1. The document describes the South African algorithm for treating eczema in sensitive skin areas. It focuses on prevention and provides diagnostic criteria. 2. The algorithm aims to minimize skin barrier dysfunction and prevent eczema flares through early detection and treatment of pre-lesions. It emphasizes emollients as the first line treatment. 3. The diagnostic criteria help identify patients who may benefit from additional anti-inflammatory therapies like topical corticosteroids depending on the severity and type of lesions present.

1. Overview of the South African algorithm
for treating Eczema in
sensitive skin areas
Willie Visser
Head: Division of Dermatology
Department of Medicine
Faculty of Medicine and Health Sciences
University of Stellenbosch
Tygerberg Academic Hospital

2. 2
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4. Atopic Dermatitis Is a Common, Chronic, Systemic Type 2 Inflammatory Disease1,2
1. Leung DY, Guttman-Yassky E. J Allergy Clin Immunol. 2014;134:769-779. 2. Weidinger S, Novak N. Lancet. 2016;387:1109-1122. 3. Boguniewicz M, et al. J Allergy Clin Immunol Pract. 2017;5:1519-1531.
4. Taylor K, et al. Br J Dermatol. 2017;176(6):1617-1623. 5. Lynde CW, et al. J Cutan Med Surg. 2018;22(1):78-83. 6. Esaki H, et al. J Allergy Clin Immunol. 2016;138(6):1639-1651. 7. Arkwright PD, et al.
J Allergy Clin Immunol Pract. 2013;1(2):142-151. 8. Guttman-Yassky E, et al. Expert Opin Biol Ther. 2013;13(4):549-561.
Disease Description
• Characterized by intense pruritus, recurrent eczematous lesions, and a relapsing and remitting course2,3
• Associated with immune dysregulation and skin barrier dysfunction2,3
• Occurs in approximately 3–10% of adults and 15–25% of children; 20–30% of patients have moderate-to-severe disease4-7
• Large unmet need for safe and effective therapeutics in both adults and children for long-term disease control7,8

5. MULTIFACTORIAL ETIOLOGY OF ATOPIC DERMATITIS
Genetic
 Mutations in structural
proteins, such as FLG
and claudin
 Polymorphisms in genes
encoding the Th2
cytokines and other
immune cells are
associated with AD
Immune
 Activation of Th2 and
other immune cell
types can weaken the
skin barrier
Environmental
 Changes in the
environment can
trigger further skin
barrier weakness
Microbiome
 Shifts in microbiome
might explain
temporal changes in
disease activity
FLG: filaggrin; AD: atopic dermatitis.
Leung DM et al. J Allergy Clin Immunol. 2014;134(4):769779. Hoffjan S et al. Arch Dermatol Res. 2015;307(8):659670. Darsow U et al. J
Eur Acad Dermatol Venereol. 2010;24(3):317328. Kim BE et al. Allergy Asthma Immunol Res. 2012;4(1):1216. Williams MR et al. Curr
Allergy Asthma Rep. 2015;15:65
Factors contributing to skin barrier
dysfunction in atopic dermatitis

6. DEFINITION: BARRIER
“……any obstacle that prevents movement or access”
Oxford Dictionary

7. Barrier Dysfunction

8. https://quizlet.com/43063566/skin-histology-flash-cards/
PHYSICAL BARRIER

9. - Bricks = corneocytes (cells)
- Iron rods = corneodesmosomes
(holding the cells together)
- Cement = lipid lamellae (around the
cells)
Adapted from: Cork et al. Academic unit of dermatology research. University of Sheffield
THE BRICK WALL MODEL OF THE SKIN BARRIER

10. THE BRICK WALL MODEL OF THE SKIN BARRIER
Adapted from: Cork et al. Academic unit of dermatology research. University of Sheffield

11. SKIN BARRIER BREAK DOWN
Adapted from: Cork et al. Academic unit of dermatology research. University of Sheffield

12. LOSS OF WATER AND ENTRY OF ALLERGENS & IRRITANTS
Williams H. Prevention of atopic dermatitis. 2012;F1000 medicine reports. 4. 24.
10.3410/M4-24.

