2型糖尿病患者血清IL-6和TNF-α水平的检测对预后的意义

目的通过测定2型糖尿病(DM)患者血清白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平的变化,探讨其在糖尿病肾病(DN)中的发病学意义,了解其对DM预后的影响.方法采用放射免疫法检测85例2型DM患者血清IL-6和TNF-α水平.并根据24 h尿白蛋白排泄率(UAER)将DM患者分为单纯DM组(SDM,n=40),隐性糖尿病肾病组(IDN,n=28)和显性糖尿病肾病组(ODN,n=17),并与32例正常人对照.结果(1)SDM,IDN,ODN 3组患者及正常对照组血清IL-6水平分别为(99±16),(112±22),(128±24),(90±15)ng/L,TNF-α水平分别为(127±15),(130±16),(148±22),(112±22)ng/L,经方差分析,各组间差异具有非常显著意义(F=19.27,13.35,P均＜0.01),其中SDM,IDN,ODN 3组均明显高于正常对照组(P＜0.05或P＜0.01),ODN组又明显高于SDM组和IDN组(P＜0.01),IDN组血清IL-6水平亦较SDM组升高(P＜0.05).(2)糖尿病病程与患者血清IL-6,TNF-α水平呈明显正相关(r=0.396,P＜0 01和r=0.277,P＜0.05),UAER与患者血清IL-6,TNF-α水平变化亦呈正相关关系(r=0.630,0.426,P均＜0.01);空腹血糖与患者血清IL-6,TNF-α水平间均未见相关关系.结论IL-6和TNF-α可能参与了糖尿病及其肾病的发生与发展.血清IL-6,TNF-α水平检测可以作为临床观察DN病情及判断DM预后的参考指标.     

败血症／感染性休克病人循环血中TNF的动态测定及意义

对15例败血症/感染性休克病人分别于入院当天、第二天和第三天动态测定循环血中肿瘤坏死因子(TNF)的浓度。结果发现与健康对照相比,败血症/感染性休克病人循环血中 TNF 的浓度明显升高(P<0.05～0.01),其中死亡组病人(N=6)血浆 TNF 水平又要明显高于存活组病人(N=9)(P<0.05～0.01),而且伴有更为严重的血浆胰高血糖素升高和高乳酸血症。上述结果提示临床败血症/感染性休克病人血浆 TNF 水平与休克严重程度有关,而且在判定病人预后方面具有重要价值。     

强直性脊柱炎患者外周血TH细胞亚群和细胞因子的检测及其临床意义

目的探讨强直性脊柱炎(AS)患者外周血辅助性T细胞(TH)亚群和细胞因子的变化水平及其临床意义。方法用流式细胞术分析27例AS患者及30例体检健康者外周血TH1、TH2和TH17细胞亚群的比例;流式微球阵列技术(cytometric beadarray,CBA)检测血清IL-2、IL-4、IL-6、IL-10、TNF、IFN-γ和IL-17A的水平。结果 AS组TH1和TH17细胞的百分率显著高于健康人对照组(P均<0.01),而TH2细胞差异无统计学意义(P>0.05)。AS患者血清IL-2、IL-6、TNF和IFN-γ表达水平也明显高于健康人对照组(P均<0.01),但IL-4、IL-10和IL-17A无显著性差异(P均>0.05)。结论 AS患者TH细胞亚群失衡,表现为TH1和TH17细胞比例及IFN-γ、TNF、IL-2和IL-6水平升高。     

脓毒症患者血清IL-3的表达情况及其临床意义

目的:检测不同程度脓毒症患者血清白介素-3(interleukin-3,IL-3)的表达情况,并探究其与疾病的相关性。方法:纳入2017年12月至2018年12月符合条件的脓毒症病例组100例,分为非休克组(n=69)和休克组(n=31),存活组(n=79)和死亡组(n=21)。并纳入同时期健康体检人群50例作为对照组。收集患者的血尿样本检测包括IL-3等相关生化指标,同时记录患者急性病生理学和长期健康评价Ⅱ(acute physiology and chronic health evaluation,APACHEⅡ)评分以及序贯器官衰竭评分(sequential organ failure assessment,SOFA),作为评估疾病严重程度的指标。结果:脓毒症病例组血清IL-3水平显著高于健康对照组(P<0.01),休克组血清IL-3水平高于非休克组(P<0.01),死亡组血清IL-3水平高于存活组(P<0.01);脓毒症患者血清IL-3水平与APACHEⅡ评分(r=0.67,P=0.02)及SOFA(r=0.59,P=0.03)呈正相关联系;脓毒症患者血清IL-3水平是患者发生死亡事件的独立危险因素(P=0.03);IL-3水平判断脓毒症死亡预后的ROC曲线下面积为0.88,灵敏度为0.86,特异度为0.72(P=0.03)。结论:脓毒症患者血清IL-3水平升高,且与疾病严重程度具有相关性,可用于评估脓毒症患者预后。     

