陈 勇,张 娜,范敬静,韩永平,蒋荣猛
自发性细菌性腹膜炎实验诊断研究进展
陈 勇,张 娜,范敬静,韩永平,蒋荣猛
自发性细菌性腹膜炎是肝硬化腹水患者常见且可致命的并发症,住院患者具有较高的病死率。延迟诊断和未能及时采用有效的抗生素治疗,可明显增加患者的死亡风险。因此,合理使用腹水分析,血清腹水检测以及腹水病原学检测等技术对实现该病早期诊断具有重要的临床意义。本文对自发性细菌性腹膜炎的实验室诊断进展进行综述。
自发性细菌性腹膜炎;失代偿期肝硬化;腹水;实验诊断
自发性细菌性腹膜炎(spontaneous bacterial peritonitis, SBP)是由于多种因素导致肠道菌群移位引起的腹腔感染,临床上须依据腹水多形核细胞(polymorphonuclear cell, PMN)计数≥250/mm3判断并排除继发性腹膜炎和腹腔内明确感染灶所致的腹膜炎[1]。SBP是失代偿期肝硬化伴腹水患者常见且可致命的感染性并发症,也有心源性、肾源性、恶性肿瘤、门静脉血栓、自身免疫性疾病相关的SBP的报道。SBP是肝硬化合并感染中最常见的类型,约占64.9%[2]。在门诊治疗的无症状肝硬化腹水患者中,SBP的患病率约为2.1%~3.5%[3-4],而在住院患者中的患病率可达11.2%[4]。有研究显示,肝硬化住院患者的病死率约为5.0%[5]。合并SBP的住院患者病死率可达16.0%~32.6%[5-7]。Kim 等[8]的研究显示,延迟诊断可使SBP住院患者的死亡风险增加2.70倍。而对于伴发脓毒性休克的肝硬化SBP患者,每延误恰当抗生素治疗时间1 h,死亡风险增加1.86倍[9]。因此,SBP的早期诊断具有重要的临床意义。本文从腹水分析,血清腹水检测,腹水病原学检测等方面对SBP的实验诊断进展进行综述。
1.1 腹水分析指征 Chinnock等[10]对144例腹水患者的研究显示,依靠医生的临床印象诊断SBP的敏感度为76%(95%CI:0.62~0.91),特异度为34%(95%CI:0.28~0.40),研究认为,依据临床特征和医生评估不足以诊断或排除SBP。因此,SBP的诊断不仅须要依靠特征性的临床表现,还须排除有病因明确的感染以及胃肠道穿孔、阑尾炎、憩室炎或胆囊炎等所致的继发性腹膜炎[1]。由于SBP的患病率较低[3-4],对于门诊治疗的肝硬化腹水患者,不建议进行常规腹水分析[11]。然而,对于所有肝硬化腹水的住院患者,均建议行腹水分析检测,以便早期诊断SBP。Kim等[8]的研究显示,入院12~72 h行腹水分析的患者,较入院12 h内行腹水检查的患者,死亡风险增加2.70倍。然而,在临床上只有60%左右的肝硬化腹水住院患者进行了腹腔穿刺术[12]。
1.2 腹水细胞计数 目前SBP实验室诊断的金标准是:通过手工细胞计数法测得腹水
PMN≥250/mm3,并排除其他病因所致的继发性腹膜炎[1]。但由于手工细胞计数与操作者的技术水平和实验室之间的经验不同,可能导致结果的差异。实验室广泛并大量应用于血细胞计数的自动化血细胞计数技术在检测腹水PMN方面显示出准确、可靠、快速的特征[13]。Riggio等[14]对52例肝硬化患者的112例腹水标本的研究显示,与手工计数相比,自动化血细胞计数诊断SBP的敏感度和特异度分别为100%和97.7%,而对抗生素治疗有效性的评价敏感度为91.0%,特异度为100%。
2种方法对感染控制的评价完全一致。然而,当腹水PMN计数水平较低,如在250/mm3左右时,有出现假阳性的可能[15]。而且,这一检测技术并未普遍用于腹水细胞计数中,因此目前的指南未作推荐。流式细胞术作为一种新型细胞分类计数技术,可用于肝硬化腹水患者的快速腹水细胞计数,其敏感度和特异度可达100%,特别是对腹水PMN计数在250/mm3以上的患者[16]。
1.3 腹水白细胞酯酶试纸条法 白细胞酯酶试纸条法最初是由Butani等[17]用于SBP的诊断。其原理是:腹水中活化的粒细胞酯酶、水解酯化的吡咯、释放的苯基吡咯与重氮盐发生反应,导致含偶氮染料的试纸条显示出紫色改变。白细胞酯酶试纸条法在快速检测腹水PMN计数增高方面的敏感性变异较大,但特异性较好,是一种方便、廉价、简单并可在床旁诊断SBP的检测技术[18],并具有较好的阴性预测值,其阴性结果可基本排除SBP的诊断[19]。
