C反应蛋白及降钙素原在小儿脓毒症血流感染及其他部位感染性疾病中的诊断价值

目的：评估入住PICU 6 h内血清CRP及PCT水平在脓毒症血流感染及其他部位感染患儿临床诊断中的价值。方法：回顾性分析2010年1月至2012年1月期间,中国医科大学附属盛京医院PICU收治的30名明确诊断SIRS患儿,脓毒症血流感染及脓毒症其他部位感染患儿各15名,收集入住6 h内的血清CRP、PCT及D-二聚体含量资料,进行差异性比较并通过ROC曲线分析其诊断价值。结果：脓毒症血流感染组患儿的血清CRP及PCT水平较脓毒症其他部位感染组显著升高（P0.05）。血清PCT水平较CRP水平在诊断与鉴别脓毒症血流感染与其他部位感染性疾病方面有明显优势,PCT10 ng/mL时诊断脓毒症血流感染具有较高的可信度（阳性预测值：77%）。结论：入院6 h内的血清PCT水平较CRP水平在早期鉴别入住PICU脓毒症血流感染与其他部位感染患儿具有更好的诊断价值;当血清PCT水平>10 ng/mL时,脓毒症血流感染的诊断可能性较大。     

血浆脑钠肽及心肌肌钙蛋白Ⅰ在小儿脓毒症诊断及评估中的意义

目的探讨血浆脑钠肽（BNP）及心肌肌钙蛋白I（cTnI）测定在小儿脓毒症诊断及评估中的意义。方法应用化学发光法检测47例脓毒症患儿和50例一般感染患儿入院时血浆BNP及cTnI的浓度,并选取同期入院的11例非感染患儿为对照组。结果（1）脓毒症组血浆BNP水平（ng／L）[中位数（四分位数间距）]为164．40（308．60）,高于一般感染组[50．35（63．97）]及对照组[28．90（12．28）],差异有非常显著性（P〈0．01）。严重脓毒症组血浆BNP水平（ng／L）[379．88（1108．70）]高于一般脓毒症组[135．30（211．88）],差异有显著性（P〈0．05）。（2）脓毒症组血浆eTnI水平（μg/L）[中位数（四分位数间距）]为0．05（0．07）,高于一般感染组[0．03（0．03）]及对照组[0．03（0．04）],差异有显著性（P〈0．05）。严重脓毒症组血浆cTnI水平（μg／L）[0．10（0．20）]高于一般脓毒症组[0．04（0．03）],差异有非常显著性（P〈0．01）。结论脓毒症患儿在除外充血性心力衰竭因素时,血浆BNP及cTnI水平有助于临床医生对脓毒症进行诊断和严重程度评估。     

脓毒症患儿外周血自然杀伤细胞比例及亚群的变化

目的 探讨脓毒症患儿外周血自然杀伤（natural killer,NK）细胞及各亚群比例的变化.方法 2009年1月至2012年12月我院住院的脓毒症患儿按病情分为脓毒症组25例和严重脓毒症组12例,同时设健康对照组37例.提取各组患儿外周血,采用流式细胞术检测NK细胞及各亚群比例.结果 脓毒症组患儿CD16^＋ NK细胞（0.44％±0.13％）较健康对照组明显减少（P＜0.01）.严重脓毒症组患儿外周血CD16^＋ NK细胞（0.73％±0.25％）较健康对照组（1.78％±0.39％）明显减少（P＜0.05）.严重脓毒症组患儿外周血CD56^＋ CD16^＋ NK细胞（4.82％±2.57％）较健康对照组（9.52％±1.16％）明显减少（P＜0.05）.严重脓毒症组患儿外周血NK细胞总数（5.90％±3.27％）较健康对照组（11.80％±2.40％）明显减少（P＜0.05）.脓毒症组与健康对照组患儿NK细胞总数差异无统计学意义（P＞0.05）.严重脓毒症组、脓毒症组、健康对照组患儿CD56^＋ NK细胞差异无统计学意义（P＞0.05）.结论 脓毒症患儿NK细胞总数减少不明显,但其亚群CD16^＋ NK细胞明显减少.严重脓毒症患儿CD16^＋ NK细胞、CD56^＋ CD16^＋ NK细胞两个亚群均减少.NK细胞总数也减少.脓毒症及严重脓毒症患儿CD56^＋ NK细胞数量无明显减少.CD16^＋ NK细胞数量减少可能是脓毒症的易感因素之一,并与严重脓毒症的发生发展有关.     

