Impetiginized Dyshidrotic Eczema.
Ontology highlight
ABSTRACT:
SUBMITTER: Tchernev G
PROVIDER: S-EPMC5535680 | biostudies-other | 2017 Jul
REPOSITORIES: biostudies-other
Similar Datasets
Project description:BackgroundHyperkeratotic hand eczema (HHE) is a typical clinical hand eczema subtype with a largely unknown pathophysiology.ObjectiveTo investigate histopathology, expression of keratins (K), epidermal barrier proteins, and adhesion molecules in HHE.MethodsPalmar skin biopsies (lesional and perilesional) were obtained from seven HHE patients and two healthy controls. Moreover, 135 candidate genes associated with palmoplantar keratoderma were screened for mutations.ResultsImmunofluorescence staining showed a significant reduction of K9 and K14 in lesional skin. Upregulation was found for K5, K6, K16, and K17 in lesional skin compared with perilesional and healthy palmar skin. Further, upregulation of involucrin and alternating loricrin staining, both in an extracellular staining pattern, was found. Filaggrin expression was similar in lesional, perilesional, and control skin. No monogenetic mutations were found.ConclusionCurrently, the phenotype of HHE is included in the hand eczema classification system; however, it can be argued whether this is justified. The evident expression of filaggrin and involucrin in lesional skin does not support a pathogenesis of atopic eczema. The upregulation of K6, K16, and K17 and reduction of K9 and K14 might contribute to the underlying pathogenesis. Unfortunately, comparison with hand eczema studies is not possible yet, because similar protein expression studies are lacking.
| S-EPMC7496397 | biostudies-literature
Project description:Hand eczema is often a chronic, multifactorial disease. It is usually related to occupational or routine household activities. Exact etiology of the disease is difficult to determine. It may become severe enough and disabling to many of patients in course of time. An estimated 2-10% of population is likely to develop hand eczema at some point of time during life. It appears to be the most common occupational skin disease, comprising 9-35% of all occupational diseases and up to 80% or more of all occupational contact dermatitis. So, it becomes important to find the exact etiology and classification of the disease and to use the appropriate preventive and treatment measures. Despite its importance in the dermatological practice, very few Indian studies have been done till date to investigate the epidemiological trends, etiology, and treatment options for hand eczema. In this review, we tried to find the etiology, epidemiology, and available treatment modalities for chronic hand eczema patients.
| S-EPMC4037938 | biostudies-other
Project description:Background: Atopic eczema (AE) is a common chronic inflammatory skin disorder. In order to dissect the genetic background several linkage and genetic association studies have been performed. Yet very little is known about specific genes involved in this complex skin disease, and the underlying molecular mechanisms are not fully understood. Results: We used human DNA microarrays to identify a molecular picture of the programmed responses of the human genome to AE. The transcriptional program was analyzed in skin biopsy samples from lesional and patch-tested skin from AE patients sensitized to Malassezia sympodialis (M. sympodialis), and corresponding biopsies from healthy individuals. The most notable feature of the global gene-expression pattern observed in AE skin was a reciprocal expression of induced inflammatory genes and repressed lipid metabolism genes. The overall transcriptional response in M. sympodialis patch-tested AE skin was similar to the gene-expression signature identified in lesional AE skin. In the constellation of genes differentially expressed in AE skin compared to healthy control skin, we have identified several potential susceptibility genes that may play a critical role in the pathological condition of AE. Many of these genes, including genes with a role in immune responses, lipid homeostasis, and epidermal differentiation, are localized on chromosomal regions previously linked to AE. Conclusion: Through genome-wide expression profiling, we were able to discover a distinct reciprocal expression pattern of induced inflammatory genes and repressed lipid metabolism genes in skin from AE patients. We found a significant enrichment of differentially expressed genes in AE with cytobands associated to the disease, and furthermore new chromosomal regions were found that could potentially guide future region-specific linkage mapping in AE. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Disease State: Skin biopsies from normal ('normal') and lesional and patch-tested ('leisonal') skin from Atopic eczema patients sensitized to Malassezia sympodialis Organism Part: location of skin biopsy Keywords: disease state analysis
2008-12-17 | GSE12511 | GEO
Project description: Not available
| S-EPMC6517242 | biostudies-literature
Project description:ObjectivesTo explore young people's experiences of eczema self-management and interacting with health professionals.DesignSecondary qualitative data analysis of data sets from two semistructured interview studies. Data were analysed using inductive thematic analysis.SettingParticipants were recruited from the UK primary care, dermatology departments and a community-based sample (eg, patient representative groups, social media).ParticipantsData included 28 interviews with young people with eczema aged 13-25 years (mean age=19.5 years; 20 female).ResultsAlthough topical treatments were generally perceived as effective, young people expressed doubts about their long-term effectiveness, and concerns around the safety and an over-reliance on topical corticosteroids. Participants welcomed the opportunity to take an active role in their eczema management, but new roles and responsibilities also came with initial apprehension and challenges, including communicating their treatment concerns and preferences with health professionals, feeling unprepared for transition to an adult clinic and obtaining treatments. Decisions regarding whether to engage in behaviours that would exacerbate their eczema (eg, irritants/triggers, scratching) were influenced by young people's beliefs regarding negative consequences of these behaviours, and perceived control over the behaviour and its negative consequences.ConclusionsBehavioural change interventions must address the treatment concerns of young people and equip them with the knowledge, skills and confidence to take an active role in their own eczema management.