13. 1. Eichenfield LF, et al. J Am Acad Dermatol. 2014;70(2):338. 2. Bieber T, et al. J Allergy Clin Immunol. 2017;139(4S):S58. 3. Weidinger S, et al. Lancet. 2016;387(10023):1109. 4. Kay J, et al. J Am Acad Dermatol. 1994;30(1):35.
5. Bantz SK, et al. J Clin Cell Immunol. 2014;5(2):202. 6. Silverberg NB, Durán-McKinster C. Dermatol Clin. 2017;35(3):351. 7. Lyons JJ, et al. Immunol Allergy Clin North Am. 2015;35(1):161. 8. Kim JP, et al. J Am Acad Dermatol.
2016;75(4):681. 9. Garmhausen D, et al. Allergy. 2013;68(4):498. 10. Mortz CG, et al. Allergy. 2015;70(7):836. 11. Irvine AD, Mina-Osorio P. British J Dermatol. 2019; doi:10.1111/bjd.17766. 12. Margolis JS, et al. JAMA
Dermatol. 2014;150(6):593.
EARLY ONSET PERSISTENT DISEASE COURSE
Disease Description
Typically, disease onset occurs early in
life1-5
• ~85–90% of patients develop AD by
5 years of age6,7
• Risk factors for persistence into
adulthood may include:
• Onset of AD later than 2 years of age2,8
• Greater severity of AD8
• AD in childhood that persists for ≥5 years8
• Family history of atopic disease11
AD in pediatric patients is a chronic disease that
can persist into adulthood5,8-10
In Pediatric Patients, Onset of AD Is Typically Early and Can Remain into Adulthood
The proportion of patients who ‘outgrow’ the disease
varies per study11
Systematic review and meta-analysis
of 45 studies with 110,651 AD
patients from 15 countries8
“80% of childhood AD did not persist
by 8 y after diagnosis, and less than
5% persisted by 20 y after diagnosis”
Analysis of the Pediatric Eczema
Elective Registry (PEER) of 7157 AD
patients from the US12
“More than 80% of PEER
participants had symptoms of AD
and/or were using medication to
treat their AD” by age 26
AD, atopic dermatitis.

14. AD Eczematous Lesions Are Clinically Heterogeneous1,2
1. European Task Force on Atopic Dermatitis. Dermatology. 1993;186:23-31. 2. Weidinger S, et al. Lancet. 2016;387:1109-1122.
Skin Lesions
Erythema
Reddening of the skin
Skin edema,
papulation, or induration
Raised or elevated skin
Excoriation
Physical signs of itching
and scratching
Xerosis
Generalized skin dryness
Oozing or crusting
Exudative lesions resulting from
epidermal edema and vesiculation
Lichenification
Accentuation
of skin markings
Characteristics of AD Lesions
AD, atopic dermatitis.

15. The Morphology and Distribution of Lesions Vary Between Infants, Children,
Adolescents, and Adults1-3
*Age range not specified in the source material.
Images reprinted from The Lancet, 387(10023), Weidinger S, et al. Atopic dermatitis, 1109-1122, © 2016, with permission from Elsevier.
1. Weidinger S, et al. Lancet. 2016;387(10023):1109-1122. 2. Siegfried EC, et al. J Clin Med. 2015;4(5):884-917. 3. Eichenfield LF, et al. Semin Cutan Med Surg. 2017;36(2 Suppl 2):S36-S38.
Skin Lesions
Infants*
Face and extensor surfaces of limbs; trunk might be
affected, diaper/napkin area is typically spared1
From age 1–2 years onwards
Polymorphous manifestations with different types
of skin lesions, particularly in flexural folds1
Adolescents* and adults
Lichenification and excoriated plaques at flexures,
wrists, ankles, and eyelids; in the head and neck
type, upper trunk, shoulders, and scalp involved1
A
B
C

16. Prevention
16

17. Diagnostic criteria

18. Impact of Atopic Dermatitis (AD)
18

19. Amongst Skin and Subcutaneous Conditions, AD (Eczema)* Is a Leading Cause of
Global Burden of Disease
The Global Burden of Disease Study 2010 estimated the burden attributable to 15 categories of skin disease from 1990 to 2010 for 187 countries.1
*Standardized disease definitions were established in several ways. With atopic dermatitis, within the broader heading of eczema, definitions such as the UK working party definition of AD were used.
†Disability was derived from an analysis of the comparative impact of the direct disabling consequences of skin disease such as itch and disfigurement against other conditions through a disability weights survey, which
involved the use of international panels of volunteers, a telephone-based survey, and a web-based tool.1
1. Hay RJ, et al. J Invest Dermatol. 2014;134(6):1527-1534.
Epidemiology
Cause Average disability weight
Non-melanoma skin cancer 0.060
Eczema cases 0.038
Psoriasis cases 0.054
Cellulitis cases 0.035
Impetigo cases 0.008
Abscess and other bacterial skin diseases cases 0.003
Scabies cases 0.016
Fungal skin diseases 0.002
Molluscum contagiosum cases 0.002
Viral warts cases 0.029
Acne vulgaris cases 0.006
Alopecia areata cases 0.035
Pruritus cases 0.008
Urticaria cases 0.031
Decubitus ulcer cases 0.108
Other skin and subcutaneous diseases 0.006
Disability weights for skin and subcutaneous diseases† – Global Burden of Disease Study, 2010
AD, atopic dermatitis.