冠心病患者血清尿酸和高敏C反应蛋白浓度变化及其意义

[目的]探讨冠心病患者血清尿酸(UA)和高敏C反应蛋白(hs-CRP)水平的变化及其临床意义.[方法]选择冠心病患者211例和非冠心病对照者(CG)72例,其中冠心病患者分为稳定型冠心病(SCHD)组(n=70)、不稳定性心绞痛(UAP)组(n=73)和急性心肌梗死(AMI)组(n=68).比较分析各组间UA、hs-CRP水平的差异及其相关性.[结果]冠心病各组血清UA、hs-CRP水平较CG组显著升高(P均<0.01),AMI组UA水平显著低于SCHD组和UAP组(P均<0.01),UAP组hs-CRP显著高于SCHD组(P<0.01),AMI组hs-CRP显著高于UAP组(P<0.01).多元Logistic回归分析显示UA、hs-CRP对冠心病的影响均有统计学意义(P<0.05).直线相关分析显示SCHD组UA与hs-CRP呈正相关(r=0.328,P<0.01),AMI组UA与hs-CRP呈负相关(r=-0.461,P<0.01).[结论]血清UA和hs-CRP水平增高是冠心病的独立危险因素,高尿酸血症可能促发低度炎症反应,AMI患者在hs-CRP水平明显增高的同时伴有UA水平降低.     

PCT、LPS和IL-6在脓毒血症中的应用价值

目的探讨降钙素原(PCT)、内毒素(LPS)及白细胞介素-6(IL-6)水平联合检测在脓毒血症中的应用价值。方法选择脓毒血症(SP组)、细菌感染(BC组)和系统性炎症反应综合征(SI组)患者共120例及20例健康志愿者(NC组)作为研究对象,测定SP组、BC组、SI组和NC组血清PCT、LPS和IL-6水平。结果 SP组和SI组PCT水平均高于BC组和NC组,差异有统计学意义(P0.01);SP组和BC组LPS水平均高于SI组和NC组,差异有统计学意义(P0.01);SP、BC和SI组血清IL-6水平高于NC组(P0.01);SP组PCT、LPS和IL-6联合检测阳性率高于非SP组,差异有统计学意义(P0.01)。结论 PCT、LPS和IL-6联合检测可作为脓毒血症早期诊断及干预治疗的有效检测方法。     

不同类型急性白血病患者血清IFN-γ、TGF-β、IL-6和IL-17水平变化及其预后判定分析

目的探讨不同类型急性白血病患者血清干扰素-γ(IFN-γ)、转化生长因子-β(TGF-β)、白介素-6(IL-6)和白介素-17(IL-17)水平变化及其预后。方法选取我院2015年6月至2017年6月接诊的100例急性白血病患者进行研究,根据疾病类型将其均分为急性淋巴细胞白血病(ALL)组和急性髓细胞白血病(AML)组,此外,选择同期健康体检的患者100例作为对照组。对三组患者治疗后的临床疗效,治疗前后的血清IFN-γ、TGF-β、IL-6和IL-17水平及其预后进行比较分析。结果 ALL组和AML组治疗总有效率比较差异无统计学意义(χ2=0.0603,P=0.8061)。治疗前,ALL组和AML组的IFN-γ水平明显低于对照组,TGF-β、IL-6和IL-17水平明显高于对照组,差异有统计学意义(P0.05)。ALL组血清IFN-γ、IL-6水平明显高于AML组(P0.05),但两组患者的血清TGF-β、IL-17水平比较差异无统计学意义(P0.05)。ALL组显效患者血清IFN-γ水平高于无效患者(t=8.6250,P=0.0000),TGF-β水平低于无效患者(t=4.5539,P=0.0000),IL-6水平低于无效患者(t=12.9912,P=0.0000),IL-17水平低于无效患者(t=10.0341,P=0.0000)。AML组显效患者血清IFN-γ水平高于无效患者(t=27.4937,P=0.0000),TGF-β水平低于无效患者(t=4.6727,P=0.0000),IL-6水平低于无效患者(t=5.5393,P=0.0000),IL-17水平均低于无效患者(t=11.7118,P=0.0000)。结论急性白血病与血清IFN-γ、TGF-β、IL-6和IL-17水平密切相关,可把患者血清水平作为临床诊断急性白血病、评价预后的指标。     

