Atopic Dermatitis: Causes, Treatment, and How to Manage Flares at Every Age

Eczema isn't caused by a single factor — it results from a collision between your genetics, your immune system, and your environment.

The genetic component often involves mutations in the filaggrin gene, which is responsible for producing a protein that helps form the outermost protective layer of your skin. When filaggrin is deficient, the skin barrier becomes 'leaky': moisture escapes more easily (leading to dryness), and irritants, allergens, and microbes penetrate more readily (triggering inflammation). This is why moisturising isn't just cosmetic — it's replacing a barrier function your skin can't perform on its own.

Once irritants cross the compromised barrier, the immune system overreacts. In eczema, the immune response is skewed toward a Th2-dominant pathway, producing excessive inflammatory signals (particularly IL-4, IL-13, and IL-31 — the 'itch cytokine'). This creates the hallmark itch-scratch cycle: inflammation causes itching, scratching damages the barrier further, and the damaged barrier lets in more irritants, producing more inflammation.

Staphylococcus aureus bacteria colonise eczematous skin in over 90% of patients, compared to only 5% of healthy skin. These bacteria produce toxins that further drive inflammation, which is why eczema flares often worsen suddenly — a bacterial bloom on already-compromised skin can escalate a mild flare into a severe one.

Common environmental triggers include dry air, harsh soaps, fragrances, wool clothing, dust mites, pet dander, pollen, and emotional stress. In young children, food allergens (particularly cow's milk, eggs, and peanuts) can trigger flares, though food allergies don't cause eczema — they aggravate an existing condition.

The foundation of eczema management is restoring the skin barrier — and that means moisturising. Apply a thick, fragrance-free emollient (ointments and creams work better than lotions) at least twice daily, and always within three minutes of bathing while the skin is still damp. This single step reduces flare frequency significantly.

Topical corticosteroids remain the first-line treatment for active flares. They come in a range of strengths — from mild hydrocortisone (suitable for the face and skin folds) to potent betamethasone (for thick plaques on the body). The key is using the right strength for the right body area for the right duration. Fears about steroid side effects are common but often exaggerated; undertreatment causes more harm than appropriate use.

Topical calcineurin inhibitors (tacrolimus and pimecrolimus) are non-steroidal anti-inflammatories ideal for sensitive areas like the face, eyelids, and groin where long-term steroid use carries more risk. They can sting initially but are well-tolerated with continued use.

Crisaborole (a PDE4 inhibitor) is a newer non-steroidal option for mild-to-moderate eczema, available as a topical ointment.

For moderate-to-severe eczema that doesn't respond to topical treatments:

Phototherapy (narrowband UVB) reduces inflammation through controlled ultraviolet light exposure, typically administered 2–3 times per week in a clinic.

Dupilumab (a biologic injection targeting IL-4 and IL-13) has transformed treatment for moderate-to-severe eczema, achieving clear or almost-clear skin in clinical trials where other treatments failed.

JAK inhibitors (abrocitinib, upadacitinib) are oral medications that block the inflammatory signalling pathways driving eczema. They work rapidly but require monitoring for side effects.

Wet wrap therapy — applying moisturiser and a damp layer of clothing or bandages — can rapidly reduce severe flares, especially in children.