小儿先天性心脏病术后脓毒症发生的危险因素

目的：探讨小儿先天性心脏病（先心病）术后脓毒症发生的危险因素,以利于疾病早期认识和诊断,改善临床转归。方法回顾性分析我院胸外科重症监护室2012年1月至2015年4月间发生的52例先心病术后合并脓毒症患儿和1∶2配对的104例非脓毒症患儿的临床资料。对患儿年龄、性别、术前感染、延迟关胸、膈肌麻痹、二次开胸、长时间体外循环、留置多个有创导管方面进行Logistic回归分析,分析脓毒症发生的危险因素,计算OR值及其95％CI。结果先心病术后合并脓毒症患儿休克发生率高、功能受累脏器数目多,住院及ICU滞留天数长,病死率高,较非脓毒症患儿差异有统计学意义[25.32％vs.6.73％,（3.5±1.1）个vs.（1.1±0.7）个,（35.1±11.2）d vs.（11.3±3.1）d,（21.3±7.1）d vs.（7.1±2.3） d,19.23％ vs.4.81％,P＜0.05]。 Logistic回归分析显示术前合并感染、延迟关胸、二次开胸、留置多个有创导管,膈肌麻痹是小儿先天性心脏病术后脓毒症发生的危险因素, OR值（95％CI）分别为10.53（1.73,64.22）、26.66（2.69,263.83）、19.47（1.87,203.02）、4.99（1.361,8.31）、8.32（0.12,16.46）（P＜0.05）。结论小儿先心病术后脓毒症发生的危险因素有术前合并感染、延迟关胸、二次开胸、留置多个有创导管及膈肌麻痹。脓毒症患儿较非脓毒症患儿临床转归差。     

血清降钙素原判断儿童脓毒症病原学的作用

目的 了解细菌、病毒及支原体感染引起脓毒症血清降钙素原（procalcitonin,PCT）的水平,明确血清PCT判断引起儿童脓毒症常见病原的作用.方法 回顾性分析2011年2月1日至2012年9月1日入住湖南省儿童医院PICU确诊细菌、病毒、支原体感染引起脓毒症患儿330例,检测其入院时及治疗3d后的PCT水平,分析不同血清PCT水平下细菌、病毒及支原体感染引起的脓毒症的分布差异.分析细菌、病毒及支原体感染引起脓毒症的血清PCT水平在入院时与治疗3d时的差异.结果 细菌感染引起的脓毒症血清PCT水平明显升高,病毒及支原体感染引起的血清PCT水平升高不明显,分别为0.71 （8.14） ng/ml、0.15 （1.68） ng/ml、0.28 （1.89） ng/ml.按PCT水平分为0.05～ ng/ml、0.5～ ng/ml、2～ng/ml、10 ～ 300 ng/ml组,四组中细菌、病毒及支原体感染引起的脓毒症的分布不同,差异有统计学意义（x2=84.50,P＜0.01）.细菌感染引起的脓毒症抗炎治疗3d后,PCT水平较入院时明显下降[0.32（5.68） ng/ml vs 0.71 （8.14） ng/ml],差异有统计学意义（U=19.34,P＜0.05）.结论 PCT判断儿童脓毒症病原学有一定作用.PCT明显升高及抗炎治疗后PCT明显降低提示细菌感染可能性大,PCT升高不明显以病毒及支原体感染为主,不能完全排除细菌感染.     

