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Eczema (dermatitis)
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
Topical corticosteroids are the most useful topical agents for the treatment of atopic dermatitis. However, these drugs are only suppressive and may need to be given over long periods to maintain a reasonable quality of life. Toxic side effects include skin atrophy, striae distensae, and pituitary–adrenal axis suppression, with the possibility of adrenal collapse and masked infection. Sudden withdrawal of corticosteroids can lead to a severe ‘rebound’ aggravation of eczema, and, thus, it is prudent to use the least potent corticosteroid preparation that is effective. Acquired tolerance or tachyphylaxis is another problem associated with the use of topical corticosteroids, which makes them less effective with continued use. However, changing to another preparation of similar potency will help regain control.
Atopic Dermatitis
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Luz Fonacier, Amanda Schneider
Atopic dermatitis has a pathogenesis of complex immune dysregulation and interplay of genetic, environmental, epidermal and psychological factors. The stratum corneum of healthy skin functions as a barrier and provides water-retaining properties. It contains an extracellular lipid matrix including ceramides, cholesterol and free fatty acids (Leung 2001). When this layer becomes dry and fissured, it becomes a portal of entry for bacteria, mostly commonly Staphylococcus aureus. Disruption of the integrity of the stratum corneum exposes epidermal and dermal extracellular matrix proteins, such as fibronectin and collagen which can serve as anchors for S. aureus binding via adhesions (Cho et al. 2001). In AD, the stratum corneum lipid composition contains decreased levels of ceramides and sphingosine which normally act as water-retaining molecules. Deficient ceramide increases secretion of ceramidases, which leads to increased transepidermal water loss, resulting in dry, cracked skin of AD (Cardona et al. 2006, Arikawa et al. 2002). Sphingosine has been shown to normally possess antimicrobial properties, thus deficiencies may favor bacterial colonization (Arikawa et al. 2002).
Eczema (dermatitis)
Published in Ronald Marks, Richard Motley, Common Skin Diseases, 2019
Topical corticosteroids are the most useful topical agents for the treatment of atopic dermatitis. However, these drugs are only suppressive and may need to be given over long periods to maintain a reasonable quality of life. Toxic side effects, such as skin atrophy, the appearance of striae distensae and pituitary–adrenal axis suppression, with the possibility of adrenal collapse and masked infection, are ever-present possibilities. Sudden withdrawal of treatment with corticosteroids can lead to a sudden and severe ‘rebound’ aggravation of the eczema and it is prudent to use the least potent corticosteroid preparation that is effective. Another problem of the use of topical corticosteroids is that they may become less clinically effective with continued use. However, changing to another preparation of similar potency will regain control. This phenomenon of acquired tolerance is known as tachyphylaxis and is as yet unexplained.
Recent insights into comorbidities in atopic dermatitis
Published in Expert Review of Clinical Immunology, 2023
Caroline Gewiss, Matthias Augustin
The pathogenesis of atopic dermatitis is complex and includes genetic and immunological factors as well as a dysfunctional skin barrier [5]. In atopic dermatitis, a dysfunctional skin barrier refers to an impaired epidermal barrier caused by several aspects, such as the dysfunction of filaggrin, a structural protein of the skin, abnormal keratinocyte differentiation, tight junction, and antimicrobial barrier dysfunction [5,21]. Atopic dermatitis is one of the type 2 inflammatory diseases. Type 2 inflammation is rooted in an imbalance of the immune system [20]. Type 2 cytokines, such as interleukins (IL) IL-4, IL-5, IL-13, and IL-31 are present in excess [22]. Different inflammatory pathways (Th2 (IL-4, IL-5, IL-13, IL-31), Th22 (IL-22), Th17 (IL-17), and Th1 (IFN-γ) are involved in mediating inflammation to varying degrees depending on the endotype of atopic dermatitis [16]. The Janus kinase (JAK) signal transducer and activator of transcription (STAT) pathways are involved in modulating inflammatory pathways [16].
Increased expression of ORMDL3 in allergic asthma: a case control and in vitro study
Published in Journal of Asthma, 2023
Joanna Nowakowska, Anna Olechnowicz, Wojciech Langwiński, Oliwia Koteluk, Żaneta Lemańska, Kacper Jóźwiak, Kacper Kamiński, Wojciech Łosiewski, John Stegmayr, Darcy Wagner, Hani N. Alsafadi, Sandra Lindstedt, Maria Dziuba, Antonina Bielicka, Zuzanna Graczyk, Aleksandra Szczepankiewicz
Clinical diagnosis of atopy depended on current or past symptoms of atopic dermatitis, or allergic rhinitis. Atopic background was confirmed with increased total IgE level (higher than the upper normal limits for age) and positive skin prick test result to at least one aero-allergen (Dermatophagoides pteronyssinus, Dermatophagoides farinae, cat, dog, Alternaria alternata, Cladosporium herbarum; pollen: grass mix, rye, birch pollen, alder, hazel – Allergopharma, Germany). Any reaction with mean wheal diameter at least 3 mm greater than negative control was regarded positive. Total serum IgE level was measured by a fluoroimmunossay with Pharmacia UniCap 100 System (Pharmacia, Uppsala, Sweden) following manufacturer’s instruction. The upper limits of normal range for total IgE was age-dependent (70 kU/l for 6 yr children; 79 KU/L for 7 yr children, 89 KU/L for 8 yr children, 98 KU/L for 9 yr children, 107.0 KU/L for children of 10 years and older).
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.