| S-EPMC7789449 | biostudies-literature
Project description:Background: Atopic eczema (AE) is a common chronic inflammatory skin disorder. In order to dissect the genetic background several linkage and genetic association studies have been performed. Yet very little is known about specific genes involved in this complex skin disease, and the underlying molecular mechanisms are not fully understood. Results: We used human DNA microarrays to identify a molecular picture of the programmed responses of the human genome to AE. The transcriptional program was analyzed in skin biopsy samples from lesional and patch-tested skin from AE patients sensitized to Malassezia sympodialis (M. sympodialis), and corresponding biopsies from healthy individuals. The most notable feature of the global gene-expression pattern observed in AE skin was a reciprocal expression of induced inflammatory genes and repressed lipid metabolism genes. The overall transcriptional response in M. sympodialis patch-tested AE skin was similar to the gene-expression signature identified in lesional AE skin. In the constellation of genes differentially expressed in AE skin compared to healthy control skin, we have identified several potential susceptibility genes that may play a critical role in the pathological condition of AE. Many of these genes, including genes with a role in immune responses, lipid homeostasis, and epidermal differentiation, are localized on chromosomal regions previously linked to AE. Conclusion: Through genome-wide expression profiling, we were able to discover a distinct reciprocal expression pattern of induced inflammatory genes and repressed lipid metabolism genes in skin from AE patients. We found a significant enrichment of differentially expressed genes in AE with cytobands associated to the disease, and furthermore new chromosomal regions were found that could potentially guide future region-specific linkage mapping in AE. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Disease State: Skin biopsies from normal ('normal') and lesional and patch-tested ('leisonal') skin from Atopic eczema patients sensitized to Malassezia sympodialis Organism Part: location of skin biopsy Keywords: disease state analysis Computed
2010-06-24 | E-GEOD-12511 | biostudies-arrayexpress
Project description: Not available
| S-EPMC6517006 | biostudies-literature
Project description: Not available
| S-EPMC1397720 | biostudies-literature
Project description:BackgroundThe "atopic march" has been considered a linear progression starting with eczema and culminating with development of asthma. Not all asthma cases, however, are preceded by eczema, and not all children with eczema go on to develop asthma.ObjectiveThe aim of this study was to explore the impact of allergic sensitization patterns on the association between early eczema and later childhood asthma. Given the numerous reported associations of the ciliary gene KIF3A with the atopic march, we also examined the impact of KIF3A risk allele rs12186803 on our analyses.MethodsWe studied 505 participants in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS), a prospective birth cohort, with longitudinal eczema and asthma outcomes as well as prospective data regarding timing of sensitization to foods and aeroallergens. KIF3A genotypes were available on all children.ResultsTwo high-risk groups were identified: one with and one without early eczema. The high-risk group with early eczema was more likely to be sensitized to food allergens, while the group without early eczema was more likely to be polysensitized to aeroallergens. The KIF3A rs12186803 risk allele interacted with food sensitization to increase asthma risk in children with eczema (P = 0.02). In children without eczema, asthma was associated with the interaction between rs12186803 and aeroallergen sensitization (P = 0.007).Conclusions & clinical relevanceKIF3A interacted differentially with sensitization pattern to increase the risk of asthma in two high-risk groups of children with and without early eczema. Given the reported role of KIF3A in epithelial cell functioning, the results add evidence to the hypothesis that an impaired epithelial barrier is a key aspect in the development of allergic disease.
| S-EPMC6546546 | biostudies-literature