三联化毒疗法治疗慢性肾功能衰竭的临床研究

目的:探讨三联化毒疗法治疗慢性肾功能衰竭(CRF)的作用机制.方法:142例CRF患者采用随机数字表法分为三联化毒疗法组(治疗组,n=82)和西药治疗组(对照组,n=60),两组基础治疗相同,治疗组加用三联化毒疗法.观察两组患者治疗前后肾功能、血脂、血浆总蛋白(TP)、血红蛋白(Hb)及血清白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNFα)的变化.结果:治疗1个疗程后,治疗组患者血尿素氮(BUN)、血肌酐(SCr)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白-胆固醇(LDL-C)及血清IL-6和TNF-α水平均明显降低,高密度脂蛋白-胆固醇(HDL-C)明显升高(P<0.05或P<0.01),对照组上述指标均无明显变化.两组CRF患者TP和Hb水平均明显升高(P<0.05或P<0.01),且治疗组明显优于对照组(P均<0.01).结论:三联化毒疗法可能是通过降低CRF患者血脂及血清IL-6和TNF-α水平而起到治疗作用.     

8周游泳运动干预对高脂饲养小鼠炎性细胞因子和脂肪因子的影响

目的:研究运动干预对高脂饲养的小鼠炎性细胞因子和脂肪因子的影响。方法:将SPF级C57BL/6小鼠41只(雄性20只,雌性21只)随机分成正常对照组(NC组,n=11,雄性5只,雌性6只)和高脂饮食组(HFD组, n=30,雄性15只,雌性15只),分别以普通饲料和高脂饲料喂养。9周后,将HFD小鼠25只随机分为肥胖运动组(OE组,n=13,雄性5只,雌性8只)与肥胖对照组(OC组,n=12,雄性5只,雌性7只)。OE组进行为期8周无负重游泳训练。8周后每组随机挑选8只(雄性4只,雌性4只)小鼠,用ELISA法测定其血清脂联素(APN)、网膜素、瘦素、内脂素、C-反应蛋白(CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)水平。结果:①OE组与OC组小鼠体重均显著高于NC组(P0.01),OE组体重显著低于OC组(P0.05)。②与NC组比较,OC组小鼠血清瘦素、内脂素、CRP、IL-6、TNF-α水平均显著上升(P0.01);脂联素和网膜素有下降趋势,但差异不显著(P0.05)。与OC组相比,OE组小鼠血清脂联素(P0.05)、网膜素(P0.01)水平显著上升;内脂素水平下降(P0.05);瘦素、CRP、IL-6、TNF-α水平均显著下降(P0.01)。③小鼠血清脂联素与血清IL-6有微弱的负相关关系(P0.05);血清脂联素与网膜素有较弱的正相关关系(P0.05);小鼠血清网膜素与血清CRP有中等程度的负相关关系(P0.01);小鼠血清瘦素、内脂素均与血清IL-6、TNF-α有中等程度的正相关关系(P0.01)。结论:8周游泳运动干预可以通过刺激能抑制炎症因子的脂联素、网膜素的分泌及抑制促炎因子瘦素、内脂素的分泌有效减轻肥胖小鼠炎症反应。     

冠状动脉综合征患者血清白细胞介素6和肿瘤坏死因子α水平及辛伐他汀的干预作用

目的：探讨辛伐他汀对急性冠状动脉综合征(acute comnary svndrome，ACS)患者血清白细胞介素6(IL-6)及肿瘤坏死因子α(TNF—α)水平变化的影响，以期发现上述因子变化与ACS发病的关系及辛伐他汀对ACS发病的影响。方法：2002—09／2003—09白求恩国际和平医院急诊科留观病人和河北医大第三医院心内科住院患者中符合纳入标准ACS患者52例，将ACS患者52例随机分为辛伐他汀组(n=26)和常规治疗组(n=26)，分别于治疗前及治疗后3周行血清IL-6及TNF—α检测，均采用放射免疫分析方法。另选本院同期健康体检的30例作为对照组，对照组采血前2周内未服任何药物，体检时对其血清IL-6及TNF—α进行检测。结果：ACS患者治疗前血清IL-6，TNF—α水平均明显高于对照组(P&;lt;0.01)。辛伐他汀组患者治疗后血清IL-6，TNF-α水平[(0．708&;#177;0．087)μg／L，(67．73&;#177;10．00)fmol／L]均明显低于治疗前[(0．800&;#177;0．083)μg／L，(79．92&;#177;14．53)fmol／L](P&;lt;0．01)，但仍高于对照组(P&;lt;0．01)。常规治疗组患者治疗后血清IL-6，TNF-α降低不明显(P&;gt;0．05)。结论：IL-6，TNF-α水平越高，则ACS发病的概率可能越大；辛伐他汀可降低ACS患者血IL-6，TNF-α水平，具有减轻病变部位炎症反应和保护内皮的作用。     

