In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance

Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation...

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Veröffentlicht in:Skin research and technology 2024-07, Vol.30 (7), p.e13811-n/a
Hauptverfasser: AbdElneam, Ahmed Ibrahim, Alhajlah, Sharif, Al‐Dhubaibi, Mohammed Saleh, Bahaj, Saleh Salem, Mohammed, Ghada Farouk, Alantry, Ahmed Kaid, Atef, Lina Mohammed
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container_issue 7
container_start_page e13811
container_title Skin research and technology
container_volume 30
creator AbdElneam, Ahmed Ibrahim
Alhajlah, Sharif
Al‐Dhubaibi, Mohammed Saleh
Bahaj, Saleh Salem
Mohammed, Ghada Farouk
Alantry, Ahmed Kaid
Atef, Lina Mohammed
description Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact. Aim The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR. Subjects and methods An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people. Results Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV. Conclusion There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.
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Aim The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR. Subjects and methods An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G &gt; A (rs1800630) and −308 G &gt; A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people. Results Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G &gt; A and −308 G &gt; A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV. Conclusion There is a correlation between AV, especially severe acne, and the −863 G &gt; A and −308 G &gt; A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.</description><identifier>ISSN: 0909-752X</identifier><identifier>ISSN: 1600-0846</identifier><identifier>EISSN: 1600-0846</identifier><identifier>DOI: 10.1111/srt.13811</identifier><identifier>PMID: 38923681</identifier><language>eng</language><publisher>England: John Wiley &amp; Sons, Inc</publisher><subject>Acne ; acne vulgaris ; Acne Vulgaris - blood ; Acne Vulgaris - genetics ; Adolescent ; Adult ; Biochemical analysis ; Blood levels ; Case-Control Studies ; Comedones ; Cross-Sectional Studies ; Fasting ; Female ; Folding ; Gene expression ; Gene polymorphism ; Genetic diversity ; Genetic Predisposition to Disease - genetics ; Genetic variance ; Glucose ; Humans ; Hyperpigmentation ; Inflammation ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Laboratory testing ; Male ; Nodules ; Original ; Polymorphism ; Polymorphism, Single Nucleotide ; Psychology ; serum TNF‐α ; Severity of Illness Index ; Skin diseases ; Skin resistance ; TNF‐α gene ; TNF‐α gene expression ; Torso ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-TNF ; Young Adult</subject><ispartof>Skin research and technology, 2024-07, Vol.30 (7), p.e13811-n/a</ispartof><rights>2024 The Author(s). published by John Wiley &amp; Sons Ltd.</rights><rights>2024 The Author(s). 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Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4041-8272752d13a299f52acf5955fa50c6d77a4446374f5759a7ff524c3019f9a07a3</cites><orcidid>0000-0001-6582-907X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11197027/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11197027/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38923681$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>AbdElneam, Ahmed Ibrahim</creatorcontrib><creatorcontrib>Alhajlah, Sharif</creatorcontrib><creatorcontrib>Al‐Dhubaibi, Mohammed Saleh</creatorcontrib><creatorcontrib>Bahaj, Saleh Salem</creatorcontrib><creatorcontrib>Mohammed, Ghada Farouk</creatorcontrib><creatorcontrib>Alantry, Ahmed Kaid</creatorcontrib><creatorcontrib>Atef, Lina Mohammed</creatorcontrib><title>In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance</title><title>Skin research and technology</title><addtitle>Skin Res Technol</addtitle><description>Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact. Aim The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR. Subjects and methods An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G &gt; A (rs1800630) and −308 G &gt; A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people. Results Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G &gt; A and −308 G &gt; A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV. Conclusion There is a correlation between AV, especially severe acne, and the −863 G &gt; A and −308 G &gt; A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.</description><subject>Acne</subject><subject>acne vulgaris</subject><subject>Acne Vulgaris - blood</subject><subject>Acne Vulgaris - genetics</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Biochemical analysis</subject><subject>Blood levels</subject><subject>Case-Control Studies</subject><subject>Comedones</subject><subject>Cross-Sectional Studies</subject><subject>Fasting</subject><subject>Female</subject><subject>Folding</subject><subject>Gene expression</subject><subject>Gene polymorphism</subject><subject>Genetic diversity</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic variance</subject><subject>Glucose</subject><subject>Humans</subject><subject>Hyperpigmentation</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Laboratory testing</subject><subject>Male</subject><subject>Nodules</subject><subject>Original</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Psychology</subject><subject>serum TNF‐α</subject><subject>Severity of Illness Index</subject><subject>Skin diseases</subject><subject>Skin resistance</subject><subject>TNF‐α gene</subject><subject>TNF‐α gene