20. The Impact of Moderate-to-Severe AD on the Overall Health of Adult Patients Is
Comparable to Other Serious Chronic Disorders1
*SF-6D weighted mean (95% CI) utility scores. A cross-sectional, population-based study in 3495 adults (mean age 52.0 ± 16.3 years) in the USA; 602 (7.4%) had AD (self-reported as 34.8% moderate, 6.9% severe), according
to modified UKWP criteria.1
AD, atopic dermatitis; CI, confidence interval; Healthy, healthy adults with no chronic disorders; SF-6D, six-dimensional health state short form; UKWP, United Kingdom Working Party.
Modified from Silverberg, et al. 2019.1
1. Silverberg JI, et al. J Allergy Clin Immunol Pract. 2019;7:1246-1252.e1.
0.79
0.73
0.67 0.67
0.65
0.63 0.63 0.63
0.61
0.55
0.60
0.65
0.70
0.75
0.80
Healthy Mild AD Food
allergy
High blood
pressure
Diabetes Moderate to
severe AD
Heart
disease
Anxiety or
depression
Autoimmune
disorder
SF-6D
utility
score*
In the same study, patients with AD and comorbid atopic disease (asthma, food allergy)
had even lower SF-6D scores than patients with AD alone1
Epidemiology
Overall health (SF-6D) of US adults with chronic disorders
SF-6D
Range: 0–1
1.0: best health
0.0: worst health

21. AD Has a Large Impact on Quality of Life of Pediatric Patients and Caregivers1
AD, atopic dermatitis; CLQI, Children’s Life Quality Index; PRO, patient-reported outcome; QoL, quality of life.
1. Beattie PE, et al. Br J Dermatol. 2006;155(1):145-151.
Children aged 5–16 years with various chronic diseases, including 106 patients with AD
• Generalized AD had the second-largest impact on QoL, following only cerebral palsy, among all chronic diseases studied
PROs: Quality of Life
CLQI scores for 540 children, 379 with chronic skin disease and 161 with other chronic diseases
0
2
4
6
8
10
12
14
16
Naevi Acne Local AD Alopecia Diabetes Enuresis Epilepsy Psoriasis Asthma Urticaria Cystic
fibrosis
Renal
disease
General
AD
Cerebral
palsy
Score

22. 22
Multidimensional Burden

23. Persistent, Debilitating Itch Is Often the Predominant Feature of Adult
Moderate-to-Severe AD1
1. O’Neill JL, et al. Acta Derm Venereol. 2011;91:537. 2. Simpson EL, et al. J Am Acad Dermatol. 2016;74:491. 3. Elman S, et al. Br J Dermatol. 2010;162:587.
4. Charman C, et al. Arch Dermatol. 2004;140:1513. 5. EuroQol Group. Health Policy. 1990;16:199.
Pruritus and Pain
SEVERE
FREQUENT
LONG LASTING
DISRUPTIVE
PAINFUL
61%
86%
63%
4 nights
77%
experienced severe or unbearable itching2,3
reported the daily presence of itch2,4
reported itching at least 12 hours a day2,3
of patients reported moderate/extreme pain or discomfort2,5
per week, on average, sleep was disturbed due to AD2,4
Characteristics of itching experienced in a study of
379 adults with moderate-to-severe AD (mean age of 37.0 ± 12.2 years)2
AD, atopic dermatitis.