The role of interleukin-10 in systemic inflammatory response syndrome with sepsis

This study was performed to demonstrate the role of interleukin (IL)-10, especially in systemic inflammatory response syndrome (SIRS) patients. In clinical observations, levels of serum tumor necrosis factor-α (TNF) and IL-10 increased in SIRS patients (TNF, n=43; IL-10, n=33), and they increased more in the patients with organ failure (n=22) than in patients without organ failure (n=24), (P<0.01). In mice, serum TNF and IL-10 began to increase at 1 hour after injection with 4mg/kg of lipopolysaccharide (LPS) and reached a maximum at 2 hours. However, the serum level of TNF decreased to an undetectable level at 6 hours, while a significant amount of IL-10 remained in serum. The TNF elevation induced by LPS injection was inhibited by pretreatment with 200 ng of IL-10 (P<0.1 in serum,P<0.05 in bronchoalveolar lavage fluid). Neutrophil reduction induced by LPS injection was also inhibited by pretreatment with 1 μg of IL-10. On human neutrophils the expression of adhesion molecules LFA-1 and MAC-1 that resulted from in vitro incubation with TNF were suppressed by the addition of IL-10 supplement. The expression of TNF receptors on the surface of human neutrophils as a result of LPS loading was also suppressed by IL-10 supplement. IL-10 seems have a protective function in the progress to organ failure in SIRS patients with sepsis. IL-10 suppresses TNF production and inhibits the expression of adhesion molecules and TNF receptors on neutrophils.     

Effects of polyenylphosphatidylcholine on cytokines,nitrite/nitrate levels,antioxidant activity and lipid peroxidation in rats with sepsis

OBJECTIVES: To determine the effect of pretreatment with polyenylphosphatidylcholine (lecithin, PPC) on plasma levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, total nitrite/nitrate (NOx), and tissue levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in septic rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: University laboratory. SUBJECTS: Forty-five Spraque-Dawley rats were divided into three groups: group C, sham-operated; group S, sepsis; and group P, sepsis pretreated with PPC. INTERVENTIONS: Rats were made septic by cecal ligation and puncture (CLP). Group P rats were treated with PPC (100 mg/day orally) for 10 days before sepsis. Twenty-four hours later CLP, plasma concentrations of TNF-alpha, IL-6 and IL-10 and plasma levels of NOx were measured. SOD and MDA were determined in liver, lung and heart homogenates. MEASUREMENTS AND MAIN RESULTS: All rats in group P survived during the 24-h observation time after CLP, whereas survival rate in group S was 66.7% (10/15; P<0.05). PPC significantly reduced plasma levels of TNF-alpha (P=0.006), IL-6 (P=0.007), IL-10 (P=0.016), NOx (P<0.001), and tissue levels of MDA (P<0.001) in group P with respect to in group S. Tissue levels of SOD significantly increased in group P when compared with group S (P<0.001). CONCLUSIONS: These results show that PPC pretreatment exerts cumulative effects in decreasing the levels of cytokines, NOx, and tissue MDA concentrations, with a concomitant increase in survival in septic rats. Lecithin therapy may be a useful adjuvant therapy in controlling of the excessive production of the inflammatory cytokines in patients with severe sepsis. DESCRIPTOR: SIRS/sepsis, experimental studies.     

