K.A. Engebretsen

The effect of environmental humidity and temperature on skin barrier function and dermatitis.

Physicians are aware that climatic conditions negatively affect the skin. In particular, people living in equator far countries such as the Northern parts of Europe and North America are exposed to harsh weather during the winter and may experience dry and itchy skin, or deterioration of already existing dermatoses. We searched the literature for studies that evaluated the mechanisms behind this phenomenon. Commonly used meteorological terms such as absolute humidity, relative humidity and dew point are explained. Furthermore, we review the negative effect of low humidity, low temperatures and different seasons on the skin barrier and on the risk of dermatitis. We conclude that low humidity and low temperatures lead to a general decrease in skin barrier function and increased susceptible towards mechanical stress. Since pro‐inflammatory cytokines and cortisol are released by keratinocytes, and the number of dermal mast cells increases, the skin also becomes more reactive towards skin irritants and allergens. Collectively, published data show that cold and dry weather increase the prevalence and risk of flares in patients with atopic dermatitis.

Skin absorption through atopic dermatitis skin : a systematic review

Patients with atopic dermatitis (AD) have skin barrier impairment in both lesional and nonlesional skin. They are typically exposed daily to emollients and intermittently to topical anti‐inflammatory medicaments, thereby increasing the risk of developing contact allergy and systemic exposure to chemical ingredients found in these topical preparations. We systematically searched for studies that investigated skin absorption of various penetrants, including medicaments, in patients with AD, but also in animals with experimentally‐induced dermatitis. We identified 40 articles: 11 human studies examining model penetrants, 26 human studies examining AD drugs, and three animal studies. We conclude that patients with AD have almost twofold increased skin absorption compared with healthy controls. There is a need for well‐designed epidemiological and dermatopharmacokinetic studies that examine to what extent AD causes patients to be systemically exposed to chemicals compared with nonatopic dermatitis.

Prevalence of atopic dermatitis in infants by domestic water hardness and season of birth: Cohort study

Background: Atopic dermatitis (AD) appears to be more common in regions with hard domestic water and in children with a fall/winter birth. However, it is unknown whether a synergistic effect exists. Objective: We sought to evaluate the association between domestic water hardness and season of birth, respectively, with onset of AD within the first 18 months of life in a large Danish birth cohort. Methods: Of children from the Danish National Birth Cohort, 52,950 were included. History of physician‐diagnosed AD and population characteristics were obtained from interviews. Birth data were obtained from the Civil Registration System, and domestic water hardness data were obtained from the Geological Survey of Denmark and Greenland. The relative prevalence (RP) of AD was calculated by using log‐linear binomial regression. Results: The prevalence of AD was 15.0% (7,942/52,950). The RP of AD was 5% (RPtrend, 1.05; 95% CI, 1.03–1.07) higher for each 5° increase in domestic water hardness (range, 6.60–35.90 German degrees of hardness [118–641 mg/L]). Although the RP of AD was higher in children with a fall (RP, 1.24; 95% CI, 1.17–1.31) or winter (RP, 1.18; 95% CI, 1.11–1.25) birth, no significant interaction was observed with domestic water hardness. The population attributable risk of hard domestic water on AD was 2%. Conclusion: We observed that early exposure to hard domestic water and a fall/winter birth was associated with an increase in the relative prevalence of AD within the first 18 months of life. Although the 2 exposures did not interact synergistically, a dose‐response relationship was observed between domestic water hardness and AD.

Current knowledge on biomarkers for contact sensitization and allergic contact dermatitis

Contact sensitization is common and affects up to 20% of the general population. The clinical manifestation of contact sensitization is allergic contact dermatitis. This is a clinical expression that is sometimes difficult to distinguish from other types of dermatitis, for example irritant and atopic dermatitis. Several studies have examined the pathogenesis and severity of allergic contact dermatitis by measuring the absence or presence of various biomarkers. In this review, we provide a non‐systematic overview of biomarkers that have been studied in allergic contact dermatitis. These include genetic variations and mutations, inflammatory mediators, alarmins, proteases, immunoproteomics, lipids, natural moisturizing factors, tight junctions, and antimicrobial peptides. We conclude that, despite the enormous amount of data, convincing specific biomarkers for allergic contact dermatitis are yet to be described.

