Common Dermatoses

Eczematous dermatitis: atopic, contact, and seborrheic

Atopic dermatitis. A chronic, relapsing, intensely pruritic eczema, the "itch that rashes." Distribution changes with age: the face and extensor surfaces in infants, and the flexural creases (antecubital and popliteal fossae) in children and adults. Loss-of-function filaggrin mutations impair the skin barrier, and the disease forms part of the atopic triad with asthma and allergic rhinitis.

• Every patient: daily emollients to repair the barrier.
• Flares: topical corticosteroids; topical calcineurin inhibitors (tacrolimus, pimecrolimus) spare steroids on the face and eyelids.
• Severe disease: dupilumab, which blocks IL-4 and IL-13 signaling.

Eczema herpeticum is HSV superinfection of eczematous skin: clustered, painful, punched-out erosions, often with fever. Treat promptly with acyclovir. Staphylococcus aureus commonly colonizes atopic skin and causes crusted, impetiginized flares.

Contact dermatitis. Lesions take the shape of the exposure: an earlobe or wrist under nickel jewelry, or linear streaks of vesicles where a plant brushed the skin. Allergic contact dermatitis is a type IV (T-cell-mediated) delayed hypersensitivity that needs prior sensitization, so it appears a day or more after re-exposure. Irritant contact dermatitis is direct chemical injury and is more common.

Seborrheic dermatitis. Erythematous patches with greasy yellow scale in sebum-rich zones: the scalp (dandruff), eyebrows, nasolabial folds, and chest. It is linked to Malassezia yeast and appears as cradle cap in infants. Treat with ketoconazole shampoo and low-potency topical steroids.

Seborrheic dermatitis is more severe and extensive in Parkinson disease and in HIV/AIDS; florid disease should prompt consideration of both.

Papulosquamous disease: psoriasis and lichen planus

Psoriasis. Well-demarcated erythematous plaques with silvery scale on the extensor surfaces (elbows, knees) and scalp, driven by accelerated keratinocyte turnover. Scraping the scale produces pinpoint bleeding (Auspitz sign) from dilated dermal capillaries beneath thin suprapapillary plates, and skin trauma seeds new lesions (Koebner phenomenon). Nail pitting and onycholysis are common, and psoriatic arthritis accompanies the skin disease in a subset of patients.

Triggers. Guttate (droplike) psoriasis erupts after streptococcal pharyngitis. β-Blockers, lithium, and antimalarials can worsen psoriasis, and withdrawing systemic steroids can provoke a severe pustular flare, so systemic steroids are avoided.

Lichen planus: the six Ps. Pruritic, purple, polygonal, planar (flat-topped) papules and plaques, classically on the wrists and ankles, with fine white lines on the surface (Wickham striae) and lacy white oral lesions. Like psoriasis, it Koebnerizes. First-line treatment is a high-potency topical steroid.

Lichen planus is associated with hepatitis C, so check hepatitis C serology. Chronic erosive oral lichen planus carries a small risk of squamous cell carcinoma.

Acne vulgaris and rosacea

Four drivers. Acne arises from follicular hyperkeratinization, androgen-driven excess sebum, Cutibacterium acnes, and inflammation. Comedones (open = blackhead, closed = whitehead) progress to inflammatory papules and pustules and then to nodulocystic lesions that scar.

Hormonal options. In women, combined oral contraceptives and spironolactone reduce androgen-driven sebum.

Isotretinoin is highly teratogenic (retinoid embryopathy). iPLEDGE requires two contraceptive methods and monthly pregnancy tests. Other effects: cheilitis and dry skin, raised triglycerides and LFTs, night blindness, and reported mood changes. Never combine it with tetracyclines, because both cause pseudotumor cerebri.

Rosacea. Central facial erythema, telangiectasias, and papulopustules in adults, with flushing triggered by heat, alcohol, spicy food, and sun. Phymatous change produces rhinophyma, and ocular involvement causes eyelid and conjunctival inflammation. Treat with topical metronidazole, azelaic acid, or ivermectin, or oral doxycycline; topical steroids worsen it.

Urticaria

Transient wheals. Urticaria produces pruritic wheals, each lasting under 24 hours, from mast cell histamine release, triggered by IgE (type I) mechanisms or physical stimuli such as pressure, cold, or stroking (dermatographism). Acute urticaria lasts under 6 weeks and often follows an infection, drug, or food; chronic urticaria lasts over 6 weeks and is usually idiopathic.

Treatment. A second-generation (non-sedating) H1 antihistamine such as cetirizine or loratadine is first-line; the dose can be increased up to 4 times the standard dose before escalating. Omalizumab (anti-IgE) is used for refractory chronic urticaria.

Hives with airway swelling, wheeze, or hypotension is anaphylaxis: give IM epinephrine. Wheals that last longer than 24 hours, burn, or leave bruising suggest urticarial vasculitis and need a biopsy.

Choosing a topical corticosteroid

Match potency to the site. Thin skin (face, eyelids, skin folds) and children absorb more steroid and atrophy easily, while thick plaques, palms, and soles need strong agents. Occlusion and higher potency both increase absorption; large areas under occlusion can cause systemic effects.