Psoriasis

Published on 05/03/2015 by admin

Filed under Dermatology

Last modified 22/04/2025

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6

Psoriasis

Key Points

Affects up to 2% of the population.

Chronic disorder in those with a polygenic predisposition combined with triggering factors such as infections (especially streptococcal pharyngitis, but also HIV infection) or medications (e.g. interferon, β-blockers, lithium, or oral CS taper).

Koebner phenomenon – elicitation of psoriatic lesions by traumatizing the skin.

Common sites.

Scalp.

Elbows and knees.

Nails, hands, feet, trunk (intergluteal fold).

Skin lesions.

Most commonly – well-demarcated, erythematous plaques with silvery scale (Fig. 6.1).

Other lesions include sterile pustules, glistening plaques in intertriginous zones.

Histopathologic findings.

Regular acanthosis, confluent parakeratosis with neutrophils, hypogranulosis, dilated blood vessels (see Chapter 1).

Major systemic association is psoriatic arthritis (see Table 6.1), most commonly presenting as asymmetric oligoarthritis of hands/feet; the metabolic syndrome is also common.

Pathogenesis.

Regarded as a T-cell-driven disease involving cytokines, including TNF-α and IL-23 (stimulates Th17 cells).

Genes that have been associated with psoriasis include those encoding caspase recruitment domain family member 14 (CARD14, a regulator of NF-κB signaling) and, for generalized pustular psoriasis, the IL-36 receptor antagonist (a regulator of IL-8 production and IL-1β responses).

Variants

Pustular Psoriasis

Generalized pustular psoriasis (von Zumbusch pattern).

Erythema and sterile pustules arising within erythematous, painful skin; lakes of pus characteristic (Fig. 6.7).

Often associated fever.

Triggering factors – pregnancy (termed impetigo herpetiformis), rapid tapering of CS, hypocalcemia, infections.

DDx: acute generalized exanthematous pustulosis (AGEP; pustular drug reaction) (see Chapter 17).

Palmoplantar (pustulosis).

Sterile pustules on palms/soles (Fig. 6.8).

May have no evidence of psoriasis elsewhere.

Triggering factors – infections, stress.

May be aggravated by smoking.

Associated with inflammatory bone lesions (see Chapter 21).

Annular pattern (Fig. 6.9).

DDx: includes Sneddon–Wilkinson disease (see below).

Exanthematic type.

Significant overlap with AGEP.

Localized pattern – within plaques, often due to irritants (Fig. 6.10).

Acrodermatitis continua (of Hallopeau).

Erythema and scale of distal digit with pustules (Fig. 6.11).

Often associated fever.

Psoriatic Arthritis (See Table 6.1)

Seen in 5–30% of patients with cutaneous psoriasis.

Most commonly is an asymmetric oligoarthritis affecting the distal interphalangeal joints (Fig. 6.15).

More rarely, but classically, is arthritis of all the interphalangeal joints.

Occasionally, presentation is rheumatoid arthritis-like, affecting small- and medium-sized joints symmetrically.

Arthritis mutilans – rare form with acute, rapidly progressive joint inflammation and destruction; softening and telescoping of the digits.

Spondylitis and sacroiliitis – axial arthritis as well as arthritis of the knees and sacroiliac joints; may be HLA-B27-positive and may have associated inflammatory bowel disease or uveitis.

DDx: reactive arthritis (previously referred to as Reiter’s disease).

Urethritis, arthritis, ocular findings (e.g., conjunctivitis), and oral ulcers in addition to psoriasiform lesions, especially on the soles (keratoderma blennorrhagicum) or genitalia (balanitis circinata) (Fig. 6.16).

More common in men.

Strongly associated with HLA-B27.

Course is often self-limited.

May be severe in HIV-positive individuals.

Treatment

Topical agents.

First-line.

CS (Table 6.2).

Vitamin D3 analogues (calcipotriene, calcitriol) (Table 6.3).

Second-line.

Calcineurin inhibitors (may be first-line for sensitive areas such as the face or flexures).

Tars (e.g. liquor carbonis detergens [LCD] 5%).

Anthralin.

Tazarotene.

Phototherapy and systemic agents.

First-line.

Phototherapy – UVB (narrowband or broadband > PUVA) (Table 6.4); if thick keratotic plaques, can combine with oral retinoids.

Methotrexate (oral or intramuscular, occasionally subcutaneous) (Table 6.5).

Oral retinoids (e.g. acitretin, isotretinoin).

Second-line systemic.

Targeted immunomodulators (‘biologic’ agents) (Tables 6.6 and 6.7).

Cyclosporine.

See Table 6.8 for treatment options in patients with comorbidities or special situations.

See Table 6.9 for the recommended laboratory evaluation for patients receiving targeted immunomodulators.

For further information see Ch. 8. From Dermatology, Third Edition.