肝衰竭继发感染患者炎性因子与细胞因子的研究

Inflammatory factors and cytokines in patients with secondary infection of liver failure

  • 摘要: 目的 探究肝衰竭继发感染患者炎性因子及细胞因子水平的临床检测价值。方法 选择2016年1月-2018年12月承德医学院附属医院收治的肝衰竭患者120例为研究对象,根据是否继发感染分为继发感染组51例与非感染组69例,入院后,两组均行营养支持、促肝细胞生长、维持电解质等常规治疗。抽取两组入院时和继发感染组出现典型感染时两个时段空腹静脉血检测降钙素原(PCT)及抗炎因子:转化生长因子-β(TGF-β)、白细胞介素-10(IL-10)、IL-17,促炎因子C-反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、IL-6和肝功能指标:丙氨酸氨基转移酶(ALT)、直接胆红素(DBil)、胆总红素(TBil)及T淋巴细胞亚群CD4+、CD8+结果 继发感染组确诊时的PCT水平(2.12±0.57)ng/ml高于非感染组的(0.28±0.24)ng/ml(P<0.001);继发感染组确诊时的CRP(30.78±5.42)mg/L、IL-6(41.87±8.29)ng/L、TNF-α(425.83±35.92)mg/L水平高于非感染组(P<0.001);继发感染组确诊时的TGF-β(148.52±20.27)mg/L、IL-10(97.38±10.14)mg/L、IL-17(228.79±17.68)ng/L水平均下降,且低于非感染组(P<0.001);继发感染组确诊时的CD4+(27.69±4.07)%、CD4+/CD8+(0.81±0.12)低于非感染组,CD8+为(36.84±6.92)%高于非感染组(P<0.001);继发感染组确诊时的ALT(217.65±21.43)U/L、DBil(231.65±20.78)μmol/L、TBil(392.52±25.64)μmol/L高于非感染组(P<0.001)。结论 肝衰竭继发感染加重肝脏负担,进一步损害肝功能,加速肝衰竭病情进展,其中血清降钙素原及抗炎因子水平上升,促炎因子水平下降,免疫功能指标下降,对肝衰竭继发感染的诊断、治疗及预后具有一定参考价值。

     

    Abstract: OBJECTIVE To explore the clinical detection value of inflammatory factors and cytokine levels in patients with secondary infection of liver failure. METHODS A total of 120 patients with liver failure treated in the affiliated hospital of Chengde medical university from Jan. 2016 to Dec. 2018 were selected as study subjects, and were divided into 51 cases of secondary infection group and 69 cases of non-infected group according to whether secondary infection. After admission, both groups received routine treatments such as nutrition support, hepatocyte growth-promoting factors, and electrolyte maintenance. Fasting venous blood was drawn in two groups at the time of admission and in the secondary infection group when a typical infection occured. Blood procalcitonin(PCT), anti-inflammatory factors(transforming growth factor-β(TGF-β), interleukin-10(IL-10), interleukin-17(IL-17), pro-inflammatory factor C-reactive protein(CRP), tumor Necrosis factor-α(TNF-α), interleukin-6(IL-6), and liver function indicators(alanine aminotransferase(ALT), direct bilirubin(DBil), total bilirubin(TBil); T lymphocyte subsets CD4+, CD8+) were detected. RESULTS The PCT level at the time of diagnosis in the secondary infection group was(2.12±0.57) ng/ml, significantly higher than that in the non-infected group(0.28±0.24) ng/ml(P<0.001). The levels of CRP(30.78±5.42)mg/L, IL-6(41.87±8.29)ng/L and TNF-α(425.83±35.92)mg/L at the time of diagnosis in the secondary infection group were significantly higher than those of the Non-infected group(P<0.001). The TGF-β(148.52±20.27) mg/L, IL-10(97.38±10.14)mg/L and IL-17(228.79±17.68)ng/L in the secondary infection groupat the time of diagnosis were decreased and significantly lower than those in non-infected group(P<0.001). The level of CD4+(27.69±4.07)% and CD4+/CD8+(0.81±0.12) levels in the secondary infection group at the time of diagnosis were significantly lower than those in the non-infected group. The level of CD8+ was(36.84±6.92)%, significantly higher than that in the non-infected group(P<0.001). The levels of ALT(217.65±21.43)U/L, DBil(231.65±20.78)μmol/L, and TBil(392.52±25.64)μmol/L in the secondary infection group at the time of diagnosis were significantly higher than those in the non-infected group(P<0.001). CONCLUSION Secondary infection of liver failure aggravated liver burden, further damaged liver function, and accelerated the progression of liver failure, with serum procalcitonin and anti-inflammatory factors increased, proinflammatory factor levels decreased and immune function indicators decreased, which had certain reference value for the diagnosis, treatment and prognosis of secondary infection of liver failure.

     

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