Topical Anti-inflammatories

Topical Corticosteroids: The Potency Ladder and the Art of Safe Use

No drug class has done more for dermatology than the topical corticosteroid — and none is more often used badly. Prescribe too weak an agent and the eczema smoulders on; prescribe too strong an agent to the wrong site and you thin the skin, stretch it with striae, or quietly suppress the adrenal axis. The whole craft lies not in knowing that steroids work, but in matching the right potency to the right skin for the right length of time — and then knowing when to step down.

Steroid-Sparing Topicals: Calcineurin Inhibitors and PDE4

Topical steroids are the workhorse of inflammatory skin disease — cheap, fast, effective. But they carry a slow-burning cost: used long enough on the wrong skin, they thin it, spread telangiectasias, and cause the very redness they were meant to treat. On the face, the eyelids, the groin — thin skin, sensitive sites, chronic disease — that cost becomes unacceptable. This is the gap the steroid-sparing topicals were built to fill. They calm the same inflammation by a completely different route, and the skin they treat does not thin. The trade is a stinging first application and a higher price at the pharmacy.

The New Topicals: JAK Inhibitors and Tapinarof

For half a century, treating an inflamed patch of skin meant one of two things: a corticosteroid or, later, a calcineurin inhibitor. Both worked; both had ceilings — steroids thin the skin, calcineurin inhibitors sting. Then, from 2022 onward, a wave of genuinely new molecules arrived that share a single ambition: to switch off inflammation precisely, at a named signalling node, without a single steroid molecule. A cream that blocks the same JAK enzymes as the pills that revolutionised rheumatology. A cream that talks to a receptor better known for sensing dioxin. This is topical immunomodulation growing up — and it is quietly rewriting what a tube of ointment can do.