Lesions are under control, but itching persists. The lesions improved, yet sleep remains disrupted. This disconnect between clinical measures and patients’ experiences was a key focus of discussions on atopic dermatitis at the 79th Congress of the Brazilian Society of Dermatology (CSBD), held on September 10-12, 2026, in Fortaleza, Ceará, Brazil.

The concept of disease modification was central to the discussion. In an interview with Medscape’s Portuguese edition, Xinaida Taligare Vasconcelos Lima, MD, PhD, associate professor, Department of Clinical Medicine, School of Medicine, Federal University of Ceará, Fortaleza, Brazil, emphasized that the concept “is still predominantly a translational and research concept.” Demonstrating a true change in the natural history of the disease requires more than keeping a patient symptom-free while receiving effective treatment. This would require sustained remission after treatment discontinuation and, potentially, a reduced risk for comorbidities or progression of the atopic march.

Long-term data, even when they do not establish disease modification, are changing treatment expectations. The ECZTEND study, published earlier this year in Dermatology and Therapy, followed 1672 adolescents aged 12 years or older and adults with moderate-to-severe atopic dermatitis in an open-label extension of tralokinumab treatment. Including exposure during previous studies, the follow-up period lasted up to 6 years. Eczema Area and Severity Index (EASI) 75 was maintained in at least 80% of the evaluated patients, while EASI-90 and clear or almost clear skin, defined by an Investigator’s Global Assessment score of 0 or 1, were maintained in at least half of the participants.

The study showed that prolonged disease control was possible; however, it also highlighted an important distinction: maintaining a response during continuous treatment does not indicate that the disease will remain controlled after treatment is discontinued.

Pruritus Needs Separate Assessment

One of the most practical changes may be recognizing pruritus as a treatment target in its own right. According to Raquel Leão Orfali, MD, PhD, a professor in the Department of Dermatology at the University of São Paulo’s School of Medicine (FMUSP) and a co-coordinator of the high-complexity Urticaria and Atopic Dermatitis outpatient clinics at Hospital das Clínicas FMUSP, pruritus results from interactions among cutaneous inflammation, epidermal barrier dysfunction, and neuroimmune mechanisms involving interleukin 31 pathways and type 2 cytokines.

“ Controlling skin lesions and controlling pruritus are closely related goals, but they are not necessarily equivalent,” Orfali said. Some patients experience objective improvement in eczema but continue to have clinically relevant pruritus. Therefore, pruritus intensity, frequency, effects on sleep, and functional impact should be independently assessed.

This distinction also provides scientific support. A post hoc analysis of four phase 3 clinical trials, published in the Journal of the European Academy of Dermatology and Venereology, showed that nemolizumab, which targets the interleukin 31 receptor, produced a rapid reduction in pruritus. The difference in the proportion of responders from the placebo group was detectable by day 2 and increased through day 14. Sleep disturbances also improved at an early stage. These data do not indicate that all atopic dermatitis should be treated by prioritizing a single pathway, but they show that the biology of pruritus is sufficiently specific to warrant considering it a therapeutic outcome.

Orfali summarized the change in clinical terms: “We no longer treat only ‘itchy skin’ but also the mechanisms that generate and perpetuate pruritus.” This distinction has several diagnostic implications. Persistent pruritus lasting more than 6 weeks, particularly when generalized or disproportionate to the skin findings or accompanied by weight loss, fever, night sweats, or lymphadenopathy, should not be automatically attributed to atopic dermatitis. In these situations, medication-related, systemic, neurologic, hematologic, and lymphoproliferative causes should be investigated.

Adults May Go Years Without a Diagnosis

Another obstacle is the perception that atopic dermatitis is primarily a childhood disease. Renata da Silveira Rodrigues Paiva, MD, a dermatologist and preceptor in the Dermatology Medical Residency at the Department of Dermatology, Hospital Universitário Lauro Wanderley, João Pessoa, Brazil, where she is responsible for the paediatric dermatology and atopic dermatitis outpatient clinics, emphasized that “atopic dermatitis can begin at any age, including in older adults.”

