Prevalence and Risk Factors for Xerosis in the Elderly: A Cross-Sectional Epidemiological Study in Primary Care

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Abstract

Background: Limited information is available concerning the prevalence and risk factors of xerosis in the elderly. Objective: To establish the prevalence of xerosis and associated factors in elderly patients. Methods: A national, multicenter, observational, cross-sectional study in patients aged 65 or older was performed. The data collected by general practitioners were demographics and medical history, including history of atopic disease. Xerosis was evaluated using the Overall Dry Skin score. Results: 756 patients were included. The prevalence of xerosis was 55.6%. Xerosis was significantly associated with older age (OR: 1.48, 95% CI: 1.16–1.89), female sex (OR: 1.80, 95 CI%: 1.29–2.53), treatments that can potentially cause xerosis (OR: 2.21, 95 CI%: 1.54–3.17), itching during sweating (OR: 7.11, 95% CI: 3.90–12.95), a history of dry skin (OR: 2.89, 95% CI: 1.65–5.08) and a history of atopic dermatitis (OR: 3.60, 95% CI: 1.99–6.52). Conclusion: Xerosis is highly prevalent in the elderly. A history of atopy, especially atopic dermatitis, is associated with an increased risk of xerosis in the elderly.

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Most cited references 21

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Epidermal barrier dysfunction in atopic dermatitis.

Michael Cork, Simon G Danby, Yiannis Vasilopoulos … (2009)

Atopic dermatitis (AD) is a multifactorial, heterogenous disease that arises as a result of the interaction between both environmental and genetic factors. Changes in at least three groups of genes encoding structural proteins, epidermal proteases, and protease inhibitors predispose to a defective epidermal barrier and increase the risk of developing AD. Loss-of-function mutations found within the FLG gene encoding the structural protein, filaggrin, represent the most significant genetic factor predisposing to AD identified to date. Enhanced protease activity and decreased synthesis of the lipid lamellae lead to exacerbated breakdown of the epidermal barrier. Environmental factors, including the use of soap and detergents, exacerbate epidermal barrier breakdown, attributed to the elevation of stratum corneum pH. A sustained increase in pH enhances the activity of degradatory proteases and decreases the activity of the lipid synthesis enzymes. The strong association between both genetic barrier defects and environmental insults to the barrier with AD suggests that epidermal barrier dysfunction is a primary event in the development of this disease. Our understanding of gene-environment interactions should lead to a better use of some topical products, avoidance of others, and the increased use and development of products that can repair the skin barrier.

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The skin barrier as an innate immune element.

Waldir P. Elias (2007)

Since life in a terrestrial environment threatens mammals continuously with desiccation, the structural, cellular, biochemical, and regulatory mechanisms that sustain permeability barrier homeostasis have justifiably comprised a major thrust of prior and recent research on epidermal barrier function. Yet, the epidermis mediates a broad set of protective 'barrier' functions that includes defense against pathogen challenges. Permeability and antimicrobial function are both co-regulated and interdependent, overlapping through the dual activities of their lipid/protein constituents. Most of the defensive (barrier) functions of the epidermis localize to the stratum corneum (SC), which limits pathogen colonization through its low water content, acidic pH, resident (normal) microflora, and surface-deposited antimicrobial lipids (1 degree free fatty acid). These various barrier functions are largely mediated by either the corneocyte or the extracellular matrix, and it is both the localization and the organization of secreted hydrophobic lipids into characteristic lamellar bilayers that is critical not only for permeability barrier function, but also for antimicrobial function through its contribution to the maintenance of SC integrity. Low constitutive levels of antimicrobial peptides under basal conditions emphasize the key role of epithelial structure in antimicrobial defense. But antimicrobial peptide synthesis and delivery to the SC interstices accelerates after external insults to the barrier.

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Gene polymorphism in Netherton and common atopic disease.

Andrew Walley, Stéphane Chavanas, Miriam Moffatt … (2001)

Atopic dermatitis (AD) and asthma are characterized by IgE-mediated atopic (allergic) responses to common proteins (allergens), many of which are proteinases. Loci influencing atopy have been localized to a number of chromosomal regions, including the chromosome 5q31 cytokine cluster. Netherton disease is a rare recessive skin disorder in which atopy is a universal accompaniment. The gene underlying Netherton disease (SPINK5) encodes a 15-domain serine proteinase inhibitor (LEKTI) which is expressed in epithelial and mucosal surfaces and in the thymus. We have identified six coding polymorphisms in SPINK5 (Table 1) and found that a Glu420-->Lys variant shows significant association with atopy and AD in two independent panels of families. Our results implicate a previously unrecognized pathway for the development of common allergic illnesses.

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Author and article information

Journal

Journal ID (publisher-id): DRM

Journal ID (nlm-ta): Dermatology

Journal ID (doi): 10.1159/issn.1018-8665

Title: Dermatology

Publisher: S. Karger AG

ISSN (Print): 1018-8665

ISSN (Electronic): 1421-9832

Publication date Subscription-year: 2011

Publication date (Print): December 2011

Publication date (Electronic): 22 November 2011

Volume: 223

Issue: 3

Pages: 260-265

Affiliations

^aPaul Sabatier University and Department of Dermatology, Hôpital Larrey, Toulouse, ^bEpidemiology and Biostatistics, ClinSearch, Bagneux, ^cLaboratoires Pierre Fabre Santé, Castres, and ^dCERPER et Laboratoires Pierre Fabre, Toulouse, France

Author notes

*Carle Paul, MD, PhD, Université Paul Sabatier, Département de Dermatologie, Hôpital Larrey, 24 Chemin de Pouvourville, FR–31059 Toulouse Cedex 9 (France), Tel. +33 5 6777 8140, E-Mail paul.c@chu-toulouse.fr

Article

Publisher ID: 334631 Other ID: Dermatology 2011;223:260–265

DOI: 10.1159/000334631

PubMed ID: 22104182

SO-VID: 24f6e591-2f1e-4646-ae68-e4ab1ebe5937

License:

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 24 June 2011

Date accepted : 20 October 2011

Page count

Figures: 2, Tables: 3, Pages: 6

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