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摘要 目的:探讨血清血管内皮生长因子-A(VEGF-A)、可溶性人类白细胞抗原-G(sHLA-G)、多配体蛋白多糖-1(Syndecan-1)水平与子宫内膜异位症(EMS)患者疾病分期和痛经程度的相关性及其联合检测的诊断价值。方法:选取2018年1月~2021年12月我院收治的120例EMS患者作为观察组,另取同期女性健康体检者120例作为对照组。检测并比较两组血清VEGF-A、sHLA-G、Syndecan-1水平。此外,分别对比不同疾病分期、不同痛经程度EMS患者上述三项指标水平的差异。采用Spearman相关系数分析血清VEGF-A、sHLA-G、Syndecan-1水平与疾病分期、痛经程度的相关性。以受试者工作特征(ROC)曲线分析上述三项指标联合检测对EMS的诊断效能。结果:观察组血清VEGF-A、sHLA-G、Syndecan-1水平均高于对照组(P<0.05)。R-AFS分期为Ⅲ~Ⅳ期的EMS患者其血清VEGF-A、sHLA-G、Syndecan-1水平均高于Ⅰ~Ⅱ期患者(P<0.05)。痛经程度为中度和重度的EMS患者其血清VEGF-A、sHLA-G、Syndecan-1水平均高于轻度痛经患者,且重度痛经患者上述指标水平均高于中度痛经患者(P<0.05)。Spearman相关性分析结果显示:EMS患者的血清VEGF-A、sHLA-G、Syndecan-1水平与疾病分期、痛经程度均呈正相关(P<0.05)。ROC曲线分析结果显示:血清VEGF-A、sHLA-G、Syndecan-1联合检测诊断EMS的曲线下面积为0.894,明显高于三指标单独检测。结论:EMS患者血清VEGF-A、sHLA-G、Syndecan-1均存在异常高表达,且和疾病分期以及痛经程度有关,可能有助于临床EMS诊断及病情评估。  相似文献   
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There is substantial evidence that abnormal concentrations of oxidised tryptophan metabolites, produced via the kynurenine pathway, contribute to progressive neurodegeneration in Huntington's disease. We have now examined the blood levels of these metabolites in patients at different stages of Huntington's disease, assessed both in terms of clinical disease severity and numbers of CAG repeats. Close relatives of the patients were included in the study as well as unrelated healthy controls. Levels of lipid peroxidation products, the pro-inflammatory cytokine interleukin (IL)-23 and the soluble human leucocyte antigen-G (sHLA-G) were also measured. There were lower levels of tryptophan and a higher kynurenine : tryptophan ratio, indicating activation of indoleamine-2,3-dioxygenase, in the most severely affected group of patients, with increased levels of IL-23 and sHLA-G. Marked correlations were noted between IL-23 and the patient severity group, anthranilic acid levels and the number of CAG repeats, and between anthranilic acid and IL-23, supporting our previous evidence of a relationship between anthranilic acid and inflammatory status. Tryptophan was negatively correlated with symptom severity and number of CAG repeats, and positively correlated with sHLA-G. The results support the proposal that tryptophan metabolism along the kynurenine pathway in Huntington's disease is related to the degree of genetic abnormality, to clinical disease severity and to aspects of immunopathogenesis.  相似文献   
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