PDF(Pubmed)
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.
OBJECTIVE: 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.
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.
CONCLUSIONS: 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.
OBJECTIVE: 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.
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.
CONCLUSIONS: 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.
摘要：
背景：寻常痤疮（AV）是一种影响毛囊皮脂腺单位的慢性炎症性皮肤病，通常表现为粉刺，丘疹,脓疱,或者脸上的结节，上肢,躯干,回来,粉刺形成是导致毁容性炎症的主要病理，色素沉着过度,疤痕,和心理影响。
目的：本研究的目的是探讨痤疮患者肿瘤坏死因子-α(TNF-α)基因启动子区两个遗传变异的意义及其与胰岛素抵抗(IR)的关系。了解这些变体如何促成AV及其相关IR。
方法：对87名AV患者和73名健康志愿者进行了病例对照设计和研究评估的分析性横断面研究。获得了两组的病史，以及痤疮患者炎症的严重程度和持续时间，以及人口统计数据。对两组参与者进行了生化分析，包括空腹血糖水平，空腹时的胰岛素水平，IR,和血清TNF-α。PCR-RFLP分析确定-863G>A（rs1800630）和-308G>A（rs1800629）变异，实时PCR分析评估了患者和健康人的TNF-α基因表达。
结果：痤疮患者表现出明显较高的IR水平，空腹血糖,空腹胰岛素，血清TNF-α，和TNF-α折叠变化，与健康对照相比。-863G>A和-308G>A变体的共显性模型在两组之间表现出显著差异。严重痤疮患者的A/A基因型为-308变体表现出更高水平的IR，血清TNF-α，和TNF-α折叠改变。IR，血清TNF-α，严重房室病变的TNF-α折叠改变。
结论：AV，尤其是严重的痤疮,-863G>A和-308G>A多态性，影响TNF-α基因表达和血清TNF-α水平。
目的：本研究的目的是探讨痤疮患者肿瘤坏死因子-α(TNF-α)基因启动子区两个遗传变异的意义及其与胰岛素抵抗(IR)的关系。了解这些变体如何促成AV及其相关IR。
方法：对87名AV患者和73名健康志愿者进行了病例对照设计和研究评估的分析性横断面研究。获得了两组的病史，以及痤疮患者炎症的严重程度和持续时间，以及人口统计数据。对两组参与者进行了生化分析，包括空腹血糖水平，空腹时的胰岛素水平，IR,和血清TNF-α。PCR-RFLP分析确定-863G>A（rs1800630）和-308G>A（rs1800629）变异，实时PCR分析评估了患者和健康人的TNF-α基因表达。
结果：痤疮患者表现出明显较高的IR水平，空腹血糖,空腹胰岛素，血清TNF-α，和TNF-α折叠变化，与健康对照相比。-863G>A和-308G>A变体的共显性模型在两组之间表现出显著差异。严重痤疮患者的A/A基因型为-308变体表现出更高水平的IR，血清TNF-α，和TNF-α折叠改变。IR，血清TNF-α，严重房室病变的TNF-α折叠改变。
结论：AV，尤其是严重的痤疮,-863G>A和-308G>A多态性，影响TNF-α基因表达和血清TNF-α水平。
