Atopic dermatitis (AD) is a complex disease traditionally involving interaction of genetic, environmental, and immunologic factors. Recent studies suggest psycho-neuro-immunologic factors and emotional stress are important in its evolution. The observations that internal (bacterial infections) or external (psycho-logic) stressors may induce AD flares is explained by studies showing that stress impairs the skin barrier function and favors a shift in immunity toward a T helper type 2 cell/allergic response. Furthermore, those with AD appear to have an inherited hypothalamic deficiency that impairs normal hypothalamic-pituitary-adrenal axis function. Neuropeptides released in the skin may also mediate neurogenic inflammation, including mast cell degranulation. AD causes significant stress and impaired quality of life in patients and their family members. Psychologic and stress-reduction interventions were recently shown to improve patient well-being, and to significantly improve cutaneous manifestations.
"The disease can
also emerge in adulthood (adult-onset atopic dermatitis).6 In addition to genetic heredity (80% agreement in
monozygotic twins and 20% in heterozygotes), other factors, such as stress, can also
affect its pathogenesis.7 "
[Show abstract][Hide abstract] ABSTRACT: BACKGROUNDatopic dermatitis is directly related to psychological stress, reduced quality of
life and psychosomatic symptoms. The Psychosomatic Scale for Atopic Dermatitis is
the only questionnaire developed specifically for assessment of psychosomatization
in atopic dermatitis. OBJECTIVESthe objective of this study was to cross-culturally adapt and validate a
Brazilian-Portuguese version of the Psychosomatic Scale for Atopic Dermatitis.
METHODSadaptation consisted of independent translation and backtranslation by three
bilingual translators, followed by a pre-test. The Psychosomatic Scale for Atopic
Dermatitis and the Dermatology Life Quality Index were self-administered to 47
patients with atopic dermatitis. Disease severity was evaluated using the Eczema
Area and Severity Index. Factor analysis was used to identify the dimensions of
the Brazilian Portuguese version of the Psychosomatic Scale for Atopic Dermatitis.
Internal consistency and convergence validity were also analyzed. Reproducibility
was assessed using the Kappa coefficient. RESULTSfactor analysis revealed a two-dimensional structure: stress/laziness/insecurity
(I) and maladjustment/social relationships (II), explaining 54.4% of total
variance. All dimensions revealed excellent internal consistency. External
construct validity was confirmed by positive correlations between the
Psychosomatic Scale for Atopic Dermatitis and the Dermatology Life Quality Index.
Test-retest reliability was excellent, with k>0.7 for all questions. CONCLUSIONSthe Brazilian Portuguese version of the Psychosomatic Scale for Atopic Dermatitis
demonstrated acceptable psychometric properties and can be used for the evaluation
of psychosomatic symptoms in patients with atopic dermatitis and as a tool in
clinical and epidemiological research.
"Oh et al.  examined atopic dermatitis patients and concluded that anxiety was associated with the induction of pruritus in atopic dermatitis. Recent studies suggest that emotional stress is an important factor in the development of atopic dermatitis . "
[Show abstract][Hide abstract] ABSTRACT: Stress is considered a causal factor in many diseases, allergic disease being one of them. The prevalence of allergic disease is increasing in Korea, but the relationship between allergic symptoms and stress is not empirically well known. We aimed to evaluate the relationship between allergy-related symptoms and stress in children and adolescents.
We investigated 698 children and adolescents living in Gwangyang Bay, Korea, using a multi-stage cluster sampling method. Using the International Study of Asthma and Allergies in Childhood and the Psychosocial Well-being Index, these subjects were surveyed on allergy-related symptoms and psychosocial stressors in their lives, respectively. We used a multivariate logistic analysis for odds ratios for the complaint rate of allergic symptoms, after adjusting for age, gender, household income, body mass index, and residence.
After adjustments, lifetime rhinitis (odds ratio [OR], 1.024), rhinoconjunctivitis (OR, 1.090), diagnosis of itchy eczema (OR, 1.040), treatment of itchy eczema (OR, 1.049), 12-month allergic conjunctivitis (OR, 1.026), diagnosis of allergic conjunctivitis (OR, 1.031), and treatment of allergic conjunctivitis (OR, 1.034) were found to be significantly associated with stress.
Our results support the notion that there is a relationship between stress and allergic symptoms in children and adolescents. Further research into any causal relationship between stress and allergies, as well as preventative public health plans for decreasing stress in children and adolescents are needed.
"The possible role of nerve-derived substances such as subtance P and adenosine triphosphate in enhancement of cutaneous inflammation during stress has been explored experimentally (Pavlovic et al., 2008; Amano et al., 2008; Seiffert et al., 2006). Interestingly, a possible role for stress reduction and avoidance behavior in ameliorating inflammatory skin disorders such as atopic dermatitis and psoriasis has been suggested (Farber and Nall, 1993; Arndt et al., 2008). These findings may suggest a mechanism by which CGRP may play a role in stress modulation of skin inflammation. "
[Show abstract][Hide abstract] ABSTRACT: This study examined whether the sensory neuropeptide calcitonin gene-related peptide (CGRP) inhibits release of chemokines by dermal microvascular endothelial cells. Dermal blood vessels are associated with nerves containing CGRP, suggesting that CGRP-containing nerves may regulate cutaneous inflammation through effects on vessels. We examined CGRP effects on stimulated chemokine production by a human dermal microvascular endothelial cell line (HMEC-1) and primary human dermal microvascular endothelial cells (pHDMECs). HMEC-1 cells and pHDMECs expressed mRNA for components of the CGRP and adrenomedullin receptors and CGRP inhibited LPS-induced production of the chemokines CXCL8, CCL2, and CXCL1 by both HMEC-1 cells and pHDMECs. The receptor activity-modifying protein (RAMP)1/calcitonin receptor-like receptor (CL)-specific antagonists CGRP₈-₃₇ and BIBN4096BS, blocked this effect of CGRP in a dose-dependent manner. CGRP prevented LPS-induced IκBα degradation and NF-κB binding to the promoters of CXCL1, CXCL8 and CCL2 in HMEC-1 cells and Bay 11-7085, an inhibitor of NF-κB activation, suppressed LPS-induced production of CXCL1, CXCL8 and CCL2. Thus, the NF-κB pathway appears to be involved in CGRP-mediated suppression of chemokine production. Accordingly, CGRP treatment of LPS-stimulated HMEC-1 cells inhibited their ability to chemoattract human neutrophils and mononuclear cells. Elucidation of this pathway may suggest new avenues for therapeutic manipulation of cutaneous inflammation.
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