CA／PEI及CA／HPC亲和膜去除肝硬化腹水中内毒素对比研究

目的观察醋酸纤维素／聚乙烯基亚胺（CA／PEI）及醋酸纤维素／疏水阳离子（CA／HPC）亲和膜对肝硬化腹水中内毒素的去除效果。方法以CA为亲和基质,分别交连PEI及HPC,制备CA／PEI及CA／HPC亲和膜;采用动态吸附法,比较吸附前后肝硬化腹水中内毒素、白蛋白、免疫球蛋白（IgG、lgA、IgM）、离子（K＆^＋、Na^＋、Cl^-）及胆红素浓度的变化。结果两种亲和膜吸附前后腹水中的内毒素浓度最著降低（P〈0．01）;腹水中的白蛋白、免疫球蛋白、电解质浓度过膜前后无明显变化;CA／PEI亲和膜能显著降低腹水中的胆红素的浓度。结论两种亲和膜均能有效吸附肝硬化腹水中的内毒素,对腹水中的白蛋白、免疫球蛋白、电解质无明娃截留,CA／PEI亲和膜可同时有效吸附腹水中的胆红素,两种亲和膜均可应用于肝硬化白体腹水回输治疗。     

CA／PEI亲和膜去除肝硬化腹水中内毒素的研究

目的观察CA／PEI亲和膜对肝硬化腹水中内毒素的去除效果。方法以醋酸纤维素（CA）为亲和基质，交联聚乙烯基亚胺（PEI），制备CA／PEI亲和膜；采用动态吸附法，比较吸附前后肝硬化患者腹水中内毒素、白蛋白、免疫球蛋白（IgG、IgA、IgM）及离子（K^＋、Na^＋、Cl^-）浓度的变化。结果CA／PEI亲和膜吸附后腹水中的内毒素浓度显著降低（P〈0．01）；腹水中的白蛋白、免疫球蛋白、电解质浓度过膜前后无明显变化。结论CA／PEI亲和膜能有效吸附肝硬化腹水中的内毒素，对腹水中的白蛋白、免疫球蛋白、电解质无明显截留，可应用于肝硬化自体腹水回输的治疗。     

亲和膜色谱用于去除腹水中胆红素的研究

目的观察不同的亲和膜色谱对腹水中胆红素的清除效果。方法以醋酸纤维素为亲和基质,分别交连聚赖氨酸、季铵盐和聚乙烯基亚胺制备三种亲和膜,采用动态吸附法处理腹水,比较吸附前后肝硬化腹水中胆红素、白蛋白和免疫球蛋白（IgG、IgA、IgM）浓度的变化。结果三种亲和膜吸附前后腹水中的胆红素浓度显著降低（P〈0．01）,其中,醋酸纤维素／聚赖氨酸膜吸附效果最好,可达60．69％;腹水中的白蛋白、免疫球蛋白浓度过膜前后无明显变化。结论三种亲和膜均能有效地吸附肝硬化腹水中的胆红素,对腹水中的白蛋白和免疫球蛋白无明显截留;在肝硬化腹水中胆红素浓度较高时,用其可降低胆红素水平,使腹水回输治疗更有益。     

中药联合腹水超滤浓缩回输法治疗肝硬化顽固性腹水的临床研究

目的：观察中药联合腹水超滤浓缩回输法治疗肝硬化顽固性腹水的疗效。方法：选择肝硬化顽固性腹水住院患者62例，随机分为两组，治疗组32例，采用中药＋腹水超滤浓缩回输＋基础治疗；对照组30-ff0，采用腹水超滤浓缩回输＋基础治疗。疗程均为1个月．腹水超滤浓缩回输的频率为2周1次，1次超滤的腹水为3000ml-8000ml，观察治疗前后患者的体重、腹围、24小时尿量、血浆白蛋白、腹水白蛋白、门脉主干的血流动力学变化及患者血浆和腹水中内毒素水平的变化。结果：两组患者的临床症状均得到较好改善，患者体重及腹围显著下降，24小时尿量增加，血浆及腹水中蛋白量增加，治疗组患者门静脉、脾静脉内径及血流量、血浆中内毒素水平较治疗前显著下降，对照组患者则无明显改善，两组比较差异有显著性意义（P〈0．05）；治疗组患者腹水Ⅰ级消退者18例，占56．3％，对照组只有4例，占13.3％，两组比较差异有显著性意义（P〈0．05）。结论：中药联合腹水超滤浓缩回输治疗肝硬化顽固性腹水有较好疗效，其作用机制可能与改善患者血浆内毒素水平有关。     

