口服肠道益生菌制剂对肝硬化患者血浆脂多糖连接蛋白水平的影响及其临床意义

目的探讨失代偿期肝硬化患者使用肠道益生菌制剂前后脂多糖连接蛋白(LBP)水平变化的临床意义。方法给予肝硬化患者口服益生菌制剂,ELISA法检测血浆LBP水平,同时检测血生化指标的变化。结果肝硬化患者使用肠道益生菌制剂后LBP水平显著降低(P<0.05);血清总胆红素和天冬氨酸氨基转移酶水平显著降低(P<0.05);血浆白蛋白(ALB)水平无显著改变(P>0.05)。结论LBP水平所反映的肠源性内毒素血症是导致肝硬化患者肝功能持续受损的主要原因之一,口服肠道益生菌制剂可以降低LBP水平,部分改善肝脏生化指标。     

LBP/sCD14在评价肝硬化伴全身炎症反应综合征预后中的意义

目的了解肝硬化伴全身炎症反应综合征（SIRS）患者血脂多糖结合蛋白（LBP）、可溶性CD14（sCD14）、C反应蛋白（CRP）水平,探讨各指标预测预后的能力。方法收集肝硬化伴SIRS患者23例,肝硬化不伴SIRS患者23例,正常对照11例,动态浊度法测定血内毒素,ELISA法测定血清LBP、sCD14水平,记录CRP实验室检查结果和院内存活情况。运用ROC曲线下面积（AUC）判断指标对预后的预测能力。结果肝硬化伴SIRS患者病死率显著升高,sCD14、CRP水平显著高于肝硬化不伴SIRS患者（P〈0.05）。血LBP浓度无肝硬化组间差异无统计学意义。肝硬化伴SIRS组院内死亡患者sCD14显著高于存活患者[（1344.58±379.99）μg/L对（1045.19±318.66）μg/L,P〈0.05],与患者预后成正相关（r=0.661,P=0.024）,LBP和CRP在死亡与存活患者中的分布差异无统计学意义。肝硬化伴SIRS组sCD14预测预后的AUC为0.9,P〈0.01;LBP、CRP的AUC值均小于0.7。结论肝硬化SIRS患者血清sCD14水平显著高于不伴SIRS患者,预测肝硬化伴SIRS患者院内预后较佳。LBP、CRP预测预后能力较差。     

肝硬化患者外周血单核细胞内毒素受体表达与慢性炎症反应关系的临床意义

背景:内毒素受体在内毒素、细胞因子等介导的炎性信号转导过程中具有重要作用。目的:了解肝硬化患者外周血单核细胞(PBMC)内毒素受体的表达变化与慢性炎症反应关系的临床意义。方法:应用荧光素标记的抗人Toll样受体(TLR)4/抗人CD14单抗,以流式细胞术检测40例肝硬化患者和15名健康志愿者PBMC内毒素受体TLR4和CD14蛋白的表达;以逆转录聚合酶链反应(RT-PCR)检测内毒素受体TLR4 mRNA、CD14 mRNA和信号转导分子MyD88 mRNA的表达;以酶联免疫吸附测定(ELISA)检测血清白细胞介素(IL)-1β、IL-10和肿瘤坏死因子(TNF)-α水平;以偶氮基质显色法测定血浆内毒素水平。结果:肝硬化患者PBMC内毒素受体TLR4和CD14蛋白的表达水平显著高于对照组(P<0.05),但不同Child-Pugh分级组间差异无统计学意义;与对照组相比,PBMC内毒素受体TLR4 mRNA、CD14 mRNA和信号转导分子MyD88 mRNA的表达水平也有增高的趋势,但差异无统计学意义(P>0.05);肝硬化患者血清细胞因子IL-1β、IL-10和TNF-α水平,以及血浆内毒素水平均较对照组显著升高(P<0.05),且高内毒素水平患者内毒素受体的表达显著高于低内毒素水平患者(P<0.05),细胞因子水平也较低内毒素水平者增高。结论:肝硬化患者PBMC内毒素受体的表达明显上调,与患者的慢性炎症反应状态一致。     

