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Dyshidrosis

Basics

Description

  • Chronic dermatitis of palms/soles

  • Includes several variants:

    • Dyshidrotic eczema: symmetric fluid-filled vesicles

    • Pompholyx: large bullae

    • Lamellar dyshidrosis: exfoliation of superficial epidermis

  • Also known as:

    • Cheiropompholyx, keratolysis exfoliativa, vesicular palmoplantar eczema

Epidemiology

  • Onset: usually ≤40 years

  • Male = female

  • Accounts for 5–20% of hand eczema

  • Prevalence: ~20/100,000

Etiology & Pathophysiology

  • Multifactorial:

    • Allergies, genetics, dermatophyte infection

    • Spongiosis in epidermis, no eccrine gland effect

    • Vesicle formation possibly due to rapid Ig rise

  • Triggers:

    • Hyperhidrosis (~40%)

    • Solvents, detergents

    • Climate extremes

    • Metal sensitivities: nickel, cobalt, chromate

    • Stress, glove use, smoking

  • Genetics:

    • ~50% have atopic dermatitis

    • Rare autosomal dominant forms (e.g., chromosome 18q22.1–3)

Risk Factors

  • Atopy

  • Dermatologic history (e.g., AD, contact dermatitis)

  • Nickel/chromate/cobalt exposure

  • Smoking

  • Certain drugs: neomycin, quinolones, OCPs

Associated Conditions

  • Atopic dermatitis

  • Contact dermatitis

  • Parkinson disease

  • HIV

Diagnosis

History

  • Episodes of pruritic rash

  • Emotional stress

  • Allergen/irritant exposure

  • Costume jewelry use, IVIG therapy, smoking

Physical Exam

  • Symmetrical vesicles on palms, soles, fingers

  • Prodrome: intense itching

  • "Tapioca pudding" vesicles (1–2 mm)

  • Late phase: desquamation, lichenification

Differential Diagnosis

  • Tinea pedis, id reaction, scabies

  • Drug eruptions, bullous disorders

  • PPP, mycosis fungoides, pustular psoriasis

Tests

  • KOH mount (rule out tinea)

  • Patch test (if allergy suspected)

  • S. aureus culture (if secondary infection suspected)

Treatment

General Measures

  • Avoid triggers: stress, metal salts, irritants

  • Emollients and barrier maintenance

  • Cotton gloves/socks, avoid leather/rubber

First-Line Therapy

  • High-potency topical steroids [C]

  • Limit to 2 weeks per flare

  • Occlusion for moderate-severe cases

  • Prednisone (40–100 mg/day) for acute flares [C]

  • PUVA therapy for recurrent disease [C]

Second-Line

  • Topical calcineurin inhibitors:

    • Tacrolimus, pimecrolimus

  • Other systemic options:

    • Cyclosporine, alitretinoin, methotrexate, azathioprine

    • Mycophenolate mofetil

    • BTXA injections (esp. if hyperhidrosis-related)

    • Tap water iontophoresis

Referral

  • Allergist (if patch testing)

  • Psychologist (if stress significant)

Alternative Therapies

  • Thalidomide, dapsone

  • UVA1, UV-free phototherapy

  • Topical bexarotene

  • Nickel-allergic patients: disulfiram, sodium cromoglycate

CAM

  • Antihistamines: hydroxyzine, cetirizine

  • Compresses/soaks (e.g., Burow’s solution)

  • Sunlight exposure

  • Dandelion juice, relaxation techniques

Follow-Up

Monitoring

  • DASI index:

    • Vesicle count, erythema, desquamation, itching, area

    • Grades: mild (0–15), moderate (16–30), severe (31–60)

  • Monitor:

    • BP, glucose (systemic steroid users)

    • Drug side effects

Diet

  • Low nickel/chromium/cobalt diet if sensitive

Patient Education

Prognosis

  • Benign, often self-resolving

  • Recurrence common

  • Rarely scars

Complications

  • Skin pain, tightness

  • S. aureus infection

  • Dystrophic nails

  • Fissures, ulceration

  • Psychological impact, lymphedema

Clinical Pearls

  • Tapioca-like vesicles are hallmark

  • Often misdiagnosed

  • Topical steroids = cornerstone

  • Long-term control = trigger avoidance + skin barrier protection

  • Watch for secondary infection