Psoriasis
Psoriasis is a common, chronic papulosquamous skin disease occurring worldwide, presenting at any age, and leading to a substantial burden for individuals and society. It is associated with several important medical conditions, including depression, psoriatic arthritis, and cardiometabolic syndrome....
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Veröffentlicht in: | The Lancet (British edition) 2021-04, Vol.397 (10281), p.1301-1315 |
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description | Psoriasis is a common, chronic papulosquamous skin disease occurring worldwide, presenting at any age, and leading to a substantial burden for individuals and society. It is associated with several important medical conditions, including depression, psoriatic arthritis, and cardiometabolic syndrome. Its most common form, chronic plaque or psoriasis vulgaris, is a consequence of genetic susceptibility, particularly in the presence of the HLA-C*06:02 risk allele, and of environmental triggers such as streptococcal infection, stress, smoking, obesity, and alcohol consumption. There are several phenotypes and research has separated pustular from chronic plaque forms. Immunological and genetic studies have identified IL-17 and IL-23 as key drivers of psoriasis pathogenesis. Immune targeting of these cytokines and of TNFα by biological therapies has revolutionised the care of severe chronic plaque disease. Psoriasis cannot currently be cured, but management should aim to minimise physical and psychological harm by treating patients early in the disease process, identifying and preventing associated multimorbidity, instilling lifestyle modifications, and employing a personalised approach to treatment. |
doi_str_mv | 10.1016/S0140-6736(20)32549-6 |
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It is associated with several important medical conditions, including depression, psoriatic arthritis, and cardiometabolic syndrome. Its most common form, chronic plaque or psoriasis vulgaris, is a consequence of genetic susceptibility, particularly in the presence of the HLA-C*06:02 risk allele, and of environmental triggers such as streptococcal infection, stress, smoking, obesity, and alcohol consumption. There are several phenotypes and research has separated pustular from chronic plaque forms. Immunological and genetic studies have identified IL-17 and IL-23 as key drivers of psoriasis pathogenesis. Immune targeting of these cytokines and of TNFα by biological therapies has revolutionised the care of severe chronic plaque disease. Psoriasis cannot currently be cured, but management should aim to minimise physical and psychological harm by treating patients early in the disease process, identifying and preventing associated multimorbidity, instilling lifestyle modifications, and employing a personalised approach to treatment.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>DOI: 10.1016/S0140-6736(20)32549-6</identifier><identifier>PMID: 33812489</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Age ; Arthritis ; Cytokines ; Depression, Mental ; Dermatitis ; Disease ; Disease susceptibility ; Erythema ; Genetic Predisposition to Disease ; Histocompatibility antigen HLA ; Histocompatibility antigens ; HLA histocompatibility antigens ; Humans ; Immunology ; Interleukin 17 ; Interleukin 23 ; Lymphoma ; Medical colleges ; Medical research ; Medicine, Experimental ; Morphology ; Pathogenesis ; Phenotype ; Phenotypes ; Pruritus ; Psoriasis ; Psoriasis - drug therapy ; Psoriasis - genetics ; Psoriasis - immunology ; Psoriasis - physiopathology ; Psoriasis vulgaris ; Psoriatic arthritis ; Risk Factors ; Skin ; Skin diseases ; Tonsillitis ; Tumor necrosis factor-α ; Womens health</subject><ispartof>The Lancet (British edition), 2021-04, Vol.397 (10281), p.1301-1315</ispartof><rights>2021 Elsevier Ltd</rights><rights>Copyright © 2021 Elsevier Ltd. All rights reserved.</rights><rights>2021. Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-8ec2d79efee92261f06403c4c7e874d4e23f2f72b49c69e6629f9530de7c223c3</citedby><cites>FETCH-LOGICAL-c476t-8ec2d79efee92261f06403c4c7e874d4e23f2f72b49c69e6629f9530de7c223c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2507944516?