Psoriasis

Published on 05/03/2015 by admin

Filed under Dermatology

Last modified 22/04/2025

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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.

[/level-membership-for-dermatology-category][not-level-membership-for-dermatology-category]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