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Atopic dermatitis (AD) is a chronic disease driven by persistent underlying inflammation2–4

Adults with moderate-to-severe AD report a multi-dimensional burden including sleep, quality of life, and psychosocial effects5

Nonlesional skin in AD is not normal skin2–4

Normal Skin

Nonlesional Skin

Lesional Skin

AD experts* proposed four types of treatment failure which patients with AD may experience despite appropriate dose, duration and adherence to a therapeutic agent5

1

Inadequate clinical
improvement

2

Failure to achieve
stable long-term
disease control

3

Adverse events or
poor tolerability with
current treatment

4

Failure to relieve
burden of disease†5,6

Adult Patient-Reported Outcomes:‡7

Patient reported outcomes in uncontrolled AD

Adolescent (14–17 years old) Patient-Reported Outcomes:§8

Patient reported outcomes in uncontrolled AD

*A steering committee that consisted of a multi-disciplinary group of AD experts, including 8 dermatologists, two allergists and a patient advocacy group representative. This group met to identify and prioritise a number of essential questions concerning the evaluation and management of moderate-to-severe AD in the era of biologic therapies.5

Presence of ongoing impairment (e.g., pruritus, pain, loss of sleep, and poor quality of life) while on treatment.6

These results are patient-reported outcomes collected at a screening for a Phase 2b clinical trial of DUPIXENT (n=380).7

§These results are patient-reported outcomes from the ISOLATE study collected in six countries by in-depth telephone interviews. Questions were developed in collaboration with national eczema patient groups and physicians.8

|A flare is defined as a sudden worsening of symptoms requiring consultation or application of prescription medication.8


AD, atopic dermatitis; ISOLATE, International Study of Life with Atopic Eczema.


References

  1. DUPIXENT Summary of Product Characteristics. Available at: https://www.medicines.org.uk/emc/product/8553/smpc. Date accessed: December 2020.
  2. Leung DYM, et al. J Clin Invest. 2004;113(5):651–657.
  3. Suárez-Fariñas M, et al. J Allergy Clin Immunol. 2011;127(4):954–964.
  4. Gittler JK, et al. J Allergy Clin Immunol. 2012;130(6):1344–1354.
  5. Boguniewicz M, et al. J Allergy Clin Immunol Pract. 2017;5:1519–1531.
  6. Ibler K & Jemec. GBE Dermatol Rep. 2011;3:e5.
  7. Simpson EL, et al. J Am Acad Dermatol. 2016;74(3):491–498.
  8. Zuberbier T, et al. J Allergy Clin Immunol. 2006;11(1):226–232.