Acne vulgaris and eczema

Overview

Acne and eczema are the two commonest chronic skin complaints in young people. Both damage confidence and sleep, and both are often mistreated with the wrong creams.

• Acne vulgaris is inflammation of the pilosebaceous unit (hair follicle plus sebaceous gland) on the face, chest and back.
• Eczema (used here to mean the same as dermatitis) is an itchy inflammatory rash caused by a damaged skin barrier, allergy or irritants.

Acne vulgaris

Pathogenesis: four steps

1. More sebum: sebaceous glands enlarge at puberty under androgen drive. Affected skin is greasy (seborrhoea).
2. Blocked follicles: abnormal keratinisation plugs the follicle opening, forming the microcomedone, the first lesion.
3. Bacteria: Cutibacterium acnes (formerly Propionibacterium acnes) grows in the trapped sebum.
4. Inflammation: the follicle wall bursts and neutrophils pour in, giving papules, pustules and nodules.

Lesions

Aggravating factors and variants

• Drugs: corticosteroids (oral and topical), anabolic steroids, isoniazid, lithium, phenytoin, vitamin B12 and EGFR inhibitors. Drug-induced acne is monomorphic and has no comedones.
• Progestogen-only contraception can worsen acne.
• Polycystic ovary syndrome: acne with hirsutism and irregular periods.
• Variants: infantile acne (maternal androgens), occupational oil acne, chloracne (dioxins), pomade acne, acne excoriée (picking), acne conglobata (severe nodulocystic acne with sinuses in young men) and acne fulminans (acne with fever, joint pain and weight loss; needs oral steroids and isotretinoin).

Management: step up by severity

Rules for antibiotics in acne:

• Never use a topical antibiotic on its own; combine with benzoyl peroxide or a retinoid to reduce resistance.
• Avoid long courses of oral antibiotics (more than about 6 months).
• Do not use different oral and topical antibiotics together.

Topical retinoids and benzoyl peroxide dry and irritate the skin; start on alternate nights and use a non-greasy, non-comedogenic moisturiser. Improvement takes several weeks, so judge response only after a full course.

Isotretinoin

• An oral retinoid (vitamin A derivative). It shrinks sebaceous glands and normalises follicle keratinisation; the only drug that acts on all four steps.
• Indications: severe nodulocystic acne, acne with scarring, acne that fails adequate treatment, or acne causing severe distress.

Adverse effects:

• Teratogenic (severe birth defects): women must use effective contraception under a pregnancy prevention programme, with pregnancy tests before, during and after treatment.
• Dry lips, skin, eyes and nose (nosebleeds): almost universal.
• Raised triglycerides and liver enzymes: check fasting lipids and liver tests.
• Mood change, depression and rare suicide: ask about mood at every visit.
• Muscle aches, night-vision problems, raised intracranial pressure (avoid combining with tetracyclines).

Rosacea and its look-alikes

• Rosacea treatment: avoid triggers, topical metronidazole, azelaic acid or ivermectin, and courses of oral tetracycline/doxycycline; brimonidine gel or laser for redness.
• Topical steroids worsen rosacea.
• Perioral dermatitis: small papules and pustules around the mouth sparing the lip margin, in young women, often triggered by steroid creams; stop the steroid and give an oral tetracycline.

Hidradenitis suppurativa ("acne inversa") gives recurrent painful nodules, abscesses, sinus tracts and scars in the axillae, groin and under the breasts. It is linked to obesity and smoking. Treat with long-term tetracyclines, clindamycin with rifampicin, adalimumab, and surgery.

Eczema (dermatitis)

Acute versus chronic eczema

Classification

• Endogenous (constitutional): atopic, seborrhoeic, discoid (nummular), pompholyx (vesicular hand and foot), venous (stasis), asteatotic, lichen simplex.
• Exogenous: irritant contact and allergic contact dermatitis.

Atopic eczema

Epidemiology: affects up to about 20% of children; usually starts before age 2; many children improve by school age and about half are clear by age 6. It often comes with asthma, hay fever and food allergy (the atopic march). If both parents are atopic, the child's risk is over half.

Causes:

• Barrier defect: loss-of-function filaggrin mutations give dry, leaky skin that lets in allergens and microbes.
• Immune shift to Th2 cells (IL-4, IL-5, IL-13) with raised IgE; IL-31 drives itch.
• Poor skin defence: fewer antimicrobial peptides, so heavy colonisation with Staph. aureus and spread of herpes simplex.
• Triggers: soaps and detergents, heat and sweating, wool, infection, stress, house-dust mite and pets; food allergy (milk, egg) matters only in a minority of infants.