慢性重型肝炎患者血清内毒素调节蛋白的水平及其临床意义

探讨内毒素结合蛋白（lipopolysaccharide binding protein、LBP）、杀菌性／通透性增加蛋白（bactericidal/permeability-increasing protein、BPI）及可溶性sCD14(soluble CD14、sCD14)水平在慢重肝患者伴肠源性内毒素血症中的临床意义。应用基质显色法和ELISA双抗体夹心法，检测24例慢重肝患者血中内毒素脂多糖（Lipopolysaccharide,LPS)、LBP、BPI和sCD14的水平，并以10例献血员和16例慢性乙型肝炎患者作为对照。结果：慢重肝患者在早期、中期、晚期，其血中LPS、LBP、BPI和sCD14的水平均明显高于慢乙肝患者及献血员；慢重肝死亡者其LPS、LBP、BPI和sCD14的水平也显著高于存活者；慢重肝患者随着病情的加重，LBP／BPI比值增大。慢重肝患者伴肠源性内毒素血症时，高水平的LBP和sCD14及相对不足的BPI，可显著提高机体对LPS的敏感性。     

慢性重型肝炎患者血浆LPS与LBP、sCD_(14)的关系

目的:探讨慢性重型肝炎(慢重肝)患者血浆内毒素(lipopolyasccharide,LPS)与内毒素结合蛋白(lipopolysaccharide binding protein,LBP)、可溶性CD_(14)(soluble CD_(14),sCD_(14))的关系。方法:应用基质显色法和ELISA双抗体夹心法,检测24例慢重肝患者血浆中LPS和LBP、sCD_(14)的水平,并以10例献血员和16例慢性乙型肝炎患者作为对照。结果:慢重肝患者在早期、中期、晚期,其血浆中LPS和LBP、sCD_(14)的水平均明显高于慢性乙型肝炎患者及献血员;慢重肝死亡者其LPS和LBP、sCD_(14)的水平也显著高于存活者。结论:慢重肝患者血浆中LBP、sCD_(14)的水平及病情与临床转归相关,可作为评估病情的严重程度与判断预后的指标。     

血浆降钙素原及内毒素水平与肝硬化伴自发性细菌性腹膜炎的关系

探讨血浆降钙素原(procalcitonin,PCT)及内毒素水平对肝硬化伴自发性细菌性腹膜炎(spontaneous bacte-rial peritonitis,SBP)的诊断价值及与病原菌分型和临床预后的关系。肝硬化腹水患者(合并SBP38例,单纯腹水51例)血浆PCT含量和内毒素水平分别采用金标兔疫层析和分光光度法检测。所有患者PCT及内毒素水平均显著高于正常,SBP组PCT阳性检出率(>10ng/ml)及内毒素水平均显著高于无SBP组(P<0.001)。G菌感染组血浆内毒素水平显著高于G~+菌感染组(P<0.01),两组PCT阳性检出率分别为100％与88.9％,差异未见显著性(P>0.05)。动态观察最初三天血浆PCT的变化对不同结局的预测性及临床疗效的指导性优于内毒素检测。动态观察PCT及内毒素水平对肝硬化伴SBP的早期诊断、病原菌初步分型、临床疗效评估和预后判断等都有重要价值。     

