail move forward pits
Following a chronic unpredictable course with exacerbation and remissions.
Can be exacerbated by some drugs (eg beta-blockers, lithium, antimalarials)
Differential diagnosis – seborrheic dermatitis; candidiasis; drug eruptions; Reiter’s syndrome
No cure – treatment is symptomatic.
Topical corticosteroids – inhibit epidermal cell mitosis and antinflammatory
Tars – inhibit DNA synthesis antipsoriatic
Anthralin – synthetic antipsoriatic
Phototherapy – ultraviolet light – generally for more severe cases
Methrotrexate – cytotoxic