Distribution by age:

Associated signs: dry skin (xerosis), Dennie–Morgan infraorbital folds, hyperlinear palms, keratosis pilaris, ichthyosis vulgaris, and pityriasis alba (pale, slightly scaly patches on the cheeks of children, often confused with vitiligo or leprosy).

Diagnosis is clinical. About 80% have raised total IgE and eosinophilia, but tests are not needed for diagnosis.

Complications:

• Secondary bacterial infection (Staph. aureus, streptococci): weeping, crusting and pustules; treat with oral flucloxacillin (erythromycin if allergic).
• Eczema herpeticum (Kaposi varicelliform eruption): HSV spreads over eczematous skin, giving clusters of painful punched-out erosions with fever. Give aciclovir urgently (intravenous if unwell).
• Widespread molluscum and warts; eye problems (keratoconjunctivitis, cataract).
• Sleep loss, poor school performance and growth problems from steroid misuse or severe disease.

Management:

1. Education; avoid soaps and irritants; cotton clothing; cut nails short.
2. Emollients liberally and often, including as soap substitutes. This is the foundation of care.
3. Topical corticosteroids for flares, matched to site and severity.
4. Topical calcineurin inhibitors (tacrolimus ointment, pimecrolimus cream) for the face and eyelids; they do not cause skin atrophy; licensed from age 2; may sting at first.
5. Antibiotics for infection; antiseptic or dilute bleach baths; sedating antihistamine at night only to help sleep.
6. Severe disease: wet wraps, narrowband UVB, systemic ciclosporin, azathioprine, methotrexate, or biologic dupilumab (blocks IL-4 and IL-13 signalling). Short oral prednisolone courses work but flares follow withdrawal.

Topical steroid potency ladder

Side effects of topical steroids: skin atrophy, striae, telangiectasia, easy bruising, steroid-induced rosacea and perioral dermatitis, acne and folliculitis, tinea incognito, glaucoma and cataract around the eyes, and adrenal suppression with long use of potent steroids on large areas or under occlusion.

Seborrhoeic dermatitis

• Red, greasy, scaly rash in oily areas: scalp (dandruff), eyebrows, nasolabial folds, sides of the nose, behind the ears, ear canals, central chest and flexures.
• Linked to the yeast Malassezia.
• More common and severe in HIV infection (an early sign) and in Parkinson disease.
• Infant form: cradle cap and non-itchy napkin rash.
• Treatment: ketoconazole shampoo and cream, other topical azoles, short mild steroid, or a calcineurin inhibitor. It relapses; treatment controls rather than cures.

Contact dermatitis

• Treatment: identify and avoid the cause, protective gloves (cotton liners), emollients, topical steroids; alitretinoin for severe chronic hand eczema.

Other eczemas

• Discoid (nummular) eczema: coin-shaped, very itchy, often oozing plaques on the limbs; needs potent steroids. Itch helps tell it from psoriasis.
• Pompholyx (dyshidrotic): deep, intensely itchy vesicles on the sides of the fingers, palms and soles.
• Venous (stasis) eczema: inner lower leg with varicose veins, haemosiderin staining and lipodermatosclerosis; treat with emollients, moderate steroid and compression; watch for contact allergy to medicated dressings.
• Asteatotic eczema (eczema craquelé): elderly, dry winter skin on the shins with a "crazy paving" pattern; emollients.
• Lichen simplex chronicus ("neurodermatitis"): a single thick lichenified plaque from habitual scratching, often at the nape, ankles or genitals; potent steroid and break the itch–scratch cycle.

Differential diagnosis of an itchy, scaly rash

• Psoriasis: well-defined silvery plaques on extensors, less itchy, nail pitting.
• Tinea: annular, asymmetrical, active edge; KOH positive.
• Scabies: burrows, night itch in family.
• Contact dermatitis: pattern matches an exposure.

Quick revision

• Acne: sebum + blocked follicle + C. acnes + inflammation; comedone is the key lesion.
• Mild: retinoid ± benzoyl peroxide. Moderate: add oral tetracycline. Severe: isotretinoin.
• Isotretinoin: teratogen; dry mucosa; lipids; mood; not with tetracyclines.
• Rosacea: central face, flushing, no comedones; steroid creams worsen it.
• Acute eczema: vesicles, oozing, spongiosis. Chronic: lichenification.
• Atopic: filaggrin, Th2, IgE; face in infants, flexures later.
• Eczema herpeticum: urgent aciclovir.
• Seborrhoeic: oily areas, Malassezia, HIV and Parkinson; ketoconazole.
• Allergic contact: type IV, nickel, patch test.
• Mild steroid for face and infants; very potent for palms and soles.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).

FAQ