血清及腹水脂多糖结合蛋白检测在肝硬化自发性细菌性腹膜炎诊断中的意义

目的 检测肝硬化患者血清及腹水中脂多糖结合蛋白(LBP)的水平,探讨血清及腹水LBP检测对自发性细菌性腹膜炎(SBP)的诊断价值. 方法 将肝硬化患者分为肝硬化SBP组、腹水非SBP组、肝硬化无腹水组3组,同时将腹水非SBP组分别以有无腹痛、血白细胞计数(WBC)增高、腹痛+血WBC升高为标准分为2组,探讨LBP对临床疑诊SBP的意义.并加设阳性和阴性对照组(腹腔脓液组、健康对照组).以酶联免疫吸附法测定各组血清及腹水LBP水平;肝硬化腹水患者同时完成腹水常规、腹水培养、腹水白蛋白等检查.组间数据比较采用t检验或独立样本的非参数检验,曲线下面积(AUC)比较采用Z检验. 结果 腹腔脓液组血清及脓液LBP水平较肝硬化腹水组血清及腹水LBP水平明显增高,对比组之间的差异具有统计学意义(P＜0.01).肝硬化SBP组血清LBP水平较,腹水非SBP组及无腹水组血清LBP水平明显增高,对比组之间的差异具有统计学意义(P＜0.01);肝硬化SBP组腹水LBP水平较腹水非SBP组腹水LBP水平差异无统计学意义(P＞0.05).临床疑诊的肝硬化SBP组血清及腹水LBP水平较肝硬化腹水非SBP组血清及腹水LBP水平明显增高,对比组之间的差异具有统计学意义(中位数分别为228.00μg/ml对比80.95 μg/ml及22.50 μg/ml对比11.45 μg/ml,P＜0.05).血清LBP测定较腹水LBP测定及腹水WBC具有更高的敏感性.结论 腹腔内革兰阴性菌感染可使患者血清及体液LBP水平明显升高.肝硬化SBP患者血清LBP水平明显增高.临床疑诊SBP的肝硬化患者血清及腹水LBP明显升高,血清LBP结合腹水LBP检测能提示腹腔内感染存在,对SBP有一定的诊断价值.     

肝硬化患者血清IL-6水平与腹水发生、内毒素血症及肠道细菌的关系

明确肝硬化患者血清IL．6水平与腹水发生、内毒素血症及肠道中大肠杆菌量的关系,并探讨其可能机制。方法：37例无感染征象的肝硬化患者纳入研究,18例健康者作为对照。分别以ELISA法、鲎试验及细菌培养法检测患者及对照者血清IL．6水平、血浆内毒素浓度及肠道太肠杆菌量。结果：肝硬化患者血清IL-6水平、血浆内毒素水平显著高于健康者。肝硬化伴腹水患者血清IL．6水平、粪太肠杆菌量均显著高于无腹水者,并发现血清IL-6水平与太肠杆菌量阃存在显著相关性。结论：肝硬化伴腹水患者血清IL-6水平显著升高,肠道中革兰阴性大肠杆菌的过度生长以及由此引起的细菌移位可能是导致此细胞因子高反应的重要因素,提示肝硬化患者血清IL-6水平可作为一个细菌移位的指标。     

肝硬化患者胃液腹水胃动素水平测定的临床意义

目的:探讨胃液中胃动素的存在,腹水及血浆胃动素测定对肝硬化患者的临床意义。方法:以非平衡放射免疫法对45例肝硬化失代偿期患者进行胃液、腹水及血浆胃动素的检测。结果:胃液与腹水胃动素分别为246.22±50.34及395.32±54.22,与血浆胃动素水平、总胆红素、血肌酐及腹水量均呈正相关(各P<0.01);与血清白蛋白呈负相关(P<0.05)。按Child分级,C级组胃液、腹水胃动素较A、B级显著升高(P<0.01),提示胃液、腹水胃动素的高低与肝功能状况呈显著正相关。结论:胃液中不但存在胃动素,而且与腹水、血浆胃动素同步显著升高,此胃动素水平,对肝硬化的诊断具一定参考价值。     

