Atopic dermatitis is often discussed as a single disease. Increasingly, science is showing that the biology underneath that diagnosis can be very different from one patient to another.
Ahead of the 2026 EADV Congress in Vienna, the European Academy of Dermatology and Venereology highlighted scientific discussion around »late-onset atopic dermatitis« and how it may differ from disease that begins in childhood.
Professor Emma Guttman-Yassky's EADV session focuses on evidence showing that while type 2 inflammation is an important feature of atopic dermatitis, different immune pathways may be activated to different degrees in different groups of patients.
Researchers describe these biologically distinct disease patterns as »endotypes«. Endotypes can be associated with characteristics including age, ethnicity, IgE levels and the age at which atopic dermatitis first appears.
One of the particularly interesting questions is whether someone whose atopic dermatitis begins in adulthood has the same underlying disease as someone who has lived with atopic dermatitis since infancy. Evidence increasingly suggests the answer may be no.
EADV's programme highlights differences in both the »cutaneous immune profile« — what is happening inside the skin — and »systemic immune characteristics«, meaning immune activity throughout the body. There can also be differences in the clinical features patients experience.
This scientific shift matters because atopic dermatitis treatment has become dramatically more targeted. Clinicians now have therapies aimed at IL-4 and IL-13 signalling, IL-13 specifically, IL-31-related pathways and JAK signalling, among others.
Yet patients do not respond to every treatment in the same way.
Understanding biological subtypes may therefore help researchers move toward a future where treatment is selected according to the individual biology driving someone's disease rather than mainly through trial and error. That is where biomarkers become especially important.
Researchers hope that measurable biological signals could eventually help identify the right therapy for the right patient and show whether treatment is changing the underlying disease process.
We are not there yet.
There is currently no simple test that can tell every person with atopic dermatitis which medicine will work best for them. But the direction of research is increasingly clear. “Atopic dermatitis” may ultimately describe a family of related inflammatory patterns rather than one biologically uniform condition.
For patients, this could help explain a familiar and sometimes frustrating experience: two people can have atopic dermatitis of apparently similar severity yet respond completely differently to the same treatment. The more researchers understand those differences, the closer atopic dermatitis care moves toward genuine precision medicine.
The future question may therefore become not simply, “How severe is your atopic dermatitis?”
It may also be: “What kind of atopic dermatitis do you have?”