Rerknimitr 等[20]对200例肝硬化腹水患者的研究显示,以腹水PMN计数为参照,白细胞酯酶尿量尺法1+诊断SBP的敏感度、特异度和阴性预测值分别为88.0%、81.0%和96.0%;而白细胞酯酶尿量尺法2+诊断SBP的敏感度、特异度和阴性预测值分别为63.0%、96.0%和81.0%。在Nousbaum等[21]的一项大型多中心研究中显示,Multistix 8SG 试纸法具有较差的敏感性、阳性预测值,且不能排除感染。而Gaya等[22]对Multistix 10SG 试纸条法床旁检测与以标准的手工实验室PMN计数法为对照的研究显示,Multistix 10SG 试纸条法的敏感度、特异度、阳性预测值、阴性预测值和精确度分别是100%、91.0%、50.0%、100%和92.0%。研究认为阴性结果可排除SBP的诊断,从而避免手工PMN计数。随后的几项研究同样观察到了白细胞酯酶试纸条法诊断SBP可靠的阴性预测值[23-25]。近期Thevenot等[4]发表的一项多中心研究显示,649例肝硬化腹水患者的1402份标本中,84份标本诊断为SBP,其中,17份标本来自9例门诊患者,67份标本来自31例住院患者。以腹水PMN计数>250/mm3为参照标准,采用以“痕量”为阳性标准的新型试纸条法诊断SBP的敏感度、特异度、阳性预测值及阴性预测值分别为91.7%、57.1%、12.0%和99.1%,并且在门诊患者中,其敏感度和阴性预测值可达100%,在住院患者中分别为 89.5%和97.9%。因此研究认为白细胞酯酶试纸条法在门诊排除SBP方面快速而高效。
然而,白细胞酯酶试纸条法也存在一些不足[18],比如受腹水PMN计数水平的影响,白细胞酯酶并不特异于中性粒细胞,在很多研究中并未区分白细胞和中性粒细胞;不适用于乳糜样腹水和结核性腹膜炎的诊断。因此该法可能更适用于急诊、基层医院等设备和人员短缺的部门或机构[26]。
1.4 其他腹水检查 Dang等[27]使用流式细胞仪对123例肝硬化腹水患者的标本中检测中性粒细胞Fcγ受体I 指数,即中性粒细胞CD64指数。研究显示中性粒细胞CD64指数与腹水PMN计数呈正相关,ROC曲线下面积为 0.894,理想的诊断界值是2.02,其敏感度和特异度分别为80.49% 和93.90%,且中性粒细胞CD64指数的升高因抗生素的使用而下调。但研究数据较少,尚不适合在临床中开展。腹水乳铁蛋白可作为一项初步的筛查方法。乳铁蛋白是PMN活化的产物和标志物,利用乳铁蛋白诊断SBP的敏感度和特异度分别为95.50%和97.00%[28]。但也有学者认为,其临床应用与手工计数相比,并未显示出明显的优势[29]。
2.1 血清-腹水蛋白梯度(serum-ascites albumin gradient, SAAG) SAAG是血清白蛋白水平与腹水白蛋白水平的差值。早期研究中,由于腹水pH值降低和乳酸脱氢酶升高可见于恶性腹水、结核性腹膜炎和胰源性腹水患者中,因此,腹水pH值降低和乳酸脱氢酶升高以及二者分别联合SAAG均无法可靠的诊断SBP;而SAAG联合腹水PMN计数在SBP的诊断中较为可靠[30]。SAAG>11 g/L时为高SAAG腹水,尤其是诊断门脉高压性腹水的准确度可达96%以上[31-32]。对于高SAAG腹水患者,尚须排除心功能衰竭或布-加氏综合征等病因,而腹水总蛋白水平也须检测。当腹水总蛋白水平>25 g/L,常提示存在心源性腹水的可能[33]。而最近Wang等[34]的一项回顾性研究显示,与非肝硬化心源性腹水患者相比,心源性肝硬化腹水患者的腹水蛋白水平更低,但两者间SAAG无显著性差异。
2.2 降钙素原(procalcitonin, PCT) 在Lesinska等[35]的研究中,血清和腹水中PCT的浓度在SBP组和非SBP组间未发现显著性差异。然而,随后较大样本的研究肯定了PCT在SBP诊断中的价值。Abdel-Razik等[36]对包括52例SBP和27例非SBP的肝硬化腹水患者的研究显示,血清PCT>0.94 ng/ml,诊断SBP的敏感度和特异度分别为94.30%和91.80%。此外,腹水钙卫蛋白>445 ng/ml,诊断SBP的敏感度和特异度分别为95.40% 和85.20%。Yang等[37]对发表的7项关于PCT的研究进行的meta分析显示,血清PCT诊断终末期肝病所致SBP的敏感度为82.00%(95% CI:0.79~0.87),特异度为86.00%(95% CI:0.82~0.89),ROC曲线下面积为0.92。Cai等[2]对129例肝硬化患者的队列研究显示,在血清PCT≥2.000 ng/ml肝硬化腹水患者中,诊断SBP的敏感度和特异度分别为68.80% 和94.20%。在吴静等[38]的研究中,以血清PCT>0.462 ng/ml为参考值,诊断SBP的敏感度和特异度分别为83.70%和94.90%,ROC曲线下面积为0.95(95%CI:0.93~0.97)。因此,血清PCT对诊断肝硬化腹水患者SBP的诊断可能具有较大的临床价值。
