Papulosquamous & Acneiform Dermatoses

Lichen planus

Clinical picture. Lichen planus (LP) is a T-cell–mediated disease of skin and mucosa remembered by its Ps: pruritic, purple, polygonal, planar (flat-topped) papules and plaques. Favorite sites are the flexor wrists, shins, lower back and genitalia. Fine white lacy lines on the papules (Wickham striae) and a reticular white network on the buccal mucosa are characteristic, and new lesions follow scratches (Koebner phenomenon).

Histology. LP is the prototype interface (lichenoid) dermatitis. A dense band of CD8⁺ T cells hugs the dermal-epidermal junction and destroys basal keratinocytes, causing vacuolar change and apoptotic keratinocytes (Civatte bodies). Above it lie compact orthokeratosis without parakeratosis, wedge-shaped hypergranulosis (the microscopic correlate of Wickham striae) and pointed, sawtooth rete ridges. Melanin dropped into the dermis from damaged basal cells leaves postinflammatory hyperpigmentation after lesions heal.

Associations and course. LP, particularly the oral form, is associated with chronic hepatitis C. Erosive oral LP is painful and carries a small risk of squamous cell carcinoma, so persistent erosions deserve biopsy and follow-up. Lichenoid drug eruptions mimic LP after thiazides, β-blockers, ACE inhibitors and antimalarials. Cutaneous LP often clears within 1–2 years, and potent topical glucocorticoids relieve itch.

Pityriasis rosea and seborrheic dermatitis

Pityriasis rosea. Teenagers and young adults develop a single herald patch: a larger salmon-pink oval with a fine collarette of scale, usually on the trunk. One to two weeks later, crops of smaller oval scaly plaques appear with their long axes along skin cleavage lines, tracing a Christmas-tree pattern on the back; itch is mild. Reactivation of HHV-6 and HHV-7 is implicated. The rash resolves on its own in about 6–8 weeks, so reassurance and antipruritics are enough.

Secondary syphilis mimics pityriasis rosea but adds palm and sole lesions, lymphadenopathy and mucous patches; order an RPR or VDRL when the picture is atypical or risk is high, and use a KOH preparation to exclude tinea corporis, which can resemble the herald patch.

Seborrheic dermatitis. Ill-defined erythema with greasy, yellowish scale appears in sebum-rich skin: scalp (dandruff), eyebrows, nasolabial folds, behind the ears and the central chest. It is an inflammatory response to lipophilic Malassezia yeasts that feed on sebum. Infants develop cradle cap, thick yellow scale on the scalp that clears within months. Severe, widespread or refractory disease is a marker of HIV infection and is typical of Parkinson disease. Antifungal shampoos and creams (ketoconazole, selenium sulfide, zinc pyrithione) with short courses of low-potency glucocorticoids control it.

Psoriasis: the contrast case

Clinical contrast. Psoriasis forms sharply demarcated salmon-pink plaques with silvery scale on the extensor elbows and knees, scalp and sacrum, with nail pitting; it also koebnerizes and is linked to psoriatic arthritis. Lifting the scale reveals pinpoint bleeding (Auspitz sign) from dilated capillaries in elongated dermal papillae beneath thinned suprapapillary plates.

Histologic contrast. IL-23/Th17 signaling drives rapid keratinocyte turnover: regular acanthosis with evenly elongated rete ridges, parakeratosis (retained nuclei in the stratum corneum), a thin or absent granular layer and neutrophil collections in the stratum corneum (Munro microabscesses; not the Pautrier microabscesses of mycosis fungoides). LP is the mirror image, with hypergranulosis, orthokeratosis and a lymphocyte band.

Acne vulgaris

Lesions. Comedones are the hallmark. Open comedones (blackheads) have a dilated pore and look dark from oxidized lipids and melanin, not dirt; closed comedones (whiteheads) have a tiny opening. Inflammatory papules, pustules, nodules and cysts involve the face, chest and upper back, and deep lesions scar.

Hormonal and drug triggers. Acne with hirsutism, irregular menses or virilization should prompt evaluation for polycystic ovary syndrome, congenital adrenal hyperplasia or anabolic steroid or testosterone use. Glucocorticoids, anabolic steroids, lithium, isoniazid, phenytoin and EGFR inhibitors (cetuximab, erlotinib) cause an abrupt, monomorphic eruption of papulopustules on the face and trunk without comedones. The EGFR-inhibitor rash is very common and often tracks tumor response (contrast the hand-foot syndrome of capecitabine).

Treatment by mechanism. Topical retinoids normalize follicular keratinization (comedolytic). Benzoyl peroxide kills C. acnes without inducing resistance. Oral tetracyclines (doxycycline, minocycline) add antibacterial and anti-inflammatory effects. Combined oral contraceptives and spironolactone blunt androgen effects in women. Isotretinoin shrinks sebaceous glands and addresses all four steps, so it is reserved for severe nodulocystic or scarring acne.

Isotretinoin is a potent teratogen: pregnancy tests and two forms of contraception are mandatory. It also causes dry skin and lips, hypertriglyceridemia and hepatotoxicity.

Rosacea and hidradenitis suppurativa

Rosacea. This chronic disorder of the central face begins in adults aged 30–50, most often fair-skinned women. Neurovascular dysregulation, innate immune activation (cathelicidin peptides) and Demodex mites contribute. Flushing is provoked by heat, sunlight, alcohol, spicy food, hot drinks and stress, and persistent erythema, telangiectasias and papulopustules follow. Comedones are absent, the key distinction from acne. Phymatous rosacea thickens skin through sebaceous hyperplasia and fibrosis, classically the bulbous nose (rhinophyma) of older men, and ocular rosacea causes gritty eyes, blepharitis, conjunctivitis and sometimes keratitis. Management is trigger avoidance, sunscreen, topical metronidazole, azelaic acid or ivermectin, and oral doxycycline.

The lupus malar rash spares the nasolabial folds and lacks pustules, telangiectasias and flushing triggers.

Hidradenitis suppurativa. The disease starts with follicular occlusion (infundibular hyperkeratosis) and rupture in apocrine gland–bearing skin: axillae, groin, inframammary folds and buttocks; it is not a primary infection of apocrine glands. Recurrent deep, painful nodules and abscesses coalesce into draining sinus tracts, with double-ended comedones and rope-like scars. Onset follows puberty, women are affected more often, and obesity and smoking worsen it; Crohn disease and metabolic syndrome are associated. Adalimumab (anti-TNF) or secukinumab (anti-IL-17A) treats moderate to severe disease, surgery removes tracts, and long-standing lesions can give rise to squamous cell carcinoma.