内生吗啡对儿童脓毒症的诊断价值

目的 检测脓毒症患儿血浆内生吗啡浓度,探讨内生吗啡对脓毒症患儿发生休克、死亡及多器官功能障碍（MODS）的预测价值。方法 符合诊断标准的脓毒症患儿（n=31）,根据是否伴有休克分为脓毒症非休克组（n=19）和休克组（n=12）;根据结局分为存活组（n=22）和死亡组（n=9）;根据是否伴有MODS分为非MODS组（n=13）和MODS组（n=18）。另设普通感染患儿（n=16）和行健康体检儿童（n=31）作为对照。用高效液相质谱串联法检测各组血浆内生吗啡浓度。用受试者工作特征曲线（ROC）评估内生吗啡对脓毒症患儿发生休克、死亡及MODS的预测价值。结果 健康对照组儿童血浆未检测到内生吗啡,普通感染组仅3例患儿血浆检测到内生吗啡;脓毒症患儿血浆中均检测到内生吗啡。休克组患儿血浆内生吗啡浓度高于非休克组（P < 0.05）;死亡患儿血浆内生吗啡浓度高于存活患儿（P < 0.05）;MODS患儿血浆内生吗啡浓度高于非MODS患儿（P < 0.05）。ROC结果显示内生吗啡对脓毒症患儿休克、死亡和MODS均有预测价值（P < 0.05）。结论 脓毒症患儿血浆内生吗啡浓度明显升高,其对脓毒症患儿休克、死亡、MODS风险的发生有较好的预测价值。     

小儿脓毒症并腹内高压的危险因素分析

目的：探讨小儿脓毒症并腹内高压（IAH）的危险因素, 为早期诊断、及时干预治疗提供理论依据。方法：采用膀胱测压法对119例脓毒症患儿进行腹内压检测,根据腹内压检测结果将患儿分为腹内压正常组(对照组,n=80)与IAH组(n=39)。采用单因素和非条件logistic回归分析对两组患儿的临床资料进行分析,以调查脓毒症患儿并发IAH的危险因素。结果：单因素分析发现小儿危重病评分（PCIS）、降钙素原（PCT）、PaCO2、血清乳酸值及肠道/腹腔感染、腹水、胃肠功能障碍、机械通气、休克和多脏器功能不全（MODS）的发生比例在IAH和对照组间比较差异均具有统计学意义（P<0.05）。Logistic回归分析显示PCIS降低、MODS、休克、胃肠功能障碍和腹水是脓毒症合并IAH的主要危险因素。结论：PCIS降低、MODS、休克、胃肠功能障碍和腹水的脓毒症患儿, 有发生IAH的可能, 应重点监测,以早期诊断并予及时干预治疗。     

脓毒症患儿血浆胆固醇、白细胞介素-6水平变化与病情危重度的关系

目的探讨脓毒症患儿血浆胆固醇、IL-6水平变化及其与病情危重程度的关系。方法脓毒症患儿（脓毒症组）60例，未达全身炎性反应综合征（SIRS）诊断标准的一般感染患儿40例（对照组），二组均于确诊次日晨取外周血2mL，采用全自动生化分析仪测定患儿血浆总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）水平，ELISA法测定其IL-6水平。并于确诊后即刻测心率、血压、呼吸、pa（O2）、pH、电解质、肾功能、血红蛋白等指标，进行危重症评分。危重症评分≤80分为危重症组，〉80分为非危重症组。结果脓毒症患儿HDL-C、LDL-C及TC水平均明显低于对照组（Pa〈0．01），IL-6水平明显高于对照组（P〈0．01）。危重症组脓毒症患儿HDL-C、LDL-C及TC水平均显著低于非危重症患儿（Pa〈0．01），IL-6水平明显高于非危重症组（P〈0．01）。HDL-C与危重症评分呈正相关（r=0．74 P〈0．01），与IL-6呈负相关（r=-0．66 P〈0．01）。结论胆固醇代谢紊乱参与脓毒症的发病过程，监测血浆胆固醇尤其HDL-C水平有助于判断病情的严重度及预后。     

UCP2 基因siRNA 转染对脓毒症血清诱导心肌细胞炎症反应的影响

目的 研究解偶联蛋白2 基因（uncoupling protein 2, UCP2）siRNA 干扰大鼠H9C2 心肌细胞株后对脓毒症血清诱导炎症反应的影响,探讨UCP2 在脓毒症心肌病可能的机制。方法 制备正常大鼠血清和脓毒症大鼠血清。体外培养大鼠心肌细胞株（H9C2）,随机分为空白对照组、正常大鼠血清、10%脓毒症大鼠血清刺激12 h 组（脓毒症血清组）、UCP2-siRNA 干扰+10%脓毒症大鼠血清刺激12 h 组（UCP2-siRNA+ 脓毒症血清组）、阴性siRNA 转染+10%脓毒症大鼠血清刺激12 h 组（阴性siRNA+ 脓毒症血清组）。RT-PCR 检测各组TNF-α mRNA,IL-1βmRNA 表达;免疫印迹法检测磷酸化p38MAPK（p-p38MAPK）表达和核转录因子（NF-κB）的表达。结果 UCP2-siRNA+ 脓毒症血清组 p-p38、NF-κB 表达量均较脓毒症血清组明显增高（PP结论 UCP2 参与脓毒症血清诱导的H9C2 心肌细胞p38MAPK 活性和NF-κB 与下游炎症介质的表达调控。     