2.3 其他炎性标志物 γ-干扰素诱导蛋白-10(interferon-gamma-induced protein 10, IP-10)属趋化因子CXC家族,又称CXCL10,由中性粒细胞、嗜酸性粒细胞、单核细胞、上皮细胞等在γ干扰素的诱导分泌,特异性活化CXCR3受体,而CXCR3受体主要表达于活化的T、B淋巴细胞、NK细胞、树突样细胞及巨噬细胞表面,体液中IP-10水平的异常可见于病毒、细菌、真菌及寄生虫等感染[39]。Abdel-Razik等[40]对425例肝硬化腹水患者的研究显示,血清和腹水IP-10在肝硬化合并SBP患者中明显升高,以1915 pg/ml为界值时,血清IP-10诊断SBP的敏感度和特异度分别为91.0%和89.0%,ROC曲线下面积为0.912;以2355 pg/ml为界值时,腹水IP-10诊断SBP的敏感度和特异度分别为92.5%和87.0%,ROC曲线下面积为0.943。此外,Lesinska 等[35]对肝硬化患者血清和腹水中巨噬细胞炎症蛋白1β(macrophage in fl ammatory protein-1 beta, MIP-1β)水平的研究显示,当以69.4 pg/ml为界值时,腹水MIP-1β诊断SBP的敏感度和特异度分别为80.0%和72.7%,ROC曲线下面积为0.770(95%CI:0.58~0.96),而血清MIP-1β水平诊断SBP的效度较低。这些炎症标志物特异性较差,且研究资料有限,限制了其临床应用。
3.1 腹水培养 腹水培养可为SBP的诊断获得病原学证据,并提供药物敏感性依据,对指导治疗具有重要价值。虽然腹穿的技术是可行的,但是在腹水PMN计数增高的患者中,至少有40%的患者腹水培养阴性[41]。国内的研究显示,SBP患者腹水培养的阳性率仅为4.6%[38]。而腹水培养阴性SBP,又称培养阴性中性粒细胞腹水,须要给予和腹水培养阳性SBP同样的治疗[42]。腹水的直接床旁接种和BACTEC培养瓶方法,较传统方法有更高的阳性率。
3.2 腹水细菌DNA检测 El-Naggar等[43]对34例腹水培养阴性无中性粒细胞增多的肝硬化患者的研究显示,腹水细菌DNA检测阳性患者发生肝肾综合征、SBP及死亡风险明显增加。Frances等[44]对226例无腹水感染的肝硬化患者,22例肝硬化并SBP患者及10例长期口服诺氟沙星的肝硬化腹水患者的比较研究中发现,无感染者腹水细菌DNA检测阳性率为34%,而在并发SBP患者中检测阳性率达100%,包括在腹水培养阴性的患者中。而Mortensen等[45]通过定量PCR检测16S rDNA的方法,对38例肝硬化患者血清及腹水中细菌DNA的研究显示,在无症状且培养阴性的SBP患者中,可发现细菌DNA的阳性率升高,但血和腹水标本检测的一致性较低,这可能提示腹水细菌DNA水平的升高,患者发生肠道菌群移位的风险增加,而对诊断SBP的临床价值有限。
3.3 其他病原体的检测 由于真菌培养、抗酸杆菌的涂片和培养,以及腹水细胞学检查等检测方法价格昂贵且阳性率低,建议临床上用于存在结核性腹膜炎、真菌性腹膜炎或恶性肿瘤风险的患者中。总之,SBP是肝硬化失代偿患者常见且重要的并发症,早期诊断及合理的抗生素治疗对改善患者临床转归具有重要意义。虽然腹水PMN计数法、腹水白细胞酯酶试纸条法、SAAG、PCT以及病原学分子生物学等实验室诊断技术具有重要的临床价值,但目前对于肝硬化腹水住院患者来说,积极的腹水分析,PMN手工计数及腹水培养仍为诊断SBP的主要手段。
[1]涂波,聂为民,赵 敏. 自发性细菌性腹膜炎诊断现状[J].传染病信息,2014,27(4):252-254.
[2]Cai ZH, Fan CL, Zheng JF, et al. Measurement of serum procalcitonin levels for the early diagnosis of spontaneous bacterial peritonitis in patients with decompensated liver cirrhosis[J].BMC Infect Dis, 2015, 15:55.
[3]Evans LT, Kim WR, Poterucha JJ, et al. Spontaneous bacterial peritonitis in asymptomatic outpatients with cirrhotic ascites[J].Hepatology, 2003, 37(4):897-901.
[4]Thévenot T, Briot C, Macé V, et al. The periscreen strip is highly efficient for the exclusion of spontaneous bacterial peritonitis in cirrhotic outpatients[J]. Am J Gastroenterol, 2016,111(10):1402-1409.