24. Sleep Disturbance and Sleep-related Impairment Are Common in Adult Patients with
Moderate-to-Severe AD1
Prospective, questionnaire-based study in 287 adults (18-69 years of age) with AD, mostly moderate to severe
(92.3% in the past week on Patient-Oriented Eczema Measure [POEM]).1
AD, atopic dermatitis; PRO, patient-reported outcome.
1. Li JC, et al. Dermatitis. 2018;29(5):270-277.
PROs: Sleep Disturbances
68.0%
of patients
(n=189/278)1
48.6%
of patients
(n=134/276)1
54.7%
of patients
(n=151/276)1
58.5%
of patients
(n=161/275)1
Don’t feel alert on waking
“felt alert when woke up”:
‘not at all’ or ‘a little bit’
Felt tired
‘quite a bit’ or
‘very much’
Unsatisfied with sleep
“satisfied”:
‘not at all’ or ‘a little bit’
Don’t feel refreshed
“refreshing sleep”:
‘not at all’ or ‘a little bit’

25. Parents Report Their Own Sleep Is Disturbed Because of Their Children’s AD
*Reported as sometimes/often/all the time.
1. Chamlin SL, et al. Arch Pediatr Adolesc Med. 2005;159:745-750. 2. Drucker AM, et al. Journal Invest Dermatol. 2017;137:26-30. 3. Zuberbier T, et al. J Allergy Clin Immunol. 2006;118:226-232.
PROs: Sleep Disturbances
Parent-reported burden on sleep* (n=270, aged 0 to 6 years)1
Child’s Sleep
Disturbed
Parents’ Sleep
Disturbed
Children Co-sleeping
with Parents
68%
30%
61%
Parents of young children (aged 0 to 6 years) with AD are burdened by the lack of
sleep and emotional weight of seeing their children suffer2
25–39% of pediatric patients (aged 2 to 17 years) have been bullied because of AD (moderate-to-severe disease)3
AD, atopic dermatitis; PRO, patient-reported outcome.

26. AD Can Impact School Attendance in Pediatric Patients with AD1
1. Eczema Society of Canada. https://eczemahelp.ca/wp-content/uploads/2019/02/ESC_Quality-of-Life-Report_Nov-2017-1.pdf. Accessed March 2021.
PROs: Work and School
Impact
Pediatric patients (0–18 years) who missed school days due to their AD
in the Eczema Society of Canada Quality of Life Insights Project (n=658)
23%
12%
0
5
10
15
20
25
30
35
40
45
50
55
60
65
70
75
80
85
90
95
100
Missed ≥10 days Missed ≥20 days
AD
patients
(%)
Of the 20% of patients who
missed school:
20%
missed
school
AD, atopic dermatitis; PRO, patient-reported outcome.

27. Adults with AD Have a High Risk of Depression and Suicidality1
Any depression: clinical depression or depressive symptoms.
Systematic review and meta-analysis to determine the relationship between AD, depression and suicidality.1
1. Patel KR, et al. J Am Acad Dermatol. 2019;80(2):402-410.
PROs: Mental Health
Depression
Healthy controls AD patients
Prevalence of any depression
in a meta-analysis of 36 studies
1 in 4
AD patients
Depressive
symptoms
Suicidality
Healthy controls AD patients
Prevalence of suicidal ideation
in a meta-analysis of 14 studies
1 in 8
AD patients
Suicidal
ideation
2.0x odds of suicidal ideation in AD
12/14 studies; 95% CI 1.2–3.3; p<0.001
1.7x odds of any depression in AD
22/36 studies; 95% CI 1.5–2.0; p<0.001
14.8%
20.1%
6.4%
12.2%
AD, atopic dermatitis; CI, confidence interval; PRO, patient-reported outcome.

28. AD Patients Have an Increased Susceptibility to a Host of Cutaneous Infections1-3
1. Weidinger S, et al. Lancet. 2016;387(10023):1109-1122. 2. Baker BS. Clin Exp Immunol. 2006;144(1):1-9. 3. Leung DY. Curr Opin Pediatr. 2003;15(4):399-404.
Staphylococcal infection Eczema herpeticum Molluscum contagiosum
Infections
AD, atopic dermatitis.

30. Treatment of Atopic Dermatitis (AD)
30

32. Emollients

33. Summary
“Moisturizers remain the cornerstone of AD treatment, and the single
most important non-pharmacological therapeutic option available.”

34. • First-line therapy
• May be steroid-sparing
• Every 6h, at least 2x per day, after swimming and bathing
• All over
Emollients

36. Which emollient is the best?
There is little difference between the various emollients on the market
Unperfumed and without a colorant
The cosmetic preference of the patient is vital
Reputable manufacturer/brand
THE NEW GENERATION MOISTURIZERS
The one that the patient will use!