尿中性粒细胞明胶酶相关脂质运载蛋白测定对危重症患儿急性肾损伤的早期诊断意义

目的 评估尿中性粒细胞明胶酶相关脂质运载蛋白（urine neutrophil gelatinase-associated lipocalin,uNGAL）对PICU患儿急性肾损伤的早期诊断价值.方法 对象是上海交通大学附属儿童医院2013年4月至6月期间PICU收治的80例危重症患儿.入PICU后连续观察72 h,根据急性肾损伤（acute kidney injury,AKI） pRIFLE标准将患儿分为AKI组15例和非AKI组65例.根据脓毒症的诊断标准将患儿分为脓毒症组31例和非脓毒症组49例,于入科6h内、24 h、48 h及72 h留取患儿尿液和血液测定uNGAL和血肌酐（serum creatinine,Scr）.比较AKI组与非AKI组、脓毒症未合并AKI组与非脓毒症非AKI组、脓毒症合并AKI组与脓毒症未合并AKI组间uNGAL水平的差异,以及AKI组Scr和uNGAL之间的相关度,绘制ROC曲线评价48 h uNGAL和Scr对危重症患儿AKI诊断的敏感性和特异性.结果 80例患儿中有13例进展为AKI.（1）AKI组6h内、24 h、48 h、72 h uNGAL[M（QR）,ng/ml]水平分别为863.00（696.00）、700.50（580.00）、365.50（285.00）、289.50（319.30）,明显高于非AKI组[20.00（106.00）、20.00 （85.30）、20.00（101.00）、20.00（36.00）] （P ＜0.01）.（2）新发展AKI组患儿uNGAL值各时间点均明显高于非AKI组,两组48 h Scr水平间差异有统计学意义.（3）脓毒症未合并AKI组uNGAL水平病初时升高,48 h后逐渐降至正常,与非脓毒症非AKI组比较差异无统计学意义.（4）脓毒症合并AKI组uNGAL水平持续明显升高,与脓毒症未合并AKI组比较差异有统计学意义（P＜0.01）.（5）48 h uNGAL和Scr的ROC曲线下面积分别为0.902（95％ CI：0.801 ～1.004）和0.874（95％ CI：0.768 ～0.981）.结论 uNGAL在儿童危重症合并AKI时较Scr提前24 ～ 48 h升高,反映疾病的严重程度,可以作为PICU患儿AKI的早期诊断标志物.     

血液系统恶性肿瘤合并脓毒症患儿的临床特点及死亡因素分析

目的血液系统恶性肿瘤合并脓毒症是儿科重症监护病房患儿死亡的重要原因之一。探寻其临床特点以及相关的死亡危险因素,有助于临床早期识别、诊断以及治疗。方法对血液系统恶性肿瘤合并脓毒症患儿进行临床特征的回顾性调查分析,并对其中严重脓毒症死亡患儿的危险因素进行Logistic回归分析。结果 36例血液系统恶性肿瘤合并脓毒症患儿中7例为脓毒症,29例为严重脓毒症。脓毒症与严重脓毒症患儿比较,小儿危重病例评分(PCIS)、碱剩余(BE)的差异有统计学意义(P均<0.05)。血液系统恶性肿瘤患儿合并脓毒症时,休克发生率高达80.56%;严重脓毒症患儿的病死率达58.62%。多因素Logistic回归分析结果显示与严重脓毒症患儿死亡相关变量为多器官功能障碍(MODS)受累脏器数、机械通气时间。结论血液系统恶性肿瘤患儿合并脓毒症时,PCIS和BE值有助于判断病情和预后。血液系统恶性肿瘤患儿合并脓毒症的休克发生率高、病死率高,MODS受累脏器数、机械通气时间是其死亡的危险因素。     