[5]Singal AK, Salameh H, Kamath PS. Prevalence and in-hospital mortality trends of infections among patients with cirrhosis: a nationwide study of hospitalised patients in the United States[J].Aliment Pharmacol Ther, 2014, 40(1):105-112.
[6]Thuluvath PJ, Morss S, Thompson R. Spontaneous bacterial peritonitis--in-hospital mortality, predictors of survival, and health care costs from 1988 to 1998[J]. Am J Gastroenterol, 2001,96(4):1232-1236.
[7]Poca M, Alvarado-Tapias E, Concepción M, et al. Predictive model of mortality in patients with spontaneous bacterial peritonitis[J].Aliment Pharmacol Ther, 2016, 44(6):629-637.
[8]Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis[J]. Am J Gastroenterol, 2014,109(9):1436-1442.
[9]Karvellas CJ, Abraldes JG, Arabi YM, et al. Appropriate and timely antimicrobial therapy in cirrhotic patients with spontaneous bacterial peritonitis-associated septic shock: a retrospective cohort study[J]. Aliment Pharmacol Ther, 2015, 41(8):747-757.
[10]Chinnock B, Afarian H, Minnigan H, et al. Physician clinical impression does not rule out spontaneous bacterial peritonitis in patients undergoing emergency department paracentesis[J]. Ann Emerg Med, 2008, 52(3):268-273.
[11]Castellote J, Girbau A, Maisterra S, et al. Spontaneous bacterial peritonitis and bacterascites prevalence in asymptomatic cirrhotic outpatients undergoing large-volume paracentesis[J]. J Gastroenterol Hepatol, 2008, 23(2):256-259.
[12]Orman ES, Hayashi PH, Bataller R, et al. Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites[J]. Clin Gastroenterol Hepatol, 2014, 12(3):496-503.
[13]Angeloni S, Nicolini G, Merli M, et al. Validation of automated blood cell counter for the determination of polymorphonuclear cell count in the ascitic fluid of cirrhotic patients with or without spontaneous bacterial peritonitis[J]. Am J Gastroenterol, 2003,98(8):844-848.
[14]Riggio O, Angeloni S, Parente A, et al. Accuracy of the automated cell counters for management of spontaneous bacterial peritonitis[J]. World J Gastroenterol, 2008, 14(37):5689-5694.