Outcomes of previously healthy pediatric patients with fulminant sepsis-induced multisystem organ failure receiving therapeutic plasma exchange

Background: Fulminant sepsis‐induced multisystem organ failure (MSOF) in pediatric patients carries substantial morbidity and mortality. Therapeutic plasma exchange (TPE) has been reported to be beneficial in sepsis‐induced MSOF. We evaluated the outcomes of previously healthy children with fulminant sepsis‐induced MSOF receiving TPE. Materials and Methods: Previously healthy pediatric ICU patients who underwent TPE for MSOF due to fulminant bacterial sepsis were retrospectively reviewed. Eleven patients (three females and eight males) with age ranging 8 months to 14 years were identified (eight meningococcemia and three other infections). All patients received daily TPE with fresh frozen plasma (FFP) as replacement fluid. Organ failure index (OFI—maximum score = 6) was assessed daily for 7 days. Results: A median of 4 TPE (1–14) were performed. Improvements in organ function and platelet count occurred in most patients with 2–4 TPE treatments. All 10 patients who were alive had reduced OFI to 2 by day 7 of initial TPE and were all fully recovered (survival rate = 10/11, 91%). The only death occurred in a patient who died the same day after his first TPE treatment, which was initiated 24 h after development of MSOF. The 10 survivors underwent early initiation of TPE (median 5.3 h) after the onset of MSOF. Conclusions: > TPE may contribute to a better outcome in previously healthy pediatric patients with fulminant sepsis‐induced MSOF, especially if instituted early in the course of multiorgan failure. J. Clin. Apheresis, 2011. © 2011 Wiley‐Liss, Inc.     

Ketamine improves survival and suppresses IL-6 and TNFalpha production in a model of Gram-negative bacterial sepsis in rats

OBJECTIVE: In a previous study, ketamine suppressed Escherichia coli-induced production of the cytokines interleukin (IL)-6 and tumor necrosis factor alpha (TNF). In other previous studies ketamine improved survival after E. coli inoculation. However, the relationship between cytokines and survival following ketamine treatment is uncertain because no study has examined both cytokines and survival after E. coli inoculation. METHODS: Rats were given E. coli (0.4 x 10(9) colony forming unit (CFU)) at time 0, followed by ketamine (50 mg/kg, n=30) or saline (n=30) at 5 min or 2 h. IL-6 and TNF were measured in serum at 6 h, and mortality was recorded for 7 days. RESULTS: Survival rate with ketamine was 57% (17/30) and was significantly increased compared to saline (27%, 8/30, P=0.01). IL-6 and TNF were lower with ketamine than saline (15,197 +/- 3444 versus 30,725 +/- 4623 pg/ml [mean +/- S.E.M.], P=0.013 and 38.5 +/- 9.5 versus 122.5 +/- 14.0 pg/ml, P=0.001, respectively). With ketamine, IL-6 (but not TNF) concentrations were lower in the survivors (10,900 +/- 776 pg/ml) as compared to the non-survivors (P=0.01). IL-6 in ketamine-treated survivors was not different from that in saline-treated survivors. Conclusion: We conclude that ketamine given 5 min or 2 h after induction of E. coli sepsis significantly improves survival, possibly by interfering with the inflammatory cascade (as evidenced by attenuation of cytokine production).     

Dysregulation of in vitro cytokine production by monocytes during sepsis.

The production by monocytes of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF alpha) in intensive care unit (ICU) patients with sepsis syndrome (n = 23) or noninfectious shock (n = 6) is reported. Plasma cytokines, cell-associated cytokines within freshly isolated monocytes and LPS-induced in vitro cytokine production were assessed at admission and at regular intervals during ICU stay. TNF alpha and IL-6 were the most frequently detected circulating cytokines. Despite the fact that IL-1 alpha is the main cytokine found within monocytes upon in vitro activation of cells from healthy individuals, it was very rarely detected within freshly isolated monocytes from septic patients, and levels of cell-associated IL-1 beta were lower than those of TNF alpha. Cell-associated IL-1 beta and TNF alpha were not correlated with corresponding levels in plasma. Upon LPS stimulation, we observed a profound decrease of in vitro IL-1 alpha production by monocytes in all patients, and of IL-1 beta, IL-6, and TNF alpha in septic patients. This reduced LPS-induced production of cytokines was most pronounced in patients with gram-negative infections. Finally, monocytes from survival patients, but not from nonsurvival ones recovered their capacity to produce normal amounts of cytokines upon LPS stimulation. In conclusion, our data indicate an in vivo activation of circulating monocytes during sepsis as well as in noninfectious shock and suggest that complex regulatory mechanisms can downregulate the production of cytokines by monocytes during severe infections.     