肝硬化患者血清CA19-9和CA125检测的临床意义

目的探讨肝硬化患者血清CA19-9和CA125水平浓度的变化及可能的意义。方法肝硬化患者67例，其中肝硬化无腹水患者37例，肝硬化伴腹水患者30例，检测所有患者血清CA19-9和CA125水平。结果两组肝硬化患者血清CA19-9和CA125水平浓度均明显高于正常人。肝硬化合并腹水患者血清CA19-9和CA125水平显著高于无腹水患者（P〈0．01），经治疗腹水消退后，血清CA19-9和CA125水平明显下降（P〈0．01）。结论肝硬化患者血清CA19-9和CA125水平升高与腹水的存在有关。     

肝硬化腹水患者腹水浓缩回输治疗前后血浆及腹水中内毒素变化

目的：研究腹水浓缩回输对肝硬化腹水患者血浆及腹水中内毒素的影响及其与临床预后的关系。方法：用鲎试剂基质偶氮显色定量法，测定30例肝硬化腹水患者腹水浓缩回输前后血浆及腹水内毒素含量，观察1个月后腹水复发的情况。结果：治疗后患者腹水内毒素含量较治疗前降低，但无统计学意义（P〉0．05）；治疗后有效者23例，其血浆内毒素水平较治疗前显著下降（P〈0．01）；而无效者7例则无明显下降（P〉0.05）。结论：血浆内毒素水平是影响肝硬化腹水患者预后的重要因素之一。     

利用血液透析机进行腹水浓缩环注治疗肝硬化顽固性腹水114例疗效分析

目的探讨腹水浓缩环注治疗肝硬化顽固性腹水的疗效。方法利用血液透析装置对114例肝硬化顽固性腹水患者进行203次腹水浓缩环注(腹腔-腹腔)治疗,观察治疗前后症状、体征、尿量及血清白蛋白、肌酐、尿素氮、电解质的变化,并分析其疗效。结果114例患者共治疗203次,平均每次超滤腹水5560±2235毫升;治疗前腹胀者占98.03%(199/203),治疗结束后腹胀减少至4.93%(10/203,P<0.01)。治疗前呼吸困难占60.01%(122/203),治疗后减至0.99%(2/203,P<0.0l),每次治疗后尿量增至1500ml/日以上者占59.11%(121/203);治疗结束后血清总蛋白及白蛋白浓度有所增高,肌酐、尿素氮水平下降,电解质浓度无明显变化。治疗结束观察3个月时,显效率54.39%(62/114),有效率35.09%(40/114),总有效率89.48%(102/114)。结论利用血液透析机进行腹水浓缩环注治疗肝硬化顽固性腹水适应症广,副作用少,安全有效。     

超滤浓缩回输治疗肝硬化首次大量腹水疗效分析

目的观察超滤浓缩回输治疗肝硬化首次大量腹水临床疗效。方法随机设立常规组与试验组,分析治疗前后总有效率,症状体征、平均住院天数、平均总住院费;电解质、白蛋白水平变化,判断疗效。结果试验组与常规组总有效率相当(P0.05);但试验组平均住院天数及总住院费较常规组显著减少(P0.01);电解质变化方面两组在治疗前后差异无显著意义;白蛋白水平在两组治疗前后均见明显升高(P0.01)。结论腹水超滤浓缩回输应用于肝硬化并首次大量腹水较常规治疗有明显优势,可明显缩短住院时间,降低住院费用,减轻患者经济负担,操作简便易行,疗效确切。     

肝硬化患者CAl25检测的临床意义

目的 观察肝硬化患者血清肿瘤标志物CAl25的变化与腹水的关系，以探讨其升高在肝硬化中的临床意义。方法 以40例健康对照组及82例住院的肝硬化病人为研究对象，检测其全部血清及部分腹水(10例)CAl25水平。结果肝硬化组血清CAl25水平显著高于正常对照组，其中肝硬化组男女无性别差异，腹水组血清CAl25显著高于无腹水组，大量腹水者显著高于中少量腹水者，腹水中CAl25浓度高于血清浓度，相关性分析显示血清CAl25与Child分级、总胆红素水平呈正相关，与白蛋白、白／球比值呈负相关。结论 血清CAl25在肝硬化时可明显升高，在腹水患者更显著，是诊断有无腹水的一个敏感指标。     