老年肝硬化腹水患者血清二胺氧化酶、内毒素及D-乳酸水平及临床意义

目的 探讨老年肝硬化腹水患者血清二胺氧化酶(DAO)、内毒素及D-乳酸水平变化特点及临床意义.方法 选择2011年3月至2012年5月在该院住院治疗的病毒性肝炎肝硬化腹水患者66例作为试验组,并选择27例健康体检者作为对照组.采用酶联免疫法检测对照组及试验组患者治疗前及治疗2～4w血清DAO、内毒素及D-乳酸水平.结果 试验组患者DAO、内毒素及D-乳酸水平均显著高于对照组,差异均具有统计学意义(P＜0.05);不同Child-Pugh分级患者DAO及D-乳酸水平均显著高于对照组(P＜0.05);B级组及C级组患者内毒素水平显著高于对照组(P＜0.05);B级组血清DAO、内毒素及D-乳酸水平均显著高于A级组(P＜0.05),且显著低于C级组(P＜0.05).血清DAO与内毒素水平相关(r =0.712,P＜0.05);血清DAO与D-乳酸水平相关(r=0.633,P＜0.05);血清内毒素与D-乳酸水平相关(r=0.742,P＜0.05).除A级组内毒素水平治疗后未见明显降低外(P＞0.05),不同Child-Pugh分级患者其余各组血清DAO、内毒素及D-乳酸水平治疗后均较治疗前显著降低(P＜0.05).结论 血清DAO、内毒素及D-乳酸水平对老年肝硬化腹水患者疾病程度的判定及肝硬化腹水的发病机制的阐明具有十分重要的意义.     

Increased lipopolysaccharide binding protein in cirrhotic patients with marked immune and hemodynamic derangement

Intestinal bacterial overgrowth and translocation, both common in cirrhosis with ascites, may lead to the activation of monocytes and lymphocytes, increased levels of proinflammatory cytokines, and enhanced synthesis of nitric oxide present in cirrhosis. Bacterial endotoxin promotes the synthesis of lipopolysaccharide (LPS)-binding protein (LBP), and forms a LPS-LBP complex that binds to CD14. This study was designed to evaluate LBP levels and their correlation to the immune response and the hemodynamic status in cirrhotic patients. Plasma LBP, endotoxin, soluble CD14 (sCD14), cytokines, renin, nitrites, and systemic vascular resistance were determined before and 4 weeks after norfloxacin or placebo in 102 cirrhotic patients and 30 controls. LBP was elevated in 42% of ascitic cirrhotic patients (15.7 +/- 0.7 versus 6.06 +/- 0.5 microg/mL, P <.01). In 60% of high LBP patients, endotoxin was within normal range. Among ascitic patients, those with high LBP showed greater (P <.05) levels of sCD14, tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), nitrites + nitrates (NOx)/creatinine, and renin, and lower vascular resistance. In the cirrhotic patients with high LBP, norfloxacin normalized (P <.01) LBP (from 16.6 +/- 0.5 to 5.82 +/- 0.8 microg/mL) and sCD14; reduced the level of cytokines, NOx/creatinine, and renin; and increased vascular resistance; but lacked effect in patients with normal LBP. Portal pressure was unchanged after norfloxacin in another group of 18 cirrhotic patients with high and 19 with normal LBP. In conclusion, the subset of ascitic cirrhotic patients with marked immune and hemodynamic derangement is identified by increased LBP levels. Amelioration of these abnormalities by norfloxacin suggests the involvement of enteric bacteria or their products in the triggering of the process.     

肝硬化患者腹水中细菌DNA与相关因素的关系

目的 探讨肝硬化患者腹水中细菌DNA与血浆内毒素、肠通透性、肠道菌群等因素的关系. 方法 选取失代偿期肝硬化伴腹水患者55例,于入院当日或次日抽取腹水行腹水中细菌DNA的提取及PCR扩增,同时行腹水常规、需氧菌及厌氧菌培养检查,于入院次日测定血浆内毒素、肠通透性并进行肠道菌群分析,同时测定血常规、肝肾功能、凝血功能等生物化学指标.30例健康成年人作为正常对照,行除腹水之外的上述检查. 结果 55例肝硬化患者腹水细菌培养均为阴性,其中19例(34.55%)患者腹水中检测到细菌DNA.与细菌DNA阴性组比较,细菌DNA阳性组患者的凝血酶原活动度明显降低(t=-3.184,P=0.002),而肝功能Child-Pugh评分(t=3.224,P=0.002)和腹水白细胞计数(t'=4.088,P=0.001)明显升高.与正常对照组比较,肝硬化患者血浆内毒素水平(t=13.705,P=0.000)、尿中乳果糖/甘露醇(L/M,t'=28.568,P=0.000)和肠道肠杆菌数量(t=2.912,P=0.005)明显升高,而肠道双歧杆菌数量明显减少(t=-3.669,P=0.000).与腹水中细菌DNA相关的指标为肠道肠杆菌数量(P=0.007)和凝血酶原活动度(P=0.011).结论 肝硬化患者发生腹水细菌移位的关键因素是肠腔细菌过度生长,并与肝病的严重程度相关.     