Late-onset and atypical presentations can be mistaken for contact dermatitis, nummular eczema, dermatophytosis, or other skin disorders, delaying effective treatment. In adults, diagnosis requires reconstructing the disease history, assessing lesion distribution and recurrence, reviewing the history of atopy, identifying relevant exposures, and considering differential diagnoses. A history of childhood eczema is not required for diagnosis in adults.

Biomarkers: Promising but Not Yet Decisive

Precision medicine may be the next major development in atopic dermatitis, but there is still no test to determine the best treatment. Paiva noted that total immunoglobulin E (IgE) can be measured routinely and may indicate an extrinsic phenotype, while lactate dehydrogenase (LDH) may reflect disease severity in certain settings; both are nonspecific. “Currently, no single biomarker is sufficient to assess the complexity of atopic dermatitis,” she said. TARC/CCL17 remains among the biomarkers with the most consistent association with disease severity; however, it is not routinely incorporated into clinical practice in Brazil and cannot, on its own, determine the appropriate treatment.

A systematic review published earlier this year in Clinical Reviews in Allergy & Immunology, which included 80 studies, reached a similar conclusion. Reductions in CCL17/TARC, LDH, and total IgE often accompanied improvements in EASI and SCORing Atopic Dermatitis after systemic treatment, but heterogeneity in study designs, laboratory platforms, and cutoff values limited individual application. CCL17 and LDH were among the more consistent markers of disease severity and response, but they were not sufficiently specific to replace clinical assessment or guide treatment selection between biologics and JAK inhibitors in a validated manner. The risk is turning population-level associations into promises of personalized medicine before these tests have adequate discriminatory ability.

In practice, four dimensions need to be assessed together: objectively measured skin disease activity, pruritus, effects on sleep and quality of life, and treatment required to keep the disease under control. An adequate response, therefore, should not be defined solely by improved skin appearance or an individual score.

Similarly, treatment should not be escalated because a new therapeutic option exists. Age, comorbidities, required speed of response, safety profile, patient preference, route of administration, and ability to monitor treatment remain relevant.

Progress in atopic dermatitis therefore lies not only in expanding the therapeutic arsenal but also in better defining what should be treated. Lesions may improve before pruritus does, persistent pruritus may have another cause, a biomarker may track disease activity without determining treatment, and remission during treatment may not indicate a change in the disease itself. More effective treatments make it increasingly important to precisely define treatment goals. The goal is no longer simply to achieve lesion-free skin but to determine whether the disease is truly under control and how long that control can be safely maintained.

Vasconcelos Lima reported having no relevant conflicts of interest.

Orfali reported participating in clinical trials and serving as a speaker for Sanofi-Aventis, Eli Lilly, AbbVie, L’Oréal, and Galderma, and serving on advisory boards for Sanofi-Aventis and Eli Lilly.

Paiva reported receiving support to attend events organized by Sanofi, AbbVie, Pfizer, Novartis, Lilly, UCB, Mölnlycke, Chiesi Pharmaceuticals, and Smith & Nephew; serving as a speaker for Sanofi, Pfizer, and LEO Pharma; participating in the preparation of scientific material for Sanofi; serving on AbbVie’s advisory board; and conducting clinical research for Urgo.

The authors’ conflicts of interest are reported in the original publication.

Hermano Rocha is a physician and professor at the Faculty of Medicine of the UFC. He is a Post-Doctorate in Applied Epidemiology at the Harvard School of Public Health and UFC. Alumnus of Harvard Medical School: Effective Writing for Healthcare. Rocha is a board member of the International Epidemiological Association and conducts research in various medical-epidemiological areas, with a main focus on nutritional health, maternal-child development, and health technology assessment.

This story was translated from Medscape’s Portuguese edition.