Suggestions regarding a more appropriate understanding of atopic dermatitis

Abstract

Etymologically, and scientifically, atopic dermatitis can only be distinctively designated as the dermatologic syndrome, which heralds the atopic diathesis. Concomitantly, atopic dermatitis without atopy would be an oxymoron. Definitions based on anachronistic criteria demand updating. IgE, like eosinophilia, must be appreciated as epiphenomena of the transient Th1/Th2 cell reversal, which clearly differentiates 'atopic eczema' from all the 'other' eczemas. Failure to recognize the isomorphic feature of the eczema of atopic dermatitis denies patients with an essential therapeutic modality, namely 'Do not scratch, nor rub'. Education regarding the 'triggers' of itch would yield greater success (from recurrences), than prescribing immunomodulation.

Abnormalities in Itch Sensation and Skin Barrier Function in Atopic NC/Tnd Mice

“…[8][9][10] The control of itch sensation is difficult because the itch sensation evokes the scratching behaviors, which worsen the disease by triggering the release of pro-inflammatory cytokines, including tumor necrosis factor α (TNF-α) and interleukin-2 (IL-2), from keratinocytes, as well as itch sensation-enhancing neuropeptides such as substance P or calcitonin gene related peptide (CGRP) from C fiber. 11,12) These factors further stimulate the vascular endothelial cells or mast cells to produce chemical mediators such as histamine, consequently producing a "vicious circle" of disease exacerbation.…”

Supplementation of the fermented soy product ImmuBalance™ effectively reduces itching behavior of atopic NC/Tnd mice

“…Strong polarization to Th 2 type responses in AD patients result in the hyperproduction of IgE [7]. Moreover, barrier dysfunction of lesional skins is understood to play a crucial role in the exacerbation of clinical conditions [8].…”

Epigallocatechin-3-gallate improves Dermatophagoides pteronissinus extract-induced atopic dermatitis-like skin lesions in NC/Nga mice by suppressing macrophage migration inhibitory factor

“…The pathogenesis of AD has been known to be related with local and systemic immunologic dysfunction that leads to Th1/Th2 imbalance as well as being related to susceptibility genes and environmental factors [7][8][9][10]. It has been especially reported that there were biphasic T helper (Th) cell responses in the AD skin lesions according to local deviation, with a Th2-predominant acute phase and a Th1-predominant chronic phase.…”