血浆、腹水中心钠素、加压素的测定及意义

本文采用放射免疫分析法测定25例肝硬化腹水患者血浆、腹水中心钠素和加压素的水平，发现血浆，腹水中心钠素水平相当，均明显高于正常血浆水平；血浆加压素升高不明显，而腹水中加压素浓度显著高于血浆。结果提示心钠素和加压素的分泌释放异常，在肝硬化钠，水潴留及腹水形成中有一定的作用。腹水中高浓度的心钠素和加压素通过腹水回输可能起到一定的治疗作用。     

肝硬化患者血浆亮啡肽,神经肽Y含量的变化及临床意义

目的　探讨肝硬化患者血浆亮啡肽（ＬＥＮＫ）、神经肽Ｙ（ＮＰＹ）含量的变化规律及其临床意义。方法用放射免疫法检测４９例肝硬化患者血浆ＬＥＮＫ、 ＮＰＹ含量，并以１８例慢性肝炎、１４例急性肝炎和１０名健康者作对照。结果　肝硬化患者血浆ＬＥＮＫ含量显著高于正常人和急、慢性肝炎（Ｐ＜０．０５），有腹水、肝性脑病者分别显著高于无腹水和无肝性脑病者（Ｐ＜０．０５）；而血浆ＮＰＹ水平肝硬化患者明显下降（Ｐ＜０．０５），有腹水或肝性脑病者下降更明显（Ｐ＜０．０５）。结论肝硬化患者血浆ＬＥＮＫ、ＮＰＹ等内源性神经肽水平明显变化，且以有腹水、肝性脑病等严重并发症者更为明显，提示这些神经肽可能参与了肝硬化患者的高动力状态循环异常，并与腹水及肝性脑病形成有关。     

Plasma erythropoietin level in patients with cirrhosis and its relationship to the severity of cirrhosis and renal function

BACKGROUND AND AIM: The level of plasma erythropoietin (EPO) in patients with cirrhosis is controversial. It is known that overproduction of nitric oxide (NO) plays, in part, a role for the development of peripheral arterial vasodilatation in cirrhosis with portal hypertension. It has also been hypothesized that a possible interaction is noted between endogenous EPO and NO production. The current study was undertaken to evaluate the relationship between plasma EPO levels and the severity of liver disease, hemodynamic values, renal functions, and plasma nitrate/nitrite levels in patients with cirrhosis. METHODS: The authors measured the biochemistry, plasma EPO and nitrate/nitrite levels in 67 patients with cirrhosis (Child-Pugh class A in 23 and Child-Pugh class B and C in 44) and compared their values with those in 34 healthy subjects. Systemic and splanchnic hemodynamic measurements and effective renal plasma flow were obtained from cirrhotic patients. RESULTS: Plasma EPO and nitrate/nitrite levels were significantly increased in patients with cirrhosis compared with healthy subjects. Additionally, plasma EPO values were higher in cirrhotic patients with ascites or with anemia than in those without ascites or without anemia, respectively. Plasma EPO levels were positively correlated to the hepatic venous pressure gradient (HVPG) and Child-Pugh score, negatively correlated to the renal and hepatic blood flows, but were not correlated to nitrate/nitrite level and systemic vascular resistance in cirrhotic patients. Multiple regression analysis showed that HVPG and renal plasma flow were independent predictors for the elevated EPO level in cirrhotic patients. CONCLUSIONS: Plasma EPO levels were increased in patients with cirrhosis compared with those in healthy subjects. The increase in plasma EPO levels is related to the degree of portal hypertension, the severity of cirrhosis and the renal plasma flow. In contrast, the EPO levels had no correlation to the nitrate/nitrite levels and systemic vascular resistance in patients with cirrhosis.     