37. Barrier dysfunction and Treatment
• Moisturisers - improve barrier function
ADD (Emollients PLUS)
• Physiological lipids (eg, ceramides, cholesterol)
• Physiological humectants (urea, glycerol)
• Anti-inflammatory (Rhamnosoft, L-isoleucine, Thermal Spring water-based)
• Patented Filaggrin technology™
• Anti-itching agents (eg, glycerol)
• Dexpanthenol —stimulates lipid synthesis and epidermal differentiation
• Occlusive agents (eg, petrolatum) that reduce water evaporation
• Wet wraps

38. Choice of emollient?
Different formulations can also be used for different
anatomical locations
The patient’s preference may also change over time.
Child Teenager Adult Older

39. • Avoid over heating
o Summer PJs in winter
o Duvet – yes, blankets – no
• Avoid irritants
o Animals not on bed
o Cigarette smoke
o Foodstuffs that irritate skin
o Rough textiles, remove labels, loose fitting
• Keep skin covered
• Keep fingernails short
• Avoid skin care products (perfumes, colourants)
General measures - Education

40. • 1x per day (max), short baths
• Luke-warm water
• Moisturizing cleanser – no soaps that foam
• Do not shampoo hair in bath
• No “bubble bath”
• Pat dry – soft towel
• Apply emollient on wet skin
Bath rules:

41. 41

42. Recalcitrant/Severe AD
Corticosteroids
Calcineurin
Inhibitors
Overview of Treatment Options for AD
*Pimecrolimus is recommended by EADV and AAD, but not by JDA.1–3 †In 2016, the FDA approved crisaborole for the topical treatment of mild-to-moderate AD in patients aged ≥2 years.4 Currently, crisaborole is not
included in treatment guidelines. ‡Approved in the US for the treatment of adult patients with moderate-to-severe AD whose disease is not adequately controlled with topical prescription therapies or when those
therapies are not advisable, in the EU for the treatment of adult patients with moderate-to-severe AD who are candidates for systemic therapy, and in Japan for the treatment of AD in adults not adequately controlled
with existing therapies.8–10 §Cyclosporine is the only approved systemic immunosuppressive drug for AD (approved in most European countries and Japan).3,11
Off-label use of cyclosporine is recommended by AAD.5 Off-label use of azathioprine, methotrexate, and mycophenolate mofetil is recommended by AAD and EADV.5,6 ¶Treatment guidelines recommend oral/injectable
corticosteroids for the short-term treatment of acute flare in patients with severe AD.3,5,6 PDE4, phosphodiesterase 4; UVA, ultraviolet A; UVB, ultraviolet B.
1. Eichenfield LF et al. J Am Acad Dermatol 2014;71:116–132. 2. Wollenberg A et al. J Eur Acad Dermatol Venereol 2018;32(5):657-682. 3. Saeki H et al. J Dermatol 2016;43:117–1145. 4. FDA.
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm533371.htm. Accessed December 2016. 5. Sidbury R et al. J Am Acad Dermatol 2014;71:327–349. 6. Wollenberg A et al. J Eur Acad Dermatol
Venereol 2018;32(6):850–878. 7. Boguniewicz M et al. J Allergy Clin Immunol Pract 2017; 5:1519–1531. 8. Sanofi Genzyme, Regeneron. DUPIXENT® (dupilumab) [US prescribing information]. March 2017. 9. Sanofi
Genzyme, Regeneron. Dupixent [EMA summary of product characteristics]. 2017. 10. Regeneron. http://investor.regeneron.com/releasedetail.cfm?releaseid=1054842. 2018. [Press Release]. 11. Bieber T, Straeter B.
Allergy 2015;70:6–11.
Topical1–4 Systemic3,5–7
Basic Treatment
Phototherapy Systemic
immunosuppressive
drugs§
Emollients Low potency Tacrolimus
Pimecrolimus*
UVA/UVB
Corticosteroids¶
(eg, prednisone)
Moisturizers Medium potency
High potency
Cyclosporine Azathioprine Methotrexate Mycophenolate
mofetil
PDE4 Inhibitor
Crisaborole†
Nonbiologics Biologics
Dupilumab‡
Mild AD
Low potency: Mild-to-moderate AD
High potency: Moderate-to-severe AD

43. Topical treatments
43

44. Treatment
Treatment should start as early as possible or as
soon as possible with the first signs of eczema
1.What grade?
2.Which area on the body?