[15]Cereto F, Genescà J, Segura R. Validation of automated blood cell counters for the diagnosis of spontaneous bacterial peritonitis[J].Am J Gastroenterol, 2004, 99(7):1400.
[16]van de Geijn GJ, van Gent M, van Pul-Bom N, et al. A new flow cytometric method for differential cell counting in ascitic fluid[J].Cytometry B Clin Cytom, 2016, 90(6):506-511.
[17]Sapey T, Mena E, Fort E, et al. Rapid diagnosis of spontaneous bacterial peritonitis with leukocyte esterase reagent strips in a European and in an American center[J]. J Gastroenterol Hepatol, 2005, 20(2):187-192.
[18]Koulaouzidis A. Diagnosis of spontaneous bacterial peritonitis:an update on leucocyte esterase reagent strips[J]. World J Gastroenterol, 2011, 17(9):1091-1094.
[19]Chugh K, Agrawal Y, Goyal V, et al. Diagnosing bacterial peritonitis made easy by use of leukocyte esterase dipsticks[J].Int J Crit Illn Inj Sci, 2015, 5(1):32-37.
[20]Rerknimitr R, Rungsangmanoon W, Kongkam P, et al. Efficacy of leukocyte esterase dipstick test as a rapid test in diagnosis of spontaneous bacterial peritonitis[J]. World J Gastroenterol,2006, 12(44):7183-7187.
[21]Nousbaum JB, Cadranel JF, Nahon P, et al. Diagnostic accuracy of the Multistix 8 SG reagent strip in diagnosis of spontaneous bacterial peritonitis[J]. Hepatology, 2007, 45(5):1275-1281.
[22]Gaya DR, David BLT, Clarke J, et al. Bedside leucocyte esterase reagent strips with spectrophotometric analysis to rapidly exclude spontaneous bacterial peritonitis: a pilot study[J]. Eur J Gastroenterol Hepatol, 2007, 19(4):289-295.
[23]de Araujo A, de Barros Lopes A, Trucollo MM, et al. Is there yet any place for reagent strips in diagnosing spontaneous bacterial peritonitis in cirrhotic patients? An accuracy and cost-effectiveness study in Brazil[J]. J Gastroenterol Hepatol, 2008, 23(12):1895-1900.
[24]Koulaouzidis A, Leontiadis GI, Abdullah M, et al. Leucocyte esterase reagent strips for the diagnosis of spontaneous bacterial peritonitis: a systematic review[J]. Eur J Gastroenterol Hepatol,2008, 20(11):1055-1060.
[25]Nobre SR, Cabral JE, Sofia C, et al. Value of reagent strips in the rapid diagnosis of spontaneous bacterial peritonitis[J].Hepatogastroenterology, 2008, 55(84):1020-1023.
[26]朱龙川,朱萱. 自发性细菌性腹膜炎实验室诊断研究进展[J].实用医学杂志,2015, (18):2943-2945.
[27]Dang Y, Lou J, Yan Y, et al. The role of the neutrophil Fcγ receptor I (CD64) index in diagnosing spontaneous bacterial peritonitis in cirrhotic patients[J]. Int J Infect Dis, 2016, 49:154-160.
[28]Parsi MA, Saadeh SN, Zein NN, et al. Ascitic fluid lactoferrin for diagnosis of spontaneous bacterial peritonitis[J].Gastroenterology, 2008, 135(3):803-807.
[29]Riggio O, Marzano C, Angeloni S, et al. Do we really need alternatives to polymorphonuclear cells counting in ascitic fluid[J].Gastroenterology, 2009, 136(2):728-729.
[30]Albillos A, Cuervas-Mons V, Millán I, et al. Ascitic fluid polymorphonuclear cell count and serum to ascites albumin gradient in the diagnosis of bacterial peritonitis[J]. Gastroenterology,1990, 98(1):134-140.
[31]Runyon BA, Montano AA, Akriviadis EA, et al. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites[J]. Ann Intern Med, 1992,117(3):215-220.
[32]Uddin MS, Hoque MI, Islam MB, et al. Serum-ascites albumin gradient in differential diagnosis of ascites[J]. Mymensingh Med J, 2013, 22(4):748-754.
[33]Runyon BA. Cardiac ascites: a characterization[J]. J Clin Gastroenterol, 1988, 10(4):410-412.