Procalcitonin,and cytokines document a dynamic inflammatory state in non-infected cirrhotic patients with ascites

AIM: To quantitate the simultaneous serum and ascitic fluid levels of procalcitonin and inflammatory markers in cirrhotics with and without ascites.METHODS: A total of 88 consecutive severe cirrhotic patients seen in a large city hospital liver clinic were studied and divided into two groups, those with and without ascites. Group 1 consisted of 41 cirrhotic patients with massive ascites, as demonstrated by necessity for therapeutic large-volume paracentesis. Group 2 consisted of 47 cirrhotic patients without any clinically documented ascites to include either a recent abdominal computed tomography scan or ultrasound study. Serum and ascitic fluid levels of an array of inflammatory markers, including procalcitonin, were measured and compared to each other and a normal plasma panel (NPP).RESULTS: The values for inflammatory markers assayed in the serum of Groups 1 and 2, and ascitic fluid of the Group 1. The plasma levels of the inflammatory cytokines interleukin (IL)-2, IL-4, IL-6, IL-8, interferon gamma (IFNγ) and epidermal growth factor (EGF) were all significantly greater in the serum of Group 1 as compared to that of the serum obtained from the Group 2 subjects (all P < 0.05). There were significantly greater serum levels of IL-6, IL-8, IL-10, monocyte chemoattractant protein-1, tumor necrosis factor-α, vascular endothelial growth factor and EGF when comparing Group 2 to the NPP. There was no significant difference for IL-1A, IL-1B, IL-2, IL-4 and IFNγ levels between these two groups. Serum procalcitonin levels were increased in cirrhotics with ascites compared to cirrhotics without ascites, but serum levels were similar to ascites levels within the ascites group. Furthermore, many of these cytokines, but not procalcitonin, demonstrate an ascites-to-serum gradient. Serum procalcitonin does not demonstrate any significant difference segregated by liver etiology in the ascites group; but ascitic fluid procalcitonin is elevated significantly in cardiac cirrhosis/miscellaneous subgroup compared to the hepatitis C virus and alcoholic cirrhosis subgroups.CONCLUSION: Procalcitonin in the ascitic fluid, but not in the serum, differentiates between cirrhotic subgroup reflecting the dynamic interplay of ascites, bacterial translocation and the peri-peritoneal cytokine.     

腹水超滤浓缩回输腹腔术治疗肝硬化顽固性腹水疗效分析

目的 探讨腹水超滤浓缩回输腹腔术治疗肝硬化顽固性腹水的疗效。方法 将56例肝硬化顽固性腹水患者随机分为2组,均给予保肝、利尿及抗病毒治疗。在此基础上,对治疗组行腹水超滤浓缩回输腹腔术加小剂量人血白蛋白静脉滴注(静滴)(每滤出1000ml腹水,静滴人血白蛋白4g),对对照组行大量放腹水加大剂量人血白蛋白静滴(每抽出1000ml腹水,静滴人血白蛋白8g)。结果 术后第14天,治疗组患者24h尿量、血清ALB水平均高于对照组(P均<0.05),且治疗组总有效率高于对照组(P<0.05)。结论 腹水超滤浓缩回输腹腔术是一种安全有效的治疗肝硬化顽固性腹水的方法。     