45. Grading of eczema
Mild
Moderate
Severe

46. Clinical Presentation of AD Ranges in Severity*
*Severity of AD lesions is determined using assessment tools (eg, IGA, EASI, and SCORAD) that include measurements of the extent of area involved,
an intensity score, and other symptoms such as pruritus and sleep loss.1–3
Photos from Bieber T, Nestle F, eds. Personalized Treatment Options in Dermatology. doi:10.1007/978-3-662-45840-2_5; Berlin Heidelberg: Springer-
Verlag; 2015, with images courtesy of Dr Thomas Bieber, from Leung DYM et al. J Allergy Clin Immunol 2014;134:769–779, from Weidinger S et al.
Lancet 2016;387:1109–1122; and from Sanofi Genzyme and Regeneron, used with permission. Photos are not representative of all patients with AD.
1. Hanifin JM et al. Exp Dermatol 2001;10:11–18. 2. European Task Force on Atopic Dermatitis. Dermatology 1993;186:23–31. 3. Rehal B et al. PLoS
ONE 2011;6:e17520.
Mild Form Moderate Form Severe Form

47. Sensitive skin areas
47

49. Sensitive areas

50. Sensitive areas

51. Regular follow up

52. *Adapted from Akdis CA, et al. J Allergy Clin Immunol. 2006;118(1):152-169.

53. Maintenance Treatment

54. Pro-active therapy

55. When to Refer?
55

56. Available Systemic Therapies Are Limited by Risk
/ Benefit Profiles
Systemic corticosteroids may temporarily suppress disease
flares – but should generally be avoided due to short- and long-
term risks1
1. Sidbury R et al. J Am Acad Dermatol. 2014;71(6):12181233. 2. Akhavan A, Rudikoff D. Semin Cutan Med Surg. 2008;27:151155.
Risks associated with oral corticosteroids include2,3
–Cataracts – Glucose intolerance – Myopathy
–Cushing’s syndrome – Hypertension – Osteopathy
–Glaucoma – Infections
Rebound phenomenon may occur2
Skin lesions may get worse after discontinuation of treatment with systemic corticosteroids

57. Systemic immunosuppressants
Representative risks with systemic immunosuppressants
Cyclosporine
 Boxed warning for
malignancies, infection,
hypertension,
and nephrotoxicity/
structural renal
damage; need for blood
monitoring of CsA4
Methotrexate
 Boxed warning for
malignancies, bone
marrow suppression,
infection, hepatic and
renal toxicity,
teratogenic, pulmonary
fibrosis5
Azathioprine
 Boxed warning for
malignancies
 Mutagenic potential
 Hematologic
toxicitites6
Mycophenolate mofetil
 Boxed warnings for
pregnancy,
loss/congenital
malformations;
malignancies, serious
infection7
3. Lindstrom J. Atopic dermatitis inadequately responsive to topical therapy.
http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/Drugs/
DermatologicandOphthalmicDrugsAdvisoryCommittee/UCM439354.pdf. Accessed December 22, 2015. 4. Neoral ®
[package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2015. 5. Methotrexate [package insert]. Lake Forest,
IL, Hospira; 2011. 6. Imuran® [package insert]. San Diego, CA. Pharmaceutics Internal Inc; 2011. 7. CellCept® [package insert].
Nutley, NJ: Roche; 2009

58. 58

59. 59

60. Th2 Pathway
DC IL-4
IL-13
IL-4
Th 2
TYPE 2
INFLAMMATION

61. Th2 Pathway Suppression
DC IL-4
IL-13
IL-4
Th 2
TYPE 2
INFLAMMATION
Targeting a central ‘driver pathway’

62. Targeting Key Proximal Drivers Of The Type-2 Pathway
Gandhi, Namita & Bennett, Brandy & Graham, Neil & Pirozzi, Gianluca & Stahl, Neil & Yancopoulos, George. (2015). Targeting key proximal drivers of type 2 inflammation in disease. Nature reviews. Drug discovery. 15. 10.1038nrd4624.

63. Small molecules; targeted therapies of atopic dermatitis
Ann Dermatol Vol. 33, No. 2, 2021

64. Conclusion
• AD dermatitis is a clinically diagnosable chronic disease
• Numerous co-morbidities associated with AD
• Severe impact on QoL
• Established treatment protocols
• BUT still an unmet need for reluctant disease
• Emollients and general skin care is the cornerstone of treatment
• TCI are the first choice of treatment for sensitive skin areas

65. A New World of
Eczema Treatment
Thank you