Sepsis in the newborn

Infections are the single largest cause of neonatal deaths globally. According to National Neonatal Perinatal Database (2002–03), the incidence of neonatal sepsis in India was 30 per 1000 live-births; klebsiella pneumoniae and staphylococcus aureus were the two most common organisms isolated. Based on the onset, neonatal sepsis is classified into two major categories: early onset sepsis, which usually presents with respiratory distress and pneumonia within 72 hours of age and late onset sepsis, that usually presents with septicemia and pneumonia after 72 hours of age. Clinical features of sepsis are non-specific in neonates and a high index of suspicion is required for the timely diagnosis of sepsis. Although blood culture is the gold standard for the diagnosis of sepsis, culture reports would be available only after 48–72 hours. A practical septic screen for the diagnosis of sepsis has been described and some suggestions for antibiotic use have been included in the protocol.     

儿童铜绿假单胞菌脓毒症临床特点及预后分析

目的探讨儿童铜绿假单胞菌脓毒症临床特点、高危因素及预后。方法回顾性分析16例铜绿假单胞菌脓毒症患儿的临床资料。结果儿童铜绿假单胞菌脓毒症以婴幼儿多见;临床以发热、出血性皮疹、腹泻、肝脏肿大多见;白血病、手术创伤、婴幼儿为铜绿假单胞菌脓毒症高危因素。16例患儿中痊愈11例、好转出院3例、死亡2例。治愈及好转14例中11例初始治疗抗生素对铜绿假单胞菌敏感。结论儿童铜绿假单胞菌脓毒症表现多样,白血病患儿、手术创伤、婴幼儿疑诊脓毒症时应警惕铜绿假单胞菌,合适初始抗生素治疗有利于改善预后。     

再论儿童脓毒症——如何早期识别和治疗严重脓毒症和脓毒性休克

儿童严重脓毒症、脓毒性休克是PICU中患儿的主要死亡原因之一,早期识别、及时诊断、尽早治疗是改善预后、降低病死率之关键。该文再次强调了儿童脓毒症新定义,并推荐国外的儿童脓毒症筛查方案及早期目标导向治疗(EGDT)方案,旨在指导国内儿科医师的诊断和治疗,改善严重脓毒症、脓毒性休克儿童的预后,提高生存率。     

Polymerase chain reaction in rapid diagnosis of neonatal sepsis

In a prospective study a total of hundred neonates who fulfilled the American College of Obstetrics and Gynecology's (ACOG) criteria for probable sepsis admitted to NICU of tertiary care armed forces hospital were investigated for evidence of sepsis. The investigation protocol included sepsis screen, blood culture and 1 mL of venous blood for molecular analysis by polymerase chain reaction (PCR) for bacterial DNA component encoding 16 s RNA in all cases. 100 newborns with probable sepsis were studied to evaluate the molecular diagnosis of sepsis using PCR amplification of 16 S RNA in newborns with risk factors for sepsis or those who have clinical evidence of sepsis. We compared the results of PCR with blood culture and other markers of sepsis screen (total leucocyte count (TLC), absolute neutrophil count (ANC), immature/total neutrophil count ratio (I/T ratio), peripheral blood smear, micro ESR and C reactive protein (CRP). Controls consisted of 30 normal healthy newborns with no overt evidence of sepsis. Sepsis screen was positive in 24 (24%) of cases in study group with sensitivity and specificity of 100% and 83.5% respectively. Blood culture was positive in 09(9%t) with sensitivity of 69.2% and specificity of 100%. PCR was positive in 13(13%) of cases (9% are both blood culture and sepsis screen positive and 4% are positive by sepsis screen); the sensitivity of PCR was 100% and specificity was 95.6%. Blood culture is the most reliable method for diagnosis of neonatal sepsis. Polymerase chain reaction is useful and superior to blood culture for early diagnosis of sepsis in neonates.     

