目的:探讨血清血管生成素样蛋白2(ANGPT2)、血管内皮细胞特异性受体VEGF受体(VEGF receptors,VEGFR)-3、抵抗素(Resistin)水平在寻常型银屑病中的临床意义。方法:选择2017年9月—2020年6月在本院皮肤科就诊的寻常型银屑病患者60例作为...目的:探讨血清血管生成素样蛋白2(ANGPT2)、血管内皮细胞特异性受体VEGF受体(VEGF receptors,VEGFR)-3、抵抗素(Resistin)水平在寻常型银屑病中的临床意义。方法:选择2017年9月—2020年6月在本院皮肤科就诊的寻常型银屑病患者60例作为病例组,同期选择本院体检的健康人员60例作为对照组。检测所有入选者的血清ANGPT2、VEGFR-3、抵抗素水平,调查病例组的银屑病面积与严重性指数(Psoriasis area and severity index,PASI)评分并进行相关性分析。结果:病例组的ANGPT2、VEGFR-3、抵抗素含量[(4.69±0.44)ng/ml、(10.83±1.47)ng/ml、(267.02±45.10)ng/ml]均高于对照组[(1.83±0.30)ng/ml、(8.02±2.15)ng/ml、(98.27±10.47)ng/ml],病例组的PASI评分高于对照组(P<0.05)。在病例组中,Pearson分析显示PASI评分与血清ANGPT2、VEGFR-3、抵抗素含量都存在相关性(P<0.05)。Cox比例风险回归模型分析显示血清ANGPT2、VEGFR-3、抵抗素含量都为影响PASI评分的影响因素(P<0.05)。结论:血清ANGPT2、VEGFR-3、抵抗素水平在寻常型银屑病中呈现高表达状况,与患者的PASI评分存在相关性,可反映患者的病情状况。展开更多
Non-alcoholic fatty liver disease(NAFLD) has a prevalence of approximately 30% in western countries, and is emerging as the first cause of liver cirrhosis and hepatocellular carcinoma(HCC). Therefore, risk stratificat...Non-alcoholic fatty liver disease(NAFLD) has a prevalence of approximately 30% in western countries, and is emerging as the first cause of liver cirrhosis and hepatocellular carcinoma(HCC). Therefore, risk stratification emerges as fundamental in order to optimize human and economic resources, and genetics displays intrinsic characteristics suitable to fulfill this task. According to the available data, heritability estimates for hepatic fat content range from 20% to 70%, and an almost 80% of shared heritability has been found between hepatic fat content and fibrosis. The rs738409 single nucleotide polymorphism(SNP) in patatin-like phospholipase domain-containing protein 3 gene and the rs58542926 SNP in transmembrane 6 superfamily member 2 gene have been robustly associated with NAFLD and with its progression, but promising results have been obtained with many other SNPs. Moreover, there has been proof of the additive role of the different SNPs in determining liver damage, and there have been preliminary experiences in which risk scores created through a few genetic variants, alone or in combination with clinical variables, were associated with a strongly potentiated risk of NAFLD, non-alcoholic steatohepatitis(NASH), NASH fibrosis or NAFLD-HCC. However, to date, clinical translation of genetics in the field of NAFLD has been poor or absent. Fortunately, the research we have done seems to have placed us on the right path: We should rely on longitudinal rather than on cross-sectional studies; we should focus on relevant outcomes rather than on simple liver fat accumulation; and we should put together the genetic and clinical information. The hope is that combined genetic/clinical scores, derived from longitudinal studies and built on a few strong genetic variants and relevant clinical variables, will reach a significant predictive power, such as to have clinical utility for risk stratification at the single patient level and even to esteem the impact of intervention on the risk of disease-related outcomes. Well-structured future studies would demonstrate if this vision can become a reality.展开更多
文摘目的:探讨血清血管生成素样蛋白2(ANGPT2)、血管内皮细胞特异性受体VEGF受体(VEGF receptors,VEGFR)-3、抵抗素(Resistin)水平在寻常型银屑病中的临床意义。方法:选择2017年9月—2020年6月在本院皮肤科就诊的寻常型银屑病患者60例作为病例组,同期选择本院体检的健康人员60例作为对照组。检测所有入选者的血清ANGPT2、VEGFR-3、抵抗素水平,调查病例组的银屑病面积与严重性指数(Psoriasis area and severity index,PASI)评分并进行相关性分析。结果:病例组的ANGPT2、VEGFR-3、抵抗素含量[(4.69±0.44)ng/ml、(10.83±1.47)ng/ml、(267.02±45.10)ng/ml]均高于对照组[(1.83±0.30)ng/ml、(8.02±2.15)ng/ml、(98.27±10.47)ng/ml],病例组的PASI评分高于对照组(P<0.05)。在病例组中,Pearson分析显示PASI评分与血清ANGPT2、VEGFR-3、抵抗素含量都存在相关性(P<0.05)。Cox比例风险回归模型分析显示血清ANGPT2、VEGFR-3、抵抗素含量都为影响PASI评分的影响因素(P<0.05)。结论:血清ANGPT2、VEGFR-3、抵抗素水平在寻常型银屑病中呈现高表达状况,与患者的PASI评分存在相关性,可反映患者的病情状况。
文摘Non-alcoholic fatty liver disease(NAFLD) has a prevalence of approximately 30% in western countries, and is emerging as the first cause of liver cirrhosis and hepatocellular carcinoma(HCC). Therefore, risk stratification emerges as fundamental in order to optimize human and economic resources, and genetics displays intrinsic characteristics suitable to fulfill this task. According to the available data, heritability estimates for hepatic fat content range from 20% to 70%, and an almost 80% of shared heritability has been found between hepatic fat content and fibrosis. The rs738409 single nucleotide polymorphism(SNP) in patatin-like phospholipase domain-containing protein 3 gene and the rs58542926 SNP in transmembrane 6 superfamily member 2 gene have been robustly associated with NAFLD and with its progression, but promising results have been obtained with many other SNPs. Moreover, there has been proof of the additive role of the different SNPs in determining liver damage, and there have been preliminary experiences in which risk scores created through a few genetic variants, alone or in combination with clinical variables, were associated with a strongly potentiated risk of NAFLD, non-alcoholic steatohepatitis(NASH), NASH fibrosis or NAFLD-HCC. However, to date, clinical translation of genetics in the field of NAFLD has been poor or absent. Fortunately, the research we have done seems to have placed us on the right path: We should rely on longitudinal rather than on cross-sectional studies; we should focus on relevant outcomes rather than on simple liver fat accumulation; and we should put together the genetic and clinical information. The hope is that combined genetic/clinical scores, derived from longitudinal studies and built on a few strong genetic variants and relevant clinical variables, will reach a significant predictive power, such as to have clinical utility for risk stratification at the single patient level and even to esteem the impact of intervention on the risk of disease-related outcomes. Well-structured future studies would demonstrate if this vision can become a reality.
