When the steroid cream stops working
You've been given a stronger cream. It worked for a fortnight. The flare came back. You were told to keep going with emollients, that they'll grow out of it, that this is just how eczema is.
Then someone mentioned injections.
There is a step between those two things, and most people are never offered it. This page explains what it is, why it exists, and how to work out whether it applies to you.
The question nobody asks
When steroids stop working, the usual response is to go stronger, then to go systemic. What's rarely asked is why they stopped working — and the answer determines whether escalating is the right move at all.
Four explanations are far more common than treatment resistance:
The skin is colonised with bacteria. This is the big one, and the most frequently missed. Staphylococcus aureus is present on the lesional skin of the great majority of people with atopic dermatitis, against a small minority of people without it. It isn't a passive passenger. Staph produces toxins that act as superantigens, driving inflammation directly and continuously.
A steroid suppresses that inflammation. It does nothing to the organism generating it. So the skin settles while the cream is on and relapses within days of stopping — which looks exactly like treatment failure, and isn't. It's a treatment aimed at half the problem.
Not enough is being used. Most people apply considerably less topical steroid than they've been prescribed, usually because they've been warned about steroids so effectively that they use them nervously. Undertreated eczema is indistinguishable from resistant eczema.
Treatment stops too soon. Skin can look settled while inflammation continues underneath. Stopping at visible clearance is a reliable route back to a flare.
The diagnosis isn't quite right. Allergic contact dermatitis, scabies and psoriasis are all mistaken for eczema, and none behave as expected on steroid creams.
Genuine tachyphylaxis — skin becoming less responsive to the drug — is described in the literature but is a far less common explanation than any of the above.
Why this matters: if the reason is colonisation or undertreatment, a biologic will work — of course it will, it suppresses inflammation powerfully — but you'll have moved to systemic immune modulation to solve a problem a better-designed topical plan addresses. That's a significant decision to make without first ruling out the simpler explanation.
The step in between
Between "topical steroids have failed" and "let's discuss injections" there is an approach most patients are never offered: an individually compounded topical preparation that treats the inflammation and the bacterial colonisation together, adjusted repeatedly as the skin changes.
This is what we do, and it's all we do.
The preparation combines a topical corticosteroid, an antimicrobial and a moisturising base, made up to individual prescription rather than taken off a shelf. The proportions are set according to severity, body site and age, and — this is the part that matters — stepped down over the following weeks as the skin settles. The aim is to reach the lowest effective treatment, not to stay on the starting one.
It is not a stronger cream. It's a differently designed one, reviewed frequently.
What it involves
A consultation, then reviews at two weeks and four weeks
Adjustment at each review rather than a single prescription
No blood tests, no injections, no hospital visits
Entirely reversible