Epidemiology of neonatal sepsis in South Korea

Background:  Neonatal sepsis is a severe clinical syndrome characterized by systemic signs of infection, shock and system organ failure; diagnosis is confirmed on positive culture from a normally sterile site(s). There are few reports comparing incidence, mortality, and risk factors between clinically diagnosed sepsis and that confirmed by culture.
Methods:  All infants diagnosed with early- (within first 72 h after birth) or late-onset (72 h–4 weeks after birth) neonatal sepsis between 1997 and 1999 from four neonatal centers in South Korea, were investigated.
Results:  The estimated incidence rate of neonatal sepsis during the 3 years was 30.5 per 1000 live births for clinical sepsis and 6.1 per 1000 live births for sepsis with positive culture, with case-fatality rates of 4.7% and 2.2%, respectively. When only early-onset sepsis was considered, the incidence and fatality rates were 25.1 per 1000 live births and 6.1% for clinical sepsis, and 4.3 per 1000 live births and 2.5% for culture-confirmed sepsis, respectively. For the 179 patients (185 causative organisms) of proven sepsis, Staphylococcus spp. including S. aureus were the most frequent isolates. In early-onset clinical sepsis, having very low birthweight (≤1500 g), a low Apgar score at 5 min (≤7), and being male were related to higher rates of case-fatality (relative risk: 11.3, 6.8 and 2.5, respectively)
Conclusions:  Clinical sepsis was more common than culture-confirmed sepsis and had a higher case-fatality rate. It seems prudent to take rapid and decisive steps toward better management of the high-risk group whether the sepsis is clinically diagnosed or culture confirmed.     

Sepsis in the newborn

Systemic infection in the newborn is the commonest cause of neonatal mortality. Data from National Neonatal Perinatal Database 2000 suggest thatKlebsiella pneumoniae andStaphylococcus aureus are the commonest causes of neonatal sepsis in India. Two forms of clinical presentations have been identified. Early onset sepsis, probably related to perinatal risk factors, usually presents with respiratory distress and pneumonia whthin 72 hours of age. Late onset sepsis, related to hospital acquired infections, usually presents with septicemia and pneumonia after 72 hours of age. Clinical features of sepsis are non-specific in neonates and a high index of suspicion is required for the timely diagnosis of sepsis. Although blood culture is the gold standard for the diagnosis of sepsis, reports are available after 48–72 hours. A practical septic screen for the diagnosis of sepsis has been described and some suggestions for antibiotic use have been included in the protocols.     

正五聚体蛋白3与脓毒症心血管功能障碍

脓毒症早期并发心血管功能障碍发生率较高,早期发现、及时治疗有利于降低脓毒症病死率,其中生物学标志物起着非常重要的作用.本文就相关标志物正五聚体蛋白3与脓毒症心血管功能障碍的关系作一综述.     

Coagulase-negative staphylococcal sepsis as a predictor of bronchopulmonary dysplasia

AIM: To determine whether sepsis caused by coagulase-negative staphylococci (CoNS) is a risk factor for developing bronchopulmonary dysplasia (BPD) in premature newborns. METHODS: All newborns born at < or = 30 wk of gestation at Orebro University Hospital during 1994-2001 with clinical sepsis caused by CoNS (group A, n = 22) or by other bacteria (group B, n = 17) were included and compared with premature newborns without sepsis (group C, n = 53). Clinical sepsis was defined as a positive blood culture (monoculture) plus clinical symptoms and laboratory findings. BPD was defined as treatment with oxygen > 21% for at least 28 d. RESULTS: The incidence of BPD differed between the three groups, as follows: CoNS sepsis (A) 64%, other sepsis (B) 41% and control (C) 24%. The difference between the control group and the sepsis groups was highly significant (p = 0.006). In a univariate model the crude estimates of relative risk (RR) for occurrence of BPD increased with presence of sepsis and particularly with presence of sepsis with CoNS (A: RR 2.6, 95% CI 1.5-4.6, p = 0.001; B: RR 1.7, CI 0.8-3.5, p = 0.17). When regression was performed with two additional predictive variables in multivariate models including sepsis, gestational age and mechanical ventilation (group A: RR 1.5, CI 1.1-2.0, p = 0.004; group B: RR 0.9, CI 0.6-1.4, p = 0.67), the estimates were lower. CONCLUSION: The relative risk for BPD is significantly increased in premature newborns with sepsis caused by CoNS compared with those with sepsis caused by other bacteria and compared with premature newborns with no sepsis.     

蛋白质组学在SIRS和脓毒症中的应用

脓毒症是由感染引起的全身炎症反应,是ICU中患者死亡的重要原因.如果能够实现脓毒症的早期诊断,并采取积极有效的治疗,则有望改善脓毒症的预后.蛋白质组学的方法能检测未知的蛋白质,该特点尤其适合于Sepsis研究,以期寻找到脓毒症的早期诊断的生物学蛋白标记.该文就蛋白质组学在脓毒症中的应用作一综述.