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目的通过检测肾综合征出血热(HFRS)患者循环内皮细胞(CEC)计数及CEC中磷酸化黏着斑激酶(FAKps910)、热休克蛋白70(HSP70)的阳性表达率,了解HFRS患者CEC计数及FAKps910、HSP70表达的动态变化,探讨其临床意义。方法 50例HFRS患者按病情分为轻型17例、中型20例、重型及危重型13例,健康对照组20例。流式细胞技术检测CEC计数及CEC中FAKps910、HSP70的表达情况。结果从发热早期至多尿期,HFRS患者CEC计数[发热早期:(13.37±5.19)个/μl;发热期末或低血压休克期:(47.73±19.89)个/μl;少尿期(41.11±16.21)个/μl;多尿期(19.29±4.81)个/μl]及HSP70的表达水平(发热早期:53.26%±10.54%;发热期末或低血压休克期:56.21%±8.83%;少尿期:40.13%±6.99%;多尿期:28.53%±6.79%)均显著高于对照组[CEC计数:(3.31±1.49)个/μl;HSP70:23.89%±4.70%],至恢复期[CEC计数:(3.86±1.98)个/μl;HSP70:26.52%±6.31%]则逐渐趋向正常。在发热期末或低血压休克期CEC及HSP70随病情加重而升高,在重型和危重型患者中达到高峰。但循环内皮细胞中FAKps910的表达水平在发热早期(59.87%±9.58%)明显升高,发热期末或低血压休克期降至正常水平以下(11.64%±2.17%),以后又恢复正常(少尿期:22.44%±4.09%;多尿期:21.05%±2.61%;恢复期:20.94%±3.15%)。且发热末或低血压期FAKps910的表达随病情加重而减少,在重型和危重型患者中降至最低。结论 HFRS中CEC计数明显增高并能反映内皮细胞损伤的程度,FAKps910、HSP70在病程中规律性变化,提示黏着斑(FAK)可能与汉坦病毒引起的整合素β3介导的血管内皮细胞损伤有关;而HFRS患者的CEC中HSP70表达增高,可能对CEC具有保护作用。CEC计数、FAKps910及HSP70还可作为早期病情的预测指标。
Objective To detect the CEC count and the expression of FAKps910 in patients with HFRS by counting the number of circulating endothelial cells (CECs) and the positive rate of phosphorylated focal adhesion kinase (FAKps910) and heat shock protein 70 (HSP70) in patients with hemorrhagic fever with renal syndrome (HFRS) , HSP70 expression in the dynamic changes, to explore its clinical significance. Methods Fifty HFRS patients were divided into mild type in 20 cases, moderate type in 20 cases, heavy type and critical type in 13 cases, and healthy control group in 20 cases. CEC count and expression of FAKps910, HSP70 in CEC were detected by flow cytometry. Results From early fever to polyuria, the CEC count of HFRS patients (early fever: (13.37 ± 5.19) / μl; end of fever or hypotensive shock period: (47.73 ± 19.89) / μl; oliguria (41.11 ± 16.21) (19.29 ± 4.81) / μl] and the expression of HSP70 (early fever: 53.26% ± 10.54%; end of fever or hypotensive shock: 56.21% ± 8.83%; oliguria: 40.13 % ± 6.99%; polyuria: 28.53% ± 6.79%) were significantly higher than the control group [CEC count: (3.31 ± 1.49) / μl; HSP70:23.89% ± 4.70% (3.86 ± 1.98) / μl; HSP70:26.52% ± 6.31%] gradually became normal. At the end of fever or shock during the hypotension, CEC and HSP70 increased with the severity of the disease, reaching peak in patients with severe and critically ill. However, the expression of FAKps910 in circulating endothelial cells was significantly increased at early fever (59.87% ± 9.58%), decreased to below normal level (11.64% ± 2.17%) at the end of febrile sera or hypotensive shock, and then returned to normal Duration: 22.44% ± 4.09%; Polyuria: 21.05% ± 2.61%; Recovery: 20.94% ± 3.15%). The expression of FAKps910 at the end of febrile or hypotensive phase decreases with the aggravation of the disease, and it is reduced to the lowest in severe and critically ill patients. Conclusions The CEC count in HFRS is significantly increased and can reflect the degree of endothelial cell injury. The regular changes of FAKps910 and HSP70 in the course of the disease suggest that FAK may be related to integrin β3-mediated endothelial cell injury induced by Hantaviruses ; HFRS patients with elevated expression of HSP70 in CEC, may have a protective effect on CEC. CEC count, FAKps910 and HSP70 can also be used as a predictor of early disease.