Atopic eczema
Samar Razaq in Difficult Cases in Primary Care, 2021
Atopic eczema is diagnosed on the basis of the presence of a typical rash associated with itching. Younger children may have the typical rash on the extensor surfaces (rather than the usual flexural surfaces) and the cheeks. A history of atopy in the child or in a first-degree relative helps aid the diagnosis. The underlying mechanisms in atopic eczema have been probed extensively. The two major causative factors are considered to be a defective skin barrier function and skin inflammation. The breakdown in the skin defensive mechanisms, through a variety of mechanisms, is thought to increase the likelihood of allergen absorption and infection with microbial colonisation. Filaggrin gene defects have recently been identified as one of the underlying mechanisms increasing the risk of developing atopic eczema and asthma via altered skin barrier function (van den Oord and Sheikh, 2009). Cutaneous inflammation is triggered and maintained by a whole host of pro-inflammatory cytokines. Various inflammatory mediators are implicated and are serving as markers for research and future targeted drug development.
The Histopathology of Eczema
Donald Rudikoff, Steven R. Cohen, Noah Scheinfeld in Atopic Dermatitis and Eczematous Disorders, 2014
Atopic eczema is usually apparent clinically based on the chronicity of the lesions and their characteristic distribution. In some instances, however, the patient may present with widespread eczema to the point of erythroderma. Biopsies are frequently performed in this setting because of the clinical concern of cutaneous T-cell lymphoma. Both cutaneous T-cell lymphoma and atopic eczema may have a similar presentation when adults are affected. In both, the dermatitis is typically of years’ duration, pruritus can be striking, and the quality of the lesions is similar, specifically scaly erythematous plaques involving truncal and other sun-protected areas. In classic atopic eczema, there may be a relative dearth of inflammatory cells. The overwhelming morphology is one dominated by epidermal changes of chronicity, including epidermal hyperplasia, hyperkeratosis, and vertically oriented superficial fibroplasias (Figs 19.9 and 19.10).
Chronic erythematous rash and lesions on trunk and limbs
Richard Ashton, Barbara Leppard in Differential Diagnosis in Dermatology, 2021
The eczema usually begins between the ages of 3 and 12 months on the scalp and face, and may or may not spread to involve the rest of the body. Asthma occurs at age 3–4 years and hay fever in the teens. When children get older the eczema may localise in the flexures, particularly the popliteal and antecubital fossae. It is very itchy so excoriations and lichenification (Fig. 8.84) may be seen. If children rub rather than scratch, the nails may become very shiny. 50% of such children will also have ichthyosis (see p. 234, also associated with a filaggrin defect) with dry skin and increased skin markings on the palms and soles. In 90% of children the eczema will clear spontaneously by puberty, but in a small minority it will persist into adult life or become active again later. A few of these will have very extensive and troublesome eczema. Less commonly, atopic eczema may develop in adult life.
Analysis of the Association of Polymorphisms rs5743708 in TLR2 and rs4986790 in TLR4 with Atopic Dermatitis Risk
Published in Immunological Investigations, 2019
Yuan Zhang, Hui-Cong Wang, Chao Feng, Min Yan
Atopic dermatitis, also known as atopic eczema, is a common, chronic, inflammatory skin disorder with atopic syndrome, infectious complications and multifaceted etiology (Ashbaugh and Kwatra 2017; Brunner et al., 2018). The pathophysiology of atopic dermatitis is driven mainly by skin barrier defects, immune response alteration, and immunoglobulin E-mediated hypersensitivity (David Boothe et al., 2017; Kaufman et al., 2018). Besides environmental factors (e.g., allergy exposure, microbiome), some genetic variants may also be associated with the susceptibility to atopic dermatitis (Bin and Leung, 2016; Li et al., 2017; Mastrorilli et al., 2017; Paternoster et al., 2011; Stemmler and Hoffjan, 2016). For instance, gene association or genome-wide association studies (GWAS) have shown that loss-of-function mutations within the Filaggrin (filaggrin) gene, the rs479844 SNP upstream of Ovo Like Transcriptional Repressor 1 gene, the rs2164983 SNP near the Actin Like 9 gene, and the rs2897442 SNP in the Kinesin Family Member 3A gene may be associated with the risk of atopic dermatitis (Bin and Leung, 2016; Paternoster et al., 2011; Stemmler and Hoffjan, 2016). The rs1893592 polymorphism of the Ubiquitin Associated And SH3 Domain Containing A gene was also reported to be associated with the susceptibility to atopic dermatitis in the Chinese Han population through a meta-analysis (Li et al., 2017).
Human mesenchymal stem cell-derived exosomes accelerate wound healing of mice eczema
Published in Journal of Dermatological Treatment, 2022
Miao Wang, Yang Zhao, Qingyi Zhang
Our results indicated that MSC-exs can inhibit the proliferation of peripheral mononuclear cells and promote their differentiation into Treg cells, suggesting that MSC-exs can regulate Th1/Th2 immune balance, inhibit local inflammatory reaction and reduce tissue damage. The exact pathogenesis of atopic eczema remains unclear. It is generally believed that based on genetic factors, allergens invade the skin, causing abnormal immune response and inflammation. Recent studies (4,25) have shown that CD4 + CD8+ T cells infiltrating in contact dermatitis can release inflammatory mediators and cause pathological reactions such as exudative edema, Tregs dysfunction and other pathological reactions. As a result, the suppressive function to Th2 cells is weakened, which leads to the hyperfunction of Th2 cells and a series of allergic reactions. Verhagen et al. (4) found that native Tregs were not detected locally in the skin lesions of patients with atopic dermatitis, and that adaptive Tregs and their cytokines and corresponding receptors were locally expressed in large quantities, suggesting that functional defects in natural regulatory Treg cells plays an important role in atopic dermatitis.
The Relationship Between Corneal Dendritic Cells, Corneal Nerve Morphology and Tear Inflammatory Mediators and Neuropeptides in Healthy Individuals
Published in Current Eye Research, 2019
Luisa H. Colorado, Maria Markoulli, Katie Edwards
One individual in this study showed an increased DC density (195 cells/mm2), a level which has previously been reported in individuals who suffer from immuno-mediated corneal inflammation such as, herpes simplex virus or adenoviral keratitis and corneal graft rejection.53 Intriguingly, this individual also had substantially increased corneal nerve branches (CNBD) and total branch points (CTBD), as compared to the mean average of the study cohort shown in Table 1. There is no known condition that increases corneal nerve density, in fact, most diseases that affect the ocular surface usually reduce corneal nerve density54 but increase corneal nerve tortuosity.55 However, epidermal nerve density is increased in inflammatory skin conditions such as atopic dermatitis.56 The cause of atopic dermatitis is unknown but believed to involve genetics and immune system dysfunction which may explain an effect of any underlying atopic condition in this particular individual. As such, we may speculate that the individual in the present study with the significantly higher DC and nerve attributes may have an unknown previous or current systemic diseases or inflammatory processes, or medication use. Upon further questioning, this healthy individual reported being a vegan from birth and exercising 5 h per week every week.
Related Knowledge Centers
- Allergic Rhinitis
- Asthma
- Contagious Disease
- Dermatitis
- Semipermeable Membrane
- Immune System
- Itch
- Skin Infection
- Genetics
- Twin