■系统性硬化症（SSc）是一种罕见的复杂疾病，以血管损伤为特征，自身免疫,广泛的皮肤和内脏器官纤维化。半乳糖凝集素-3（Gal-3）由基因LGALS3（凝集素，半乳糖苷结合,可溶性,3;14q22.3)，据报道，它在自我宽容中起着核心作用，炎症,和纤维化。
■研究LGALS3单核苷酸多态性（SNPs）与血清Gal-3和SSc易感性及其临床特征之间的关联。
■进行了一项病例对照研究，其中有88名患者和151名匹配的对照。通过TaqMan实时聚合酶链反应（PCR）系统分析LGALS3变体，而Gal-3血清水平通过夹心酶联免疫吸附测定（ELISA）测量。基因型之间的关联，临床特征,和Gal-3水平通过统计软件包进行单变量和多变量分析。
■根据超显性模型，SSc患者的LGALS3rs4652A/C基因型比对照组更常见[OR1.89（CI95％1.01-3.52）；p=.046]。此外，LGALS3rs4652C/C多态性基因型与较低的患者Gal-3水平（p=0.03）和对照组（p=0.005）相关，如广义线性模型(GLM)所示。LGALS3rs1009977G/T对照显示出比野生型和多态基因型更高的Gal-3水平(p=.03);然而,在SSc患者中，没有发现差异。在SSc患者中，LGALS3SNP或Gal-3水平均与临床表现无关。仅考虑SSc组，GLM分析指出LGALS3rs4652和rs2075601，肺动脉高压（PAH），肌病,健康评估问卷（HAQ）和硬皮病健康评估问卷（SHAQ）是Gal-3水平的重要预测因子。
■LGALS3rs4652A/C在SSc患者中更常见，并且与较低的Gal-3水平有关。通过GLM证实了这些发现以估计Gal-3值。此外，通过模型方程，Gal-3水平可以通过HAQ预测，SHAQ,PAH,肌病,和LGALS3rs4652和rs2075601因素。在这些方面,我们建议半乳糖凝集素可能是有希望的生物标志物，以确定对SSc的易感性以及确定HAQ，SHAQ,PAH,和肌病的结果。
UNASSIGNED: Systemic sclerosis (SSc) is a rare complex disease characterized by vascular damage, autoimmunity, and extensive skin and internal organs fibrosis. Galectin-3 (Gal-3) is encoded by gene LGALS3 (Lectin, Galactoside-Binding, Soluble, 3; 14q22.3) and it has been reported to play a central role in self-tolerance, inflammation, and fibrosis.
UNASSIGNED: To investigate associations among LGALS3 single nucleotide polymorphisms (SNPs) and serum levels Gal-3 and SSc susceptibility and their clinical features.
UNASSIGNED: A
case-control study with 88 patients and 151 matched controls was performed. LGALS3 variants were analyzed by the TaqMan real-time polymerase chain reaction (PCR) system whereas Gal-3 serum levels were measured by sandwich enzyme linked immunosorbent assay (ELISA). Associations among genotypes, clinical features, and Gal-3 levels were performed by univariable and multivariable analysis through statistical packages.
UNASSIGNED: The LGALS3 rs4652 A/C genotype was more frequent in SSc patients than controls according to overdominant model [OR 1.89 (CI 95% 1.01 - 3.52); p = .046]. Also, LGALS3 rs4652 C/C polymorphic genotype was associated with lower patient Gal-3 levels (p = .03) and control group (p = 0.005), as noted by generalized linear model (GLM). The LGALS3 rs1009977 G/T controls showed higher Gal-3 levels than wild-type and polymorphic genotypes (p = .03); however, in SSc patients, no difference was found. None of the LGALS3 SNPs or Gal-3 levels was associated with clinical manifestations in SSc patients. Considering only the SSc group, GLM analysis pointed LGALS3 rs4652 and rs2075601, pulmonary arterial hypertension (PAH), myopathy, and health assessment questionnaire (HAQ) and scleroderma health assessment questionnaire (SHAQ) as important predictors for Gal-3 levels.
UNASSIGNED: The LGALS3 rs4652 A/C was more frequent in SSc patients and related to lower Gal-3 levels. These findings were corroborated through a GLM to estimate Gal-3 values. Also, by model equations, Gal-3 levels may be predicted by HAQ, SHAQ, PAH, myopathy, and LGALS3 rs4652 and rs2075601 factors. In these ways, we suggest that galectins may be promising biomarkers to identify susceptibility to SSc as well as to identify HAQ, SHAQ, PAH, and myopathy outcomes.
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