The American Journal of Managed Care has surfaced a clinical thesis that dermatologists cannot afford to overlook: treating hidradenitis suppurativa early may prevent permanent scarring in patients with skin of color.

That single claim reshapes a conversation that has long centered on symptom control rather than lasting skin damage. Black, Hispanic, and other patients with skin of color already bear the heaviest scarring burden after inflammatory skin disease. Post-inflammatory hyperpigmentation and keloid-like remodeling can persist for years after each HS lesion heals.

What is HS, and why does timing matter?

Hidradenitis suppurativa is a chronic, relapsing inflammatory disease of the apocrine gland-bearing skin. It targets the axillae, groin, inframammary folds, perianal area, and buttocks. Painful nodules, deep abscesses, and sinus tracts define its course. Hurley stage III disease can render sitting, walking, or arm movement agonizing.

The disease carries an average diagnostic delay that often stretches past seven years. By the time many patients reach a dermatologist, scarring has already set in. Each inflammatory flare remodels the dermis through repeated cycles of abscess, drainage, fibrosis, and contracture. Once sinus tracts form, topical therapy alone rarely reverses them.

Early treatment interrupts that dermal remodeling before it begins.

Why does skin of color change the calculus?

Hypertrophic and keloid scarring patterns differ across racial and ethnic groups in measurable ways. The biology extends well beyond cosmetics. Keloid HS scars burn, itch, and restrict motion in ways atrophic scars do not. Post-inflammatory hyperpigmentation can linger for years after the active lesion clears, particularly in Fitzpatrick IV through VI skin.

Patients routinely describe the scars as affecting them as much as the active disease itself, sometimes more. Treating early — before those scars form — gives the skin a chance to heal with less visible, less symptomatic damage. For darker phototypes, the difference between early and late treatment shows up in the mirror for decades.

What should clinicians do now?

The AJMC framing should prompt three practical moves:

• Lower the threshold for suspecting HS in any patient of color with recurrent groin, axillary, or buttock lesions.
• Refer early — within weeks, not months — to a dermatologist comfortable with HS staging and biologic therapy.
• Counsel patients that the goal extends beyond symptom relief to scar prevention, and document that conversation.

For payers, the message is similar. Covering early biologic use in moderate HS may cost less in the long run than the surgical reconstruction required for advanced disease. Topical and oral therapy is far cheaper than scar revision surgery, which itself carries keloid risk in skin of color patients.

Early action is the cheapest, safest scar prevention available.

What does the field still need to see?

The AJMC piece foregrounds the principle rather than a specific trial dataset. Dermatology still needs prospective studies that quantify scar outcomes by Fitzpatrick type across HS treatment pathways. Until those data arrive, the conservative clinical posture is clear: treat early, treat aggressively, and treat with the scar in view.

Payers and providers who invest in early HS care now may see measurable reductions in scarring-related costs and patient-reported morbidity within five years. For skin of color patients, the dividend is something simpler than a number. It is a mirror that looks the way it did before the disease arrived.