上皮细胞钙粘蛋白与β-连环蛋白在恶性腹水鉴别诊断中的价值

目的通过检测不同病因腹水中上皮细胞钙粘蛋白（E—cadherin）和β-连环蛋白（β-catenin）的含量,探讨其在鉴别良、恶性腹水性质中的意义。方法收集41例来自临床上已确诊患者的腹水标本,分为结核组（5例）、肝硬化组（11例）和恶性肿瘤组（25例）3组,采用酶联免疫吸附法（ELISA）检测E—cadherin和β—catenin的含量。结果结核性腹水E—cadherin水平为（7．57±0．48）ng／L,肝硬化腹水水平为（8．18±0．81）ng／L,恶性腹水水平为（9．35±1．84）ng／L。结核性腹水β-catenin水平为（0．76±0．13）ng／L,肝硬化腹水为（0．93±0．06）ng／L,恶性腹水为（1．67±1．16）ng／L。恶性腹水E—cadherin和β-catenin水平明显高于结核性腹水和肝硬化性腹水（P〈0．05）,两者水平在结核性腹水和肝硬化腹水之间比较差异无显著性（P〉0．05）。相关分析表明E—cadherin和β—catenin的表达具有正相关性（P〈0.01,r=0．479）。结论E-cadherin和β-catenin与肿瘤的浸润和转移有关,恶性腹水中两者的水平显著增高。E—cadherin和β—catenin对良、恶性腹水鉴别诊断有重要价值。     

High interleukin-6 production within the peritoneal cavity in decompensated cirrhosis and malignancy-related ascites

Abstract: To assess the diagnostic and prognostic value of interleukin-6, interleukin 1β, and tumor necrosis factor-α assays in plasma and ascites, we measured these cytokines in eight patients with malignancy-related ascites and 32 patients with decompensated cirrhosis. Five patients had an episode of bacterial peritonitis, during which one or more ascitic fluid samples were analyzed. Interleukin-6 and tumor necrosis factor-α were not significantly different between the cirrhotic and the malignant groups: ascitic interleukin-6 13 816±15 314 vs 28 138±23 403 pg/ml, plasma interleukin-6 542±719 vs 559±604 pg/ml; ascitic tumor necrosis factor-α 19±50 vs 12±31 pg/ml, plasma tumor necrosis factor-α 3.4±8.2 vs 6.1±13.8 pg/ml. During an episode of bacterial peritonitis there was a significant increase only in ascitic interleukin-6 (133 268±99 743 pg/ml), which declined after antibiotic treatment. None of the parameters was associated with 6-month survival (11 of the 40 patients died within 6 months). There was a correlation (r=0.675; p=0.002) between plasma interleukin-6 levels and the Child-Pugh score in patients with cirrhosis, but not with the etiology of the liver disorder. Plasma interleukin-6 levels correlated with IgA levels (r=0.649; p=0.004) but not with C reactive protein, sedimentation rate, fibrinogen, IgM or IgG. These results do suggest that interleukin-6 is produced within the peritoneal cavity in hepatic and malignant ascites. There is a sharp increase in the local production of interleukin-6 during an episode of bacterial peritonitis. This increase was not detectable for tumor necrosis factor-α. The physiological meaning of this over-production of locally generated cytokines and whether it relates to the poor prognosis of patients with cirrhosis and infectious disorders remain to be assessed.     

Bactericidal and opsonic activity of ascitic fluid from cirrhotic and noncirrhotic patients

Cirrhotic patients with ascites are highly susceptible to spontaneous bacterial peritonitis. Patients with ascites due to causes other than cirrhosis very seldom develop peritonitis. The antibacterial activity of these ascitic fluids is not known. The present study was undertaken to evaluate the bactericidal and opsonic activity in ascitic fluid from patients with and without cirrhosis and in normal (nonascitic) peritoneal fluid. Normal peritoneal fluids of 20 control subjects and ascitic fluids of 22 patients with noncirrhotic ascites all had normal bactericidal activity. The bactericidal activity of ascitic fluid was diminished in all 25 patients with cirrhosis (P less than 0.00005 by Fisher's exact test). Similar results were found when opsonic activity was evaluated. Complement and immunoglobulin concentrations in cirrhotic ascites were significantly lower than those in the other two groups. The present study demonstrates that noncirrhotic ascitic fluid has antibacterial activity similar to normal peritoneal fluid, whereas cirrhotic ascitic fluid has a marked reduction of both bactericidal and opsonic activities. These defects may explain the high incidence of peritonitis in cirrhotic patients.