People with AD or PN can stop their itch if they just stop scratching.

• Majority of patients with AD or PN start scratching only in response to itching; scratching is not a proactive behavior but a reflex that patients cannot control¹.   

For patients with PN, skin nodules are the most burdensome symptom of the disease.

• In a study,100% of surveyed physicians treating patients with PN said that itch was their patients’ primary complaint².

Eczema/AD is just a skin rash.

• While AD primarily affects the skin, it's not just a simple rash. It's a chronic inflammatory condition that accompanies persistent and severe itch, often leading to sleep disturbances and a reduced quality of life. Itch is one of the main complaints from patients and does not necessarily correlate with rash intensity. As such, both itch and rash intensity need to be considered^3,4. 

Itch in AD and PN is only skin-deep.

• The itching associated with eczema can extend beyond the skin. It can affect a person's overall well-being, sleep, and daily life, leading to emotional and psychological distress^2,5,6.

In AD and PN, chronic itch does not affect patients’ sleep. 

• Patients with itch have reported sleep deprivation, with some selecting it among the top three most problematic symptoms^2,7. 

In AD and PN, the impact of chronic itch on patients’ quality of life is minimal.

• Quality of life indicators such as self-image, social relationships, and intimacy can be diminished in patients with AD and PN^7,8.   

Only Th2 cells produce and/or respond to IL-31.

• According to multiple animal studies, in addition to lymphoid immune cells, such as Th2 lymphocytes, many other immune and nonimmune cells produce IL-31 and/or respond to IL-31, including basophils, eosinophils, monocytes, myeloid cells, mast cells, DRG neurons, keratinocytes, microvascular endothelial cells, and dermal fibroblasts⁹. 

IL-31 is only an itch cytokine. 

• Although IL-31 is one of the main drivers of itch, it also contributes to inflammation and skin abnormalities observed in AD and PN as shown in multiple animal studies^9,10. 

IL-31 signaling does not impact the structural cells in the skin.

• IL-31 is involved in skin barrier function and skin abnormalities by inhibiting keratinocyte differentiation and the expression of filaggrin as shown in multiple animal studies. IL-31 contributes to fibrosis and skin remodeling by affecting dermal basal cells and boosting collagen production in dermal fibroblasts, resulting in increased epidermal cell proliferation and thickening^11,12,13. 

Itch severity cannot be measured or quantified because it is subjective and differs from patient to patient.

• Patient-reported outcome tools, such as NRS, VAS, and VRS, are reliable tools to measure patient itch during the most intense itching episodes¹⁴. 

References:

1. Steinke S, Zeidler C, Riepe C, et al. Humanistic burden of chronic pruritus in patients with inflammatory dermatoses: results of the European Academy of Dermatology and Venereology Network on Assessment of Severity and Burden of Pruritus (PruNet) cross-sectional trial. J Am Acad Dermatol. 2018;79(3):457–463.e5. doi:10.1016/j.jaad.2018.04.044
2. Pereira MP, Basta S, Moore J, Ständer S. Prurigo nodularis: a physician survey to evaluate current perceptions of its classification, clinical experience and unmet need. J Eur Acad Dermatol Venereol. 2018;32(12):2224-2229. doi:10.1111/jdv.15107
3. Ständer S. Atopic dermatitis. New England J Med. 2021; 384(12):1136–1143. doi:10.1056/NEJMra2023911
4. Silverberg JI, Mohawk JA, Cirulli J, et al. Burden of disease and unmet needs in atopic dermatitis: results from a patient survey. Dermatitis. 2023; 34(2), 135–144. doi:10.1089/derm.2022.29015.jsi 
5. Silverberg JI. Comorbidities and the impact of atopic dermatitis. Ann Allergy Asthma Immunol. 2019;123(2):144–151. doi:10.1016/j.anai.2019.04.020
6. Konda D, Chandrashekar L, Rajappa M, Kattimani S, Thappa DM, Ananthanarayanan PH. Serotonin and interleukin-6: association with pruritus severity, sleep quality and depression severity in prurigo nodularis. Asian J Psychiatr.2015;17:24–28. doi:10.1016/j.ajp.2015.07.010
7. McCleary KK; More Than Skin Deep Initiative. Understanding the lived experience of eczema: the “Voice of the Patient” report on the eczema patient-focused drug development meeting. Published March 2020. Accessed September 27, 2023. http://www.morethanskindeep-eczema.org/uploads/1/2/5/3/125377765/mtsd_report_-_digital_file.pdf
8. Rodriguez D, Kwatra SG, Dias-Barbosa C, et al. Patient perspectives on living with severe prurigo nodularis. JAMA Dermatol. 2023;159(11):1205–1212. doi:10.1001/jamadermatol.2023.3251
9. Borgia F, Custurone P, Li Pomi F, Cordiano R, Alessandrello C, Gangemi S. IL-31: State of the art for an inflammation-oriented interleukin. Int J Mol Sci. 2022;23(12):6507. doi:10.3390/ijms23126507. 
10. Williams KA, Huang AH, Bezberg M, Kwatra SG. Prurigo nodularis: pathogenesis and management. J Am Acad Dermatol. 2020;83(6):1567-1575. doi:10.1016/j.jaad.2020.04.182
11. Furue M, Furue M. Interleukin-31 and pruritic skin. J Clin Med. 2021;10(9):1906. doi:10.3390/jcm1009190
12. Singh B, Jegga AG, Shanmukhappa KS, Edukulla R, Khurana GH, Medvedovic M, et al. IL-31-driven skin remodeling involves epidermal cell proliferation and thickening that lead to impaired skin-barrier function. PLoS ONE. 2016;11(8):e0161877. doi:10.1371/journal.pone.0161877
13. Hänel KH, Pfaff CM, Cornelissen C, et al. Control of the physical and antimicrobial skin barrier by an IL-31-IL-1 signaling network. J Immunol. 2016;196(8):3233–3244. doi:10.4049/jimmunol.1402943
14. Pereira MP, Ständer S. Measurement tools for chronic pruritus: assessment of the symptom and the associated burden: a review. Itch. 2019;4(4):e29. doi:10.1097/itx.0000000000000029