Skin Barrier Function and Allergens

The skin is an important barrier protecting us from mechanical insults, microorganisms, chemicals and allergens, but, importantly, also reducing water loss. A common hallmark for many dermatoses is a compromised skin barrier function, and one could suspect an elevated risk of contact sensitization (CS) and allergy following increased penetration of potential allergens. However, the relationship between common dermatoses such as psoriasis, atopic dermatitis (AD) and irritant contact dermatitis (ICD) and the development of contact allergy (CA) is complex, and depends on immunologic responses and skin barrier status. Psoriasis has traditionally been regarded a Th1-dominated disease, but the discovery of Th17 cells and IL-17 provides new and interesting information regarding the pathogenesis of the disease. Research suggests an inverse relationship between psoriasis and CA, possibly due to increased levels of Th17 cells and its associated cytokines. As for AD, a positive association to CS has been established in epidemiological studies, but is still unresolved. Experimental studies show, however, an inverse relationship between AD and CS. The opposing and antagonistic influences of Th1 (CS) and Th2 (AD) have been proposed as an explanation. Finally, there is convincing evidence that exposure to irritants increases the risk of CS, and patients with ICD are, therefore, at great risk of developing CA. Skin irritation leads to the release of IL-1 and TNF-α, which affects the function of antigen-presenting cells and promotes their migration to local lymph nodes, thus increasing the probability of CS and ultimately the development of CA.

Changes in filaggrin degradation products and corneocyte surface texture by season

During the winter in northern countries, the risk of dermatitis is increased due to low temperature and humidity. Dermatitis is particularly common on weather‐exposed skin such as the cheeks and hands. Recently, increased numbers of unidentified nanosized protrusions on the corneocyte surface were associated with dermatitis and deficiency of natural moisturizing factor (NMF).

Nickel released from children's toys is deposited on the skin

Nickel allergy is common in both children and adults, and sensitized individuals may develop allergic contact dermatitis after repetitive or prolonged skin contact with metallic items releasing nickel in excessive amounts, for example jewellery, belt buckles, buttons, and work tools (1). However, the prevalence of nickel allergy has decreased significantly since the EU restricted nickel release from selected consumer products (2, 3). Although children have an overall lower prevalence of nickel allergy than adults, it is still disturbingly high (4). The reasons remain unclear, but studies have suggested that children are sensitized at an early age, and, interestingly, a recent survey found that 34.4% of 212 children’s toys purchased in Denmark and the United States with exposed metal components released nickel when screened with the dimethylglyoxime (DMG) test (5–7). Importantly, cases of allergic contact dermatitis in children resulting from toy exposure have been reported, making this a relevant source of nickel allergy and dermatitis (6–8). Here, we examined whether short skin contact with three DMG test-positive children’s toys from the recent survey resulted in nickel deposition on the skin (5).

The association between atopic dermatitis and hand eczema: a systematic review and meta‐analysis

Atopic dermatitis (AD) and hand eczema (HE) are common chronic and relapsing inflammatory skin conditions that often co‐occur.

Allergic contact dermatitis caused by an antiseptic containing cetrimide.

Antiseptic solutions are used to reduce the levels of pathogenic microorganisms on the skin prior to surgical interventions. Chlorhexidine is widely used for such purposes, as it is active against both gram-negative bacteria and yeast, but in particular against gram-positive bacteria. Chlorhexidine allergy, either immediate type I (1) or as delayed type IV allergic contact dermatitis reactions, is well known (2). Notably, in a French study evaluating patients suspected of having contact allergy to antiseptics, it was found that 18.7% of 75 patients were allergic to chlorhexidine (3). Cetrimide may be combined with chlorhexidine to enhance its action. Cetrimide, a mixture of different quaternary ammonium salts, of which the primary surfactant is cetrimonium bromide, is active against both gram-negative and gram-positive bacteria. In addition, it breaks down surface tension, permitting wetting of the surface, enabling disinfection

Xerosis is associated with asthma in men independent of atopic dermatitis and filaggrin gene mutations

Epidermal filaggrin deficiency due to common filaggrin gene (FLG) mutations causes xerosis and strongly increases the risk of atopic dermatitis and even asthma. However, it is unknown whether xerosis independent of FLG mutations could also increase the risk of asthma.