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33812489$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Griffiths, Christopher E M</creatorcontrib><creatorcontrib>Armstrong, April W</creatorcontrib><creatorcontrib>Gudjonsson, Johann E</creatorcontrib><creatorcontrib>Barker, Jonathan N W N</creatorcontrib><title>Psoriasis</title><title>The Lancet (British edition)</title><addtitle>Lancet</addtitle><description>Psoriasis is a common, chronic papulosquamous skin disease occurring worldwide, presenting at any age, and leading to a substantial burden for individuals and society. It is associated with several important medical conditions, including depression, psoriatic arthritis, and cardiometabolic syndrome. Its most common form, chronic plaque or psoriasis vulgaris, is a consequence of genetic susceptibility, particularly in the presence of the HLA-C*06:02 risk allele, and of environmental triggers such as streptococcal infection, stress, smoking, obesity, and alcohol consumption. There are several phenotypes and research has separated pustular from chronic plaque forms. Immunological and genetic studies have identified IL-17 and IL-23 as key drivers of psoriasis pathogenesis. Immune targeting of these cytokines and of TNFα by biological therapies has revolutionised the care of severe chronic plaque disease. Psoriasis cannot currently be cured, but management should aim to minimise physical and psychological harm by treating patients early in the disease process, identifying and preventing associated multimorbidity, instilling lifestyle modifications, and employing a personalised approach to treatment.</description><subject>Age</subject><subject>Arthritis</subject><subject>Cytokines</subject><subject>Depression, Mental</subject><subject>Dermatitis</subject><subject>Disease</subject><subject>Disease susceptibility</subject><subject>Erythema</subject><subject>Genetic Predisposition to Disease</subject><subject>Histocompatibility antigen HLA</subject><subject>Histocompatibility antigens</subject><subject>HLA histocompatibility antigens</subject><subject>Humans</subject><subject>Immunology</subject><subject>Interleukin 17</subject><subject>Interleukin 23</subject><subject>Lymphoma</subject><subject>Medical colleges</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Morphology</subject><subject>Pathogenesis</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Pruritus</subject><subject>Psoriasis</subject><subject>Psoriasis - drug therapy</subject><subject>Psoriasis - genetics</subject><subject>Psoriasis - immunology</subject><subject>Psoriasis - physiopathology</subject><subject>Psoriasis vulgaris</subject><subject>Psoriatic arthritis</subject><subject>Risk Factors</subject><subject>Skin</subject><subject>Skin diseases</subject><subject>Tonsillitis</subject><subject>Tumor necrosis factor-α</subject><subject>Womens health</subject><issn>0140-6736</issn><issn>1474-547X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkMtKw0AUhgdRbKw-gm4EqYvo3CezklK8QUFBBXdDOjkpU3KpM4no25s0tQs3ns3ZfOc_Px9CpwRfEUzk9QsmHMdSMTmh-JJRwXUs91BEuOKx4Op9H0U7ZISOQlhhjLnE4hCNGEsI5YmOUPQcau_S4MIxOsjTIsDJdo_R293t6-whnj_dP86m89hyJZs4AUszpSEH0JRKkmPJMbPcKkgUzzhQltNc0QXXVmqQkupcC4YzUJZSZtkYTYbcta8_WgiNKV2wUBRpBXUbDBU46aar16Hnf9BV3fqqa9dTSnMuiOyoi4FapgUYV9m6auCrWaZtCMZMpVCEMZr0cWIAra9D8JCbtXdl6r8NwaaXajZSTW_MUGw2Uk3_4Gxbo12UkO2ufi12wM0AQOft04E3wTqoLGTOg21MVrt_XvwAv8qB7A</recordid><startdate>20210403</startdate><enddate>20210403</enddate><creator>Griffiths, Christopher E M</creator><creator>Armstrong, April W</creator><creator>Gudjonsson, Johann E</creator><creator>Barker, Jonathan N W N</creator><general>Elsevier Ltd</general><general>Elsevier B.V</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0TT</scope><scope>0TZ</scope><scope>0U~</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88C</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8C2</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K6X</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>KB~</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20210403</creationdate><title>Psoriasis</title><author>Griffiths, Christopher E M ; Armstrong, April W ; Gudjonsson, Johann E ; Barker, Jonathan N W N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-8ec2d79efee92261f06403c4c7e874d4e23f2f72b49c69e6629f9530de7c223c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Age</topic><topic>Arthritis</topic><topic>Cytokines</topic><topic>Depression, Mental</topic><topic>Dermatitis</topic><topic>Disease</topic><topic>Disease susceptibility</topic><topic>Erythema</topic><topic>Genetic Predisposition to