慢性阻塞性肺疾病合并肺气肿患者血清不规则趋化因子变化及临床意义

目的 分析慢性阻塞性肺疾病(COPD)合并肺气肿患者血清不规则趋化因子(CX3CL1/FKN)变化及临床意义.方法 我院收治的106例COPD患者,按是否合并肺气肿分为COPD合并肺气肿组(n=46)和COPD组(n=60),选取同期我院体检的40例健康者作为对照组;随访28 d,根据预后将COPD合并肺气肿组分为存活...     

急性肾功能衰竭预后危险因素研究

目的 探讨影响急性肾功能衰竭（ARF）患者肾功能恢复率、病死率的危险因素，以指导诊疗，改善预后。方法 通过Logistic回归等方法回顾性分析44例ARF患者的多系统器官功能衰竭（MSOF）发生率，比较高、低分解代谢、伴否MSOF的ARF患者其肾功能恢复率及病死率。结果 高、低分解代谢型ARF患者肾功能恢复率、病死率差异均有显著性（P〈0．01、P〈0．05）。伴否MSOF的ARF患者问其肾功能恢复率，病死率差异均有显著性（均为P〈0．01）。脏器衰竭数目与肾功能恢复率呈显著负相关（r=-0．517，P〈0．01），与病死率呈显著正相关（r=0．78，P〈0．01）。低分解代谢型ARF患者肾功能恢复率是高分解代谢型的13．7倍，不伴MSOF的ARF患者肾功能恢复率是伴MSOF者的27倍，伴MSOF的ARF患者其病死率是不伴MSOF者的68．7倍。结论 对ARF患者应积极寻找并去除导致高分解代谢的原发病因，治疗选药时避免使用损害肾外脏器药物，力争不伴发或少伴发MSOF，这对改善ARF预后有利。     

新生儿急性呼吸窘迫综合征患者血清miR-183-5p的表达及与IL-1β，IL-6和TNF-α水平的相关性

目的　探讨新生儿急性呼吸窘迫综合征（acute respiratory distress syndrome, ARDS）患者血清miR-183-5p的表达及其与白细胞介素-1β(IL-1β)、白细胞介素-6（IL-6）及肿瘤坏死因子-α（TNF-α）的相关性。方法　选取保定市第二中心医院收治的87例ARDS新生儿为研究对象。根据ARDS患儿出院时生存情况分为生存组（n=68）和死亡组（n=24）,按照新生儿危重评分结果分为非危重组（n=53,>90 分）、危重组（n=24, 70～90 分）、极危重组（n=15, <70 分）,比较各组血清miR-183-5p,IL-1β,IL-6及TNF-α水平差异。ARDS患儿miR-183-5p与IL-1β,IL-6及TNF-α的相关性采用Pearson相关分析。结果　与生存组比较,死亡组血清miR-183-5p（2.15±0.94 vs 0.96±0.38）,IL-1β（168.20±30.62 vs 110.25±19.30,pg/mL）,IL-6（217.28±44.27 vs 151.30±32.46,pg/mL）及TNF-α（81.16±19.24 vs 48.27±14.30,pg/mL）水平均明显升高（P<0.001）。随着病情加重ARDS患儿血清miR-183-5p,IL-1β,IL-6及TNF-α水平逐渐升高,极危重组>危重组>非危重组（P<0.001）。相关分析显示,ARDS患儿血清miR-183-5p表达水平与IL-1β,IL-6及TNF-α均呈正相关（P<0.001）。结论　ARDS患儿血清miR-183-5p高表达与IL-1β,IL-6,TNF-α水平及病情严重程度相关,可能是预测ARDS患儿病情严重程度的生物学指标。     

老年腹部手术患者围手术期细胞因子的变化及临床意义

目的:探讨老年患者腹部手术前后肿瘤坏死因子(TNF)、白细胞介素-6(IL-6)和白细胞介素-8(IL-8)的变化及其临床意义。方法:随机选取老年腹部手术患者56例,其中伴腹腔感染28例为观察组,另28例为对照组,均采用放射免疫法检测手术前后静脉血TNF、IL-6和IL-8的变化。结果:术前观察组静脉血TNF、IL-6和IL-8水平均显著高于对照组(P<0.01);术后1d两组TNF、IL-6和IL-8水平均显著高于术前(P<0.05);术后7d观察组TNF、IL-6和IL-8水平均较术前显著下降(P<0.01);经相关性分析证明患者静脉血TNF、IL-6与IL-8之间存在正相关关系。结论:腹部感染患者静脉血中TNF、IL-6和IL-8水平明显增高,监测三者的变化可作为观察老年腹部感染患者病情转归的重要指标。