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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Published in | Skin research and technology Vol. 30; no. 7; pp. e13811 - n/a |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
John Wiley & Sons, Inc
01.07.2024
John Wiley and Sons Inc |
Subjects | |
Online Access | Get full text |
ISSN | 0909-752X 1600-0846 1600-0846 |
DOI | 10.1111/srt.13811 |
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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 > 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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AbstractList | 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. 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. 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.BACKGROUNDAcne 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.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.AIMThe 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.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.SUBJECTS AND METHODSAn 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.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.RESULTSAcne 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.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.CONCLUSIONThere 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. 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. 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. 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. 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. 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. |
Author | AbdElneam, Ahmed Ibrahim Al‐Dhubaibi, Mohammed Saleh Alantry, Ahmed Kaid Atef, Lina Mohammed Alhajlah, Sharif Bahaj, Saleh Salem Mohammed, Ghada Farouk |
AuthorAffiliation | 5 Department of Microbiology and Immunology Faculty of Medicine and Health Sciences Sana'a University Sana'a Yemen 6 Department of Dermatology, Venereology, and Sexology Faculty of Medicine Suez Canal University Ismailia Egypt 2 Molecular Genetics and Enzymology Department Human Genetics and Genome Research Institute National Research Center Dokki Cairo Egypt 3 Department of Medical Laboratories College of Applied Medical Sciences Shaqra University Shaqra Saudi Arabia 7 Basic Medical Sciences Department, Physiology unit Uniazah College of Medicine and Medical Sciences Qassim University Unaizah Saudi Arabia 1 Department of Clinical Biochemistry Department of Basic Medical Sciences College of Medicine Shaqra University Dawadmi Saudi Arabia 4 Departments of Dermatology College of Medicine Shaqra University Dawadmi Saudi Arabia |
AuthorAffiliation_xml | – name: 2 Molecular Genetics and Enzymology Department Human Genetics and Genome Research Institute National Research Center Dokki Cairo Egypt – name: 3 Department of Medical Laboratories College of Applied Medical Sciences Shaqra University Shaqra Saudi Arabia – name: 4 Departments of Dermatology College of Medicine Shaqra University Dawadmi Saudi Arabia – name: 5 Department of Microbiology and Immunology Faculty of Medicine and Health Sciences Sana'a University Sana'a Yemen – name: 6 Department of Dermatology, Venereology, and Sexology Faculty of Medicine Suez Canal University Ismailia Egypt – name: 7 Basic Medical Sciences Department, Physiology unit Uniazah College of Medicine and Medical Sciences Qassim University Unaizah Saudi Arabia – name: 1 Department of Clinical Biochemistry Department of Basic Medical Sciences College of Medicine Shaqra University Dawadmi Saudi Arabia |
Author_xml | – sequence: 1 givenname: Ahmed Ibrahim surname: AbdElneam fullname: AbdElneam, Ahmed Ibrahim organization: National Research Center – sequence: 2 givenname: Sharif surname: Alhajlah fullname: Alhajlah, Sharif organization: Shaqra University – sequence: 3 givenname: Mohammed Saleh surname: Al‐Dhubaibi fullname: Al‐Dhubaibi, Mohammed Saleh organization: Shaqra University – sequence: 4 givenname: Saleh Salem orcidid: 0000-0001-6582-907X surname: Bahaj fullname: Bahaj, Saleh Salem email: salehbahaj2025@hotmail.com organization: Sana'a University – sequence: 5 givenname: Ghada Farouk surname: Mohammed fullname: Mohammed, Ghada Farouk organization: Suez Canal University – sequence: 6 givenname: Ahmed Kaid surname: Alantry fullname: Alantry, Ahmed Kaid organization: Qassim University – sequence: 7 givenname: Lina Mohammed surname: Atef fullname: Atef, Lina Mohammed organization: Suez Canal University |