Disease</topic><topic>Histocompatibility antigen HLA</topic><topic>Histocompatibility antigens</topic><topic>HLA histocompatibility antigens</topic><topic>Humans</topic><topic>Immunology</topic><topic>Interleukin 17</topic><topic>Interleukin 23</topic><topic>Lymphoma</topic><topic>Medical colleges</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Morphology</topic><topic>Pathogenesis</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>Pruritus</topic><topic>Psoriasis</topic><topic>Psoriasis - drug therapy</topic><topic>Psoriasis - genetics</topic><topic>Psoriasis - immunology</topic><topic>Psoriasis - physiopathology</topic><topic>Psoriasis vulgaris</topic><topic>Psoriatic arthritis</topic><topic>Risk Factors</topic><topic>Skin</topic><topic>Skin diseases</topic><topic>Tonsillitis</topic><topic>Tumor necrosis factor-α</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Griffiths, Christopher E M</creatorcontrib><creatorcontrib>Armstrong, April W</creatorcontrib><creatorcontrib>Gudjonsson, Johann E</creatorcontrib><creatorcontrib>Barker, Jonathan N W N</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>News PRO</collection><collection>Pharma and Biotech Premium PRO</collection><collection>Global News & ABI/Inform Professional</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Healthcare Administration Database (Alumni)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Lancet Titles</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>British Nursing Index</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>British Nursing Index (BNI) (1985 to Present)</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>British Nursing Index</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Newsstand Professional</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>The Lancet (British edition)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Griffiths, Christopher E M</au><au>Armstrong, April W</au><au>Gudjonsson, Johann E</au><au>Barker, Jonathan N W N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Psoriasis</atitle><jtitle>The Lancet (British edition)</jtitle><addtitle>Lancet</addtitle><date>2021-04-03</date><risdate>2021</risdate><volume>397</volume><issue>10281</issue><spage>1301</spage><epage>1315</epage><pages>1301-1315</pages><issn>0140-6736</issn><eissn>1474-547X</eissn><abstract>Psoriasis is a common, chronic papulosquamous skin disease occurring worldwide, presenting at any age, and leading to a substantial burden for individuals and society. It is associated with several important medical conditions, including depression, psoriatic arthritis, and cardiometabolic syndrome. Its most common form, chronic plaque or psoriasis vulgaris, is a consequence of genetic susceptibility, particularly in the presence of the HLA-C*06:02 risk allele, and of environmental triggers such as streptococcal infection, stress, smoking, obesity, and alcohol consumption. There are several phenotypes and research has separated pustular from chronic plaque forms. Immunological and genetic studies have identified IL-17 and IL-23 as key drivers of psoriasis pathogenesis. Immune targeting of these cytokines and of TNFα by biological therapies has revolutionised the care of severe chronic plaque disease. Psoriasis cannot currently be cured, but management should aim to minimise physical and psychological harm by treating patients early in the disease process, identifying and preventing associated multimorbidity, instilling lifestyle modifications, and employing a personalised approach to treatment.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>33812489</pmid><doi>10.1016/S0140-6736(20)32549-6</doi><tpages>15</tpages></addata></record> |
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subjects | Age Arthritis Cytokines Depression, Mental Dermatitis Disease Disease susceptibility Erythema Genetic Predisposition to Disease Histocompatibility antigen HLA Histocompatibility antigens HLA histocompatibility antigens Humans Immunology Interleukin 17 Interleukin 23 Lymphoma Medical colleges Medical research Medicine, Experimental Morphology Pathogenesis Phenotype Phenotypes Pruritus Psoriasis Psoriasis - drug therapy Psoriasis - genetics Psoriasis - immunology Psoriasis - physiopathology Psoriasis vulgaris Psoriatic arthritis Risk Factors Skin Skin diseases Tonsillitis Tumor necrosis factor-α Womens health |
title | Psoriasis |
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