expression</subject><subject>Torso</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-TNF</subject><subject>Young Adult</subject><issn>0909-752X</issn><issn>1600-0846</issn><issn>1600-0846</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp1kdFqFDEUhoNY7Fq98AUk4I2C0yaTySS5EimtLRQFXcG7cMycWVNmk20ys7Ze-Qi-ii_Sh_BJTLu1WMHchPz58p__5BDyhLNdXtZeTuMuF5rze2TGW8Yqppv2Ppkxw0ylZP1pmzzM-ZQxJg0XD8i20KYWreYz8u040IxrTEjBBaTraVhA8vklnb89_PX9x-VPusArvYgQxkyhkC6GgG7Ejo6R-uASQi6Huy_wfJUwZx8DhdAVLE-DD7RoPo8QHD4iWz0MGR_f7Dvk4-HBfP-oOnn35nj_9UnlGtbwSteqLj10XEBtTC9rcL00UvYgmWs7paBpmlaoppdKGlB9QRonGDe9AaZA7JBXG9_V9HmJncMwJhjsKvklpAsbwdu7N8F_sYu4tuVrjWK1Kg7PbxxSPJswj3bps8NhgIBxylawEtHoVuuCPvsHPY1TCqW_QmlZm8bItlAvNpRLMeeE_W0azq7KcltGaq9HWtinf8e_Jf_MsAB7G-CrH_Di_072w_v5xvI31dSu8g</recordid><startdate>202407</startdate><enddate>202407</enddate><creator>AbdElneam, Ahmed Ibrahim</creator><creator>Alhajlah, Sharif</creator><creator>Al‐Dhubaibi, Mohammed Saleh</creator><creator>Bahaj, Saleh Salem</creator><creator>Mohammed, Ghada Farouk</creator><creator>Alantry, Ahmed Kaid</creator><creator>Atef, Lina Mohammed</creator><general>John Wiley &amp; Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><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>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6582-907X</orcidid></search><sort><creationdate>202407</creationdate><title>In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance</title><author>AbdElneam, Ahmed Ibrahim ; Alhajlah, Sharif ; Al‐Dhubaibi, Mohammed Saleh ; Bahaj, Saleh Salem ; Mohammed, Ghada Farouk ; Alantry, Ahmed Kaid ; Atef, Lina Mohammed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4041-8272752d13a299f52acf5955fa50c6d77a4446374f5759a7ff524c3019f9a07a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acne</topic><topic>acne vulgaris</topic><topic>Acne Vulgaris - blood</topic><topic>Acne Vulgaris - genetics</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Biochemical analysis</topic><topic>Blood levels</topic><topic>Case-Control Studies</topic><topic>Comedones</topic><topic>Cross-Sectional Studies</topic><topic>Fasting</topic><topic>Female</topic><topic>Folding</topic><topic>Gene expression</topic><topic>Gene polymorphism</topic><topic>Genetic diversity</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genetic variance</topic><topic>Glucose</topic><topic>Humans</topic><topic>Hyperpigmentation</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Laboratory testing</topic><topic>Male</topic><topic>Nodules</topic><topic>Original</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Psychology</topic><topic>serum TNF‐α</topic><topic>Severity of Illness Index</topic><topic>Skin diseases</topic><topic>Skin resistance</topic><topic>TNF‐α gene</topic><topic>TNF‐α gene expression</topic><topic>Torso</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor necrosis factor-TNF</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>AbdElneam, Ahmed Ibrahim</creatorcontrib><creatorcontrib>Alhajlah, Sharif</creatorcontrib><creatorcontrib>Al‐Dhubaibi, Mohammed Saleh</creatorcontrib><creatorcontrib>Bahaj, Saleh Salem</creatorcontrib><creatorcontrib>Mohammed, Ghada Farouk</creatorcontrib><creatorcontrib>Alantry, Ahmed Kaid</creatorcontrib><creatorcontrib>Atef, Lina Mohammed</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Skin research and technology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>AbdElneam, Ahmed Ibrahim</au><au>Alhajlah, Sharif</au><au>Al‐Dhubaibi, Mohammed Saleh</au><au>Bahaj, Saleh Salem</au><au>Mohammed, Ghada Farouk</au><au>Alantry, Ahmed Kaid</au><au>Atef, Lina Mohammed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance</atitle><jtitle>Skin research and technology</jtitle><addtitle>Skin Res Technol</addtitle><date>2024-07</date><risdate>2024</risdate><volume>30</volume><issue>7</issue><spage>e13811</spage><epage>n/a</epage><pages>e13811-n/a</pages><issn>0909-752X</issn><issn>1600-0846</issn><eissn>1600-0846</eissn><abstract>Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact. Aim The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR. Subjects and methods An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G &gt; A (rs1800630) and −308 G &gt; A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people. Results Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G &gt; A and −308 G &gt; A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV. Conclusion There is a correlation between AV, especially severe acne, and the −863 G &gt; A and −308 G &gt; A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.</abstract><cop>England</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>38923681</pmid><doi>10.1111/srt.13811</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6582-907X</orcidid><oa>free_for_read</oa></addata></record>
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subjects Acne
acne vulgaris
Acne Vulgaris - blood
Acne Vulgaris - genetics
Adolescent
Adult
Biochemical analysis
Blood levels
Case-Control Studies
Comedones
Cross-Sectional Studies
Fasting
Female
Folding
Gene expression
Gene polymorphism
Genetic diversity
Genetic Predisposition to Disease - genetics
Genetic variance
Glucose
Humans
Hyperpigmentation
Inflammation
Insulin
Insulin resistance
Insulin Resistance - genetics
Laboratory testing
Male
Nodules
Original
Polymorphism
Polymorphism, Single Nucleotide
Psychology
serum TNF‐α
Severity of Illness Index
Skin diseases
Skin resistance
TNF‐α gene
TNF‐α gene expression
Torso
Tumor necrosis factor
Tumor Necrosis Factor-alpha - blood
Tumor Necrosis Factor-alpha - genetics
Tumor necrosis factor-TNF
Young Adult
title In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance
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