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系统性硬化症患者中黑人和白人之间的种族差异。

Racial differences between blacks and whites with systemic sclerosis.

机构信息

Division of Rheumatology and Immunology, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

出版信息

Curr Opin Rheumatol. 2012 Nov;24(6):642-8. doi: 10.1097/BOR.0b013e328356d9dc.

DOI:10.1097/BOR.0b013e328356d9dc
PMID:22955018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3756312/
Abstract

PURPOSE OF REVIEW

Racial disparities appear to exist in the susceptibility and severity of systemic sclerosis (SSc, scleroderma) and are responsible for a greater health burden in blacks as compared with whites. Disparities in socioeconomic status and access to healthcare do not sufficiently explain the observed differences in prevalence and mortality. It is important to determine whether there might be a biologic basis for the racial disparities observed in SSc.

RECENT FINDINGS

We present data to suggest that the increased susceptibility and severity of SSc in blacks may result in part from an imbalance of profibrotic and antifibrotic factors. Racial differences in the expression of transforming growth factor-β1 (TGF-β1) and caveolin-1, as well as differences in the expression of hepatocyte growth factor and PPAR-γ, have been demonstrated in blacks with SSc, as well as in normal black individuals. A genetic predisposition to fibrosis may account for much of the racial disparities between black and white patients with SSc.

SUMMARY

A better understanding of the biologic basis for the racial disparities observed in SSc may lead to improved therapies, along with the recognition that different therapies may need to be adapted for different groups of patients.

摘要

综述目的

系统性硬化症(SSc,硬皮病)的易感性和严重程度似乎存在种族差异,与白人相比,黑种人患病的负担更重。社会经济地位和获得医疗保健方面的差异并不能充分解释观察到的患病率和死亡率的差异。重要的是要确定在 SSc 中观察到的种族差异是否可能存在生物学基础。

最近的发现

我们提供的数据表明,黑人 SSc 的易感性和严重程度增加可能部分是由于促纤维化和抗纤维化因子的失衡所致。黑人 SSc 患者以及正常黑人个体中,转化生长因子-β1(TGF-β1)和窖蛋白-1的表达存在差异,以及肝细胞生长因子和 PPAR-γ的表达存在差异。纤维化的遗传易感性可能是 SSc 黑人和白人患者之间种族差异的主要原因。

总结

更好地了解 SSc 中观察到的种族差异的生物学基础可能会导致改善治疗方法,同时认识到不同的治疗方法可能需要针对不同的患者群体进行调整。

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本文引用的文献

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A clinical and serologic comparison of African American and Caucasian patients with systemic sclerosis.非裔美国人和白人系统性硬化症患者的临床及血清学比较
Arthritis Rheum. 2012 Sep;64(9):2986-94. doi: 10.1002/art.34482.
2
The PPARγ Agonist Rosiglitazone Is Antifibrotic for Scleroderma Lung Fibroblasts: Mechanisms of Action and Differential Racial Effects.过氧化物酶体增殖物激活受体γ激动剂罗格列酮对硬皮病肺成纤维细胞具有抗纤维化作用:作用机制及种族差异效应
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Localized expression of tenascin in systemic sclerosis-associated pulmonary fibrosis and its regulation by insulin-like growth factor binding protein 3.肌腱蛋白在系统性硬化症相关肺纤维化中的局部表达及其受胰岛素样生长因子结合蛋白3的调控
Arthritis Rheum. 2012 Jan;64(1):272-80. doi: 10.1002/art.30647.
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Altered monocyte and fibrocyte phenotype and function in scleroderma interstitial lung disease: reversal by caveolin-1 scaffolding domain peptide.硬皮病间质性肺病中单核细胞和成纤维细胞表型及功能的改变:小窝蛋白-1支架结构域肽的逆转作用
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Association of hepatocyte growth factor promoter polymorphism with severity of interstitial lung disease in Japanese patients with systemic sclerosis.肝细胞生长因子启动子多态性与日本系统性硬化症患者间质性肺疾病严重程度的关联
Arthritis Rheum. 2011 Aug;63(8):2465-72. doi: 10.1002/art.30415.
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PPARγ downregulation by TGFß in fibroblast and impaired expression and function in systemic sclerosis: a novel mechanism for progressive fibrogenesis.TGFβ下调成纤维细胞中的 PPARγ及其在系统性硬化症中的表达和功能障碍:进行性纤维化的新机制。
PLoS One. 2010 Nov 2;5(11):e13778. doi: 10.1371/journal.pone.0013778.
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Fibrosis in systemic sclerosis: emerging concepts and implications for targeted therapy.系统性硬皮病中的纤维化:新出现的概念及其对靶向治疗的影响。
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The skin of patients with systemic sclerosis softened during the treatment with anti-IL-6 receptor antibody tocilizumab.系统性硬皮病患者在接受抗白细胞介素-6 受体抗体托珠单抗治疗后皮肤变软。
Rheumatology (Oxford). 2010 Dec;49(12):2408-12. doi: 10.1093/rheumatology/keq275. Epub 2010 Sep 5.
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Does over-expression of transforming growth factor-beta account for the increased morbidity in African-Americans?: possible clinical study and therapeutic implications.转化生长因子-β的过度表达是否解释了非裔美国人发病率增加的原因?:可能的临床研究和治疗意义。
Med Hypotheses. 2010 Nov;75(5):418-21. doi: 10.1016/j.mehy.2010.04.009. Epub 2010 May 8.
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