[34]Wang Y, Attar BM, Gandhi S, et al. Characterization of ascites in cardiac cirrhosis: the value of ascitic fluid protein to screen for concurrent cardiac cirrhosis[J]. Scand J Gastroenterol, 2017,52(8):898-903.
[35]Lesińska M, Hartleb M, Gutkowski K, et al. Procalcitonin and macrophage inflammatory protein-1 beta (MIP-1β) in serum and peritoneal fluid of patients with decompensated cirrhosis and spontaneous bacterial peritonitis[J]. Adv Med Sci, 2014,59(1):52-56.
[36]Abdel-Razik A, Mousa N, Elhammady D, et al. Ascitic fluid calprotectin and serum procalcitonin as accurate diagnostic markers for spontaneous bacterial peritonitis[J]. Gut Liver,2016, 10(4):624-631.
[37]Yang Y, Li L, Qu C, et al. Diagnostic accuracy of serum procalcitonin for spontaneous bacterial peritonitis due to end-stage liver disease: a meta-analysis[J]. Medicine (Baltimore), 2015,94(49):e2077.
[38]吴静,蒋凤,曾藤,等. 降钙素原在晚期肝病自发性细菌性腹膜炎中的诊断价值[J]. 中国医学科学院学报,2014,36(1):37-41.
[39]Liu M, Guo S, Hibbert JM, et al. CXCL10/IP-10 in infectious diseases pathogenesis and potential therapeutic implications[J].Cytokine Growth Factor Rev, 2011, 22(3):121-130.
[40]Abdel-Razik A, Mousa N, Elbaz S, et al. Diagnostic utility of interferon gamma-induced protein 10 kDa in spontaneous bacterial peritonitis: single-center study[J]. Eur J Gastroenterol Hepatol,2015, 27(9):1087-1093.
[41]Runyon BA, Canawati HN, Akriviadis EA. Optimization of ascitic fluid culture technique[J]. Gastroenterology, 1988, 95(5):1351-1355.
[42]Sajjad M, Khan ZA, Khan MS. Ascitic fluid culture in cirrhotic patients with spontaneous bacterial peritonitis[J]. J Coll Physicians Surg Pak, 2016, 26(8):658-661.
[43]El-Naggar MM, el-SA K, El-Daker MA, et al. Bacterial DNA and its consequences in patients with cirrhosis and culture-negative,non-neutrocytic ascites[J]. J Med Microbiol, 2008, 57(Pt 12):1533-1538.
[44]Francés R, Zapater P, González-Navajas JM, et al. Bacterial DNA in patients with cirrhosis and noninfected ascites mimics the soluble immune response established in patients with spontaneous bacterial peritonitis[J]. Hepatology, 2008, 47(3):978-985.
[45]Mortensen C, Jensen JS, Hobolth L, et al. Association of markers of bacterial translocation with immune activation in decompensated cirrhosis[J]. Eur J Gastroenterol Hepatol, 2014, 26(12):1360-1366.
Research progress in laboratory diagnosis of spontaneous bacterial peritonitis
CHEN Yong, ZHANG Na, FAN Jing-jing, HAN Yong-ping, JIANG Rong-meng*
Department of Infectious Diseases, the First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China
, E-mail: 13911900791@163.com
Spontaneous bacterial peritonitis (SBP) is a common bur fatal complication in patients who developed cirrhosis with ascites, and can induce a high mortality in the in-hospital patients. Delaying diagnosis and lacking appropriate and timely antibiotic therapy can increase the risk of mortality significantly. Therefore, reasonable application of ascites fluid analysis, serum-ascites examination and ascites etiologic detecting technique are critical for early diagnosis of SBP. This article reviews the progress of laboratory diagnosis of SBP.
spontaneous bacterial peritonitis; decompensated cirrhosis; ascites; laboratory diagnosis
R575.2
A
1007-8134(2017)05-0310-05
10.3969/j.issn.1007-8134.2017.05.016
河北省医学科学研究重点课题计划(20160036);张家口市科技计划(1521072D)
075000 张家口,河北北方学院附属第一医院感染内科(陈勇、张娜、范敬静、韩永平);100015,首都医科大学附属北京地坛医院感染病科(蒋荣猛)
蒋荣猛,E-mail: 13911900791@163.com
(2017-03-11收稿 2017-09-02修回)
(本文编辑 胡 玫)