Atopic Eczema
Atopic dermatitis (AD), a chronic inflammatory dermatosis, most often begins in infants as young as 3 months old and ceases in most cases by the age of 7, although it can persist into adulthood.
The mechanisms of AD are complex, combining immunological, genetic and environmental factors with skin hyperreactivity to allergens.
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AD combines skin dryness with inflammatory flare-ups that take the form of red plaques that ooze at first, then scab over. It progresses through alternating flare-ups and phases of remission.
To support your patients
Tips sheets
Co-prescription
To remember
suffers from atopic dermatitis*
suffers from atopic dermatitis*
from itching**
from dry skin**
from red plaques**
* S. Langan. A. lrwine. S Veidimger ; Atopic Dermatitis, The lancet Volume 396 (2020)
** Etude Arcane, Dermattte Atopique (2018)
Physical consequences
AD, chronic inflammatory dermatosis, involves a number of factors and major dysfunctions including a deterioration of the skin barrier and inflammatory reactions, maintained and exacerbated by skin dryness, pruritus and microbiome imbalance.
In babies and infants, red plaques are mainly located on the face (cheeks, under and behind the ears), neck and limbs. The torso can also be affected.
In children, red plaques appear mainly in the folds (neck, elbows, knees) and on the extremities (hands, wrists, ankles).
In adults, plaques persist most often on the face (eyelids, cheeks), torso and limbs, mainly localized in the folds (elbows, knees) and on the hands.
Psychological consequences
AD is experienced as a real burden by patients and their families.
The repercussions are significant, both for their health: stress, anxiety, loss of self-confidence... and in their daily lives (quality of life, social and professional life...).
The psychological impact is particularly linked to the symptoms and the difficulty of managing them, especially during flare-ups, which are more visible. The physical impact has psychological repercussions that compound the damage to self-esteem. that compounds the damage to self-esteem. In the background, acceptance of the disease, treatment-hopping, the constraint of treatments and fear of their side effects contribute to the malaise expressed by patients.
The vicious cycle of atopic dermatitis
The symptoms of atopic dermatitis are numerous: skin dryness, skin barrier deterioration, inflammation, itching, microbiome imbalance.
The deteriorated skin barrier lets in external agents, leading to type 2 inflammation. What’s more, this exaggerated and exacerbated response affects the structure and function of the epidermis, increasing itching sensations and further damaging the skin barrier. The result is a vicious cycle that maintains and aggravates the itching/scratching cycle.
Skin barrier
The stratum corneum results from the formation of keratin filaments thanks to filaggrin (which enables the formation of NMF*) and the intercellular lipid cement (fatty acids 15%, ceramides 50%, cholesterol 25%). Interactions between proteins in the corneal envelope and lipids, as well as their structural organization, ensure the barrier function.
Atopic patients have abnormal levels of the major skin barrier components, NMF and ceramides, as well as a deficiency in gamma-Linolenic acid (Omega 6), which is both functionally and metabolically essential for the skin's barrier function. This deficiency is at the root of xerosis, caused by excessive water loss, and the deterioration of the barrier function.
NMF: Natural Moisturizing Factor
Atopic inflammation
The deterioration of the barrier allows irritants, bacteria and allergens to penetrate the dermis. Activated defense cells (T lymphocytes, mast cells, etc.) produce inflammatory cytokines, notably IL-4 and IL-13, which are key to the pathophysiology of AD. These phenomena give rise to a type 2 inflammatory response (Th2), right from the start of AD. This excessive inflammation lasts over time, is self-sustaining and also involves other defense agents (TH22, TH17, TH1 lymphocytes) in its chronic phase. Skin inflammation is delayed hypersensitivity mediated by T lymphocytes that down-regulate antimicrobial peptides, which explains why AD patients are predisposed to the development of bacterial skin infections.
Today, the inflammatory process is THE field of investigation for the treatment of atopic dermatitis, and scientific data proves that atopic skin is always inflammatory. In the flare-up phase, inflammation is visible on the skin (irritation, red plaques). In the remission phase, no clinical signs of inflammation are visible, although inflammatory markers are present in the epidermis. This invisible inflammation is called micro-inflammation.
Atopic dermatitis; S. Weidinger and N. Novak. LANCET, 2015
Cutaneous barrier dysfunction in allergic diseases Donald Y. M. Leung, MD and Emma Guttman-Yassky, MD, JACI, 2020 TSLP, IL31, IL33 and sST2 are new biomarkers in endophenotypic profiling of adult and childhood atopic dermatitis. JEADV, 2016.
Non lesional AD skin is characterized by broad terminal differentiation defects and variable immune abnormalities. Suárez-Fariñas M et al. JACI, 2011
The skin microbiome is a key element in the pathogenesis of AD.
Healthy skin is home to a wide variety of microbes. Antimicrobial peptide (AMP) production by commensal strains shapes the microbial community to prevent colonization by pathogens such as S. aureus.
In atopic skin outside of flare-ups, microbial dysbiosis occurs, with a reduction in Dermacoccus and an increased abundance of Streptococcus and Gemella species. During flare-ups, pathogens such as S. aureus proliferate, and microbial diversity is reduced. Biofilm production by S. aureus promotes colonization and leads to pathogenesis. Commensal strains are depleted.
Skin microbiome of atopic dermatitis, Li Fang Koh, Ruo Yan Ong, John E. Common, Allergology International
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