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Cites_doi | 10.1001/jamadermatol.2015.4499 10.1007/s12020‐012‐9647‐6 10.1002/jcb.26174 10.4103/0378‐6323.110765 10.1016/j.mgene.2016.06.001 10.1007/s00403‐010‐1050‐7 10.1016/j.sjbs.2021.07.042 10.1006/meth.2001.1262 10.1111/ced.12660 10.3390/biomedicines11082294 10.1186/1471‐2350‐11‐63 10.1159/000356388 10.1007/s00403‐008‐0871‐0 10.1111/j.1600‐0625.2009.00890.x 10.1111/srt.13503 10.1111/j.1468‐3083.2008.02858.x 10.1111/ijd.12426 10.1111/ced.12757 10.1016/j.jdermsci.2012.07.001 10.1016/j.jaad.2011.09.005 10.4103/ijd.ijd_396_21 10.1111/srt.13424 10.3748/wjg.14.4652 10.5114/pdia.2015.53047 10.3109/09546634.2012.751482 10.3855/jidc.10949 10.1111/srt.13333 |
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Keywords | acne vulgaris insulin resistance serum TNF‐α TNF‐α gene expression TNF‐α gene |
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References | 2009; 23 2010; 11 2023; 11 2019; 13 2021; 28 2015; 32 2015; 54 2022; 67 2008; 14 2014; 25 2008; 300 2001; 25 2011; 303 2014; 228 2023 2023; 29 2018; 119 2013; 79 2015; 40 2016; 41 2012; 68 2012; 67 2016; 9 2016; 152 2012; 42 2009; 18 2016; 151 e_1_2_12_4_1 e_1_2_12_3_1 e_1_2_12_6_1 e_1_2_12_5_1 e_1_2_12_19_1 e_1_2_12_18_1 e_1_2_12_17_1 e_1_2_12_16_1 e_1_2_12_21_1 e_1_2_12_22_1 e_1_2_12_23_1 e_1_2_12_24_1 e_1_2_12_25_1 e_1_2_12_26_1 Sutaria AH (e_1_2_12_2_1) 2023 e_1_2_12_27_1 e_1_2_12_28_1 e_1_2_12_29_1 e_1_2_12_30_1 Kartal D (e_1_2_12_20_1) 2016; 151 e_1_2_12_15_1 e_1_2_12_14_1 e_1_2_12_13_1 e_1_2_12_12_1 e_1_2_12_8_1 e_1_2_12_11_1 e_1_2_12_7_1 e_1_2_12_10_1 e_1_2_12_9_1 |
References_xml | – volume: 11 start-page: 2294 issue: 8 year: 2023 article-title: Insulin resistance in patients with acne vulgaris publication-title: Biomedicines – volume: 25 start-page: 119 issue: 2 year: 2014 end-page: 122 article-title: Insulin sensitivity, androgens and isotretinoin therapy in women with severe acne publication-title: J Dermatolog Treat – volume: 151 start-page: 353 issue: 4 year: 2016 end-page: 357 article-title: Association between isolated female acne and insulin resistance: a prospective study publication-title: G Ital Dermatol Venereol – volume: 29 issue: 11 year: 2023 article-title: Effect of interleukin‐12 gene expression on insulin resistance in patients with acne vulgaris publication-title: Skin Res Technol – volume: 79 start-page: 322 issue: 3 year: 2013 end-page: 337 article-title: Hormone therapy in acne publication-title: Indian J Dermatol Venereol Leprol – volume: 32 start-page: 281 issue: 4 year: 2015 end-page: 285 article-title: Insulin resistance in severe acne vulgaris publication-title: Postepy Dermatol Alergol – volume: 41 start-page: 297 issue: 3 year: 2016 end-page: 301 article-title: Association between tumour necrosis‐α gene polymorphisms and AV in a Pakistani population publication-title: Clin Exp Dermatol – volume: 9 start-page: 128 year: 2016 end-page: 136 article-title: Tumor necrosis factor‐α (TNF‐α)‐308G/A promoter polymorphism in colorectal cancer in ethnic Kashmiri population—a case control study in a detailed perspective publication-title: Meta Gene – volume: 300 start-page: 371 issue: 7 year: 2008 end-page: 376 article-title: Association between tumor necrosis factor‐alpha gene promoter polymorphism at position ‐308 and acne in Turkish patients publication-title: Arch Dermatol Res – volume: 14 start-page: 4652 issue: 29 year: 2008 end-page: 4661 article-title: Single nucleotide polymorphism in the tumor necrosis factor‐alpha gene affects inflammatory bowel diseases risk publication-title: World J Gastroenterol – volume: 119 start-page: 105 issue: 1 year: 2018 end-page: 110 article-title: Tumor necrosis factor‐alpha: role in development of insulin resistance and pathogenesis of type 2 diabetes mellitus publication-title: J Cell Biochem – volume: 42 start-page: 555 issue: 3 year: 2012 end-page: 560 article-title: Insulin resistance and acne: a new risk factor for men? publication-title: Endocrine – volume: 228 start-page: 152 issue: 2 year: 2014 end-page: 157 article-title: Impact of TNF haplotypes in the physical course of acne vulgaris publication-title: Dermatology – volume: 54 start-page: 662 issue: 6 year: 2015 end-page: 666 article-title: Insulin resistance in patients with post‐adolescent acne publication-title: Int J Dermatol – volume: 67 start-page: 187 issue: 2 year: 2012 end-page: 193 article-title: Acne severity grading: determining essential clinical components and features using a Delphi consensus publication-title: J Am Acad Dermatol – volume: 18 start-page: 821 issue: 10 year: 2009 end-page: 832 article-title: New developments in our understanding of acne pathogenesis and treatment publication-title: Exp Dermatol – volume: 303 start-page: 19 issue: 1 year: 2011 end-page: 27 article-title: TNFα gene polymorphisms in the pathogenesis of acne vulgaris publication-title: Arch Dermatol Res – volume: 40 start-page: 682 issue: 6 year: 2015 end-page: 687 article-title: The tumour necrosis factor‐α 308G>A genetic polymorphism may contribute to the pathogenesis of acne: a meta‐analysis publication-title: Clin Exp Dermatol – volume: 13 start-page: 419 issue: 5 year: 2019 end-page: 425 article-title: Relevance of TNF‐α, IL‐6 and IRAK1 gene expression for assessing disease severity and therapy effects in tuberculosis patients publication-title: J Infect Dev Ctries – volume: 25 start-page: 402 issue: 4 year: 2001 end-page: 408 article-title: Analysis of relative gene expression data using real‐time quantitative PCR and the 2− ΔΔCT method publication-title: methods – volume: 68 start-page: 52 issue: 1 year: 2012 end-page: 55 article-title: Tumor necrosis factor‐α ‐308 G/A and interleukin 10 ‐1082 A/G gene polymorphisms in patients with acne vulgaris publication-title: J Dermatol Sci – volume: 152 start-page: 399 issue: 4 year: 2016 end-page: 404 article-title: Insulin resistance and metabolic syndrome in young men with acne publication-title: JAMA Dermatol – volume: 29 issue: 8 year: 2023 article-title: Role of macrophage scavenger receptor 1 in the progression of dyslipidemia in acne vulgaris patients publication-title: Skin Res Technol – year: 2023 – volume: 29 year: 2023 article-title: Absence of GSTT1 and polymorphisms in GSTP1 and TP53 are associated with the incidence of acne vulgaris publication-title: Skin Res Technol – volume: 23 start-page: 331 issue: 3 year: 2009 end-page: 332 article-title: Lack of association between the promoter polymorphisms at positions ‐238 and ‐308 of the tumour necrosis factor alpha gene and AVin Polish patients publication-title: J Eur Acad Dermatol Venereol – volume: 67 start-page: 205 issue: 2 year: 2022 article-title: Insulin resistance in moderate to severe acne vulgaris publication-title: Indian J Dermatol – volume: 11 start-page: 63 year: 2010 article-title: Effect of TNF‐alpha genetic variants and CCR5 Delta 32 on the vulnerability to HIV‐1 infection and disease progression in Caucasian Spaniards publication-title: BMC Med Genet – volume: 28 start-page: 6615 issue: 11 year: 2021 end-page: 6620 article-title: Association of TNF‐α polymorphisms (‐857, ‐863 and ‐1031), TNF‐α serum level and lipid profile with acne vulgaris publication-title: Saudi J Biol Sci – ident: e_1_2_12_18_1 doi: 10.1001/jamadermatol.2015.4499 – ident: e_1_2_12_19_1 doi: 10.1007/s12020‐012‐9647‐6 – volume: 151 start-page: 353 issue: 4 year: 2016 ident: e_1_2_12_20_1 article-title: Association between isolated female acne and insulin resistance: a prospective study publication-title: G Ital Dermatol Venereol – ident: e_1_2_12_16_1 doi: 10.1002/jcb.26174 – ident: e_1_2_12_17_1 doi: 10.4103/0378‐6323.110765 – ident: e_1_2_12_8_1 doi: 10.1016/j.mgene.2016.06.001 – ident: e_1_2_12_14_1 doi: 10.1007/s00403‐010‐1050‐7 – ident: e_1_2_12_5_1 doi: 10.1016/j.sjbs.2021.07.042 – ident: e_1_2_12_10_1 doi: 10.1006/meth.2001.1262 – ident: e_1_2_12_24_1 doi: 10.1111/ced.12660 – ident: e_1_2_12_4_1 doi: 10.3390/biomedicines11082294 – ident: e_1_2_12_7_1 doi: 10.1186/1471‐2350‐11‐63 – volume-title: StatPearls [Internet] year: 2023 ident: e_1_2_12_2_1 – ident: e_1_2_12_27_1 doi: 10.1159/000356388 – ident: e_1_2_12_25_1 doi: 10.1007/s00403‐008‐0871‐0 – ident: e_1_2_12_11_1 doi: 10.1111/j.1600‐0625.2009.00890.x – ident: e_1_2_12_15_1 doi: 10.1111/srt.13503 – ident: e_1_2_12_29_1 doi: 10.1111/j.1468‐3083.2008.02858.x – ident: e_1_2_12_22_1 doi: 10.1111/ijd.12426 – ident: e_1_2_12_28_1 doi: 10.1111/ced.12757 – ident: e_1_2_12_26_1 doi: 10.1016/j.jdermsci.2012.07.001 – ident: e_1_2_12_6_1 doi: 10.1016/j.jaad.2011.09.005 – ident: e_1_2_12_3_1 doi: 10.4103/ijd.ijd_396_21 – ident: e_1_2_12_13_1 doi: 10.1111/srt.13424 – ident: e_1_2_12_30_1 doi: 10.3748/wjg.14.4652 – ident: e_1_2_12_21_1 doi: 10.5114/pdia.2015.53047 – ident: e_1_2_12_23_1 doi: 10.3109/09546634.2012.751482 – ident: e_1_2_12_9_1 doi: 10.3855/jidc.10949 – ident: e_1_2_12_12_1 doi: 10.1111/srt.13333 |
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Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules,... Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules... Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules,... |
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SubjectTerms | 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 |
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Title | In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance |
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