腹水超滤浓缩腹腔回输治疗难治性腹水的疗效

目的探讨应用WLFHY-500型伟力腹水超滤浓缩回输系统行腹腔回输治疗难治性腹水的临床疗效及对肝肾功能的影响.方法常规进行腹腔穿刺与超滤回输系统连接形成抽吸-超滤-浓缩-回输状态对各类顽固性腹水进行治疗.结果共治疗36例,61次.治疗后的患者在体重、腹围、腹压、24 h尿量方面与治疗前比差异有显著性（P＜0.01）.腹水浓缩回输前后血尿素氮、谷丙转氨酶及总胆红素没有变化（P＞0.05）,血浆总蛋白、白蛋白增加（P＜0.01）,血肌酐下降（P＜0.01）.超滤浓缩后的腹水较超滤前腹水中的总蛋白、胆红素增加（P＜0.01）,电解质无变化（P＞0.05）.临床总有效率为78.57%.结论本组资料表明腹水超滤浓缩行腹腔回输是一种安全可靠、简便有效的方法.     

Plasma endotoxin concentrations in patients with alcoholic and non-alcoholic liver disease: reevaluation with an improved chromogenic assay

Plasma endotoxin concentration was measured in 85 patients with alcoholic liver disease (alcoholic cirrhosis (n = 64), alcoholic hepatitis without cirrhosis (n = 11), fatty liver (n = 10), and in patients with non-alcoholic cirrhosis (n = 15]. Endotoxin concentration was determined with an improved chromogenic substrate assay, using individual standard curves for each plasma sample. In patients with alcoholic cirrhosis the mean endotoxin concentration was significantly higher than in patients with non-alcoholic cirrhosis (p less than 0.05). In addition, distinctly higher endotoxin concentrations (greater than 20 pg/ml) were more frequently observed in patients with alcoholic cirrhosis than in non-alcoholic cirrhosis (34.4 vs. 14.3%, p less than 0.05). Mean endotoxin concentration was not significantly higher in cirrhotics with ascites or esophageal varices as compared with the subgroup without ascites or esophageal varices. The endotoxin concentration did not correlate with serum bilirubin, prothrombin concentration or serum enzyme activities. In patients with alcoholic liver disease, however, endotoxin concentration revealed a negative correlation (p less than 0.05) with the concentration of high density lipoprotein cholesterol. On admission endotoxin concentrations in alcoholics with fatty liver were similarly elevated as observed in alcoholic cirrhosis. In six out of 12 patients with fatty liver or alcoholic hepatitis, in whom a second sample of plasma was investigated after 6 to 8 days, endotoxemia was no longer detectable; in the remaining patients, the endotoxin concentration decreased markedly. The results indicate that, irrespective of the stage of liver disease, alcohol abuse favours the development of endotoxemia. They support the hypothesis that gut-derived endotoxins might play a role in the initiation and aggravation of alcohol-induced liver disease.     

Endotoxin levels in cirrhotic rats with sterile and infected ascites.

Endotoxin levels were measured in sterile and bacterially infected ascites in a rat model of phenobarbital and carbon tetrachloride induced cirrhosis was used. An improved chromogenic substrate assay was used to measure endotoxin. All rat ascites specimens were positive for endotoxin. In culture-negative ascites (n = 8), it ranged from 0.05 EU/ml to 0.14 EU/ml (0.08 +/- 0.04 EU/ml, mean +/- SD) (Escherichia coli 0111:B4 endotoxin was used as a reference). In culture-positive ascites (premortem n = 3, postmortem n = 1), it ranged from 0.78 EU/ml to 1.8 EU/ml (1.29 +/- 0.59 EU/ml, mean +/- SD). All rats with premortem culture-positive ascites died within two days. This model is useful to study ascites endotoxin levels. In this study, increasing levels of ascites endotoxin correlated with spontaneous bacterial peritonitis and death.     

肝素涂层体外循环管道中聚乙烯亚胺的作用研究

目的: 探讨聚乙烯亚胺(PEI)的浓度、平均相对分子量对涂层肝素的影响,筛选出合适的各种底物的浓度及反应条件,优化涂层工艺。方法: 将PEI的平均相对分子量（3 000、10 000、20 000）和质量浓度（1 g/dl、2 g/dl、5 g/dl）交叉组合分为9个组,制成PEI-戊二醛-肝素涂层体外循环管道。利用红外光谱对结合肝素的表征定性,用甲苯胺蓝分光光度法测量肝素的结合含量。结果: 通过PEI-戊二醛-肝素涂层体外循环管道肝素的结合量,受PEI的分子量及浓度的影响,最适质量浓度及平均相对分子量分别为2 g/dl和20 000。结论: 各组肝素涂层材料肝素的浓度随PEI平均相对分子量的递增而增加,在一定范围内,PEI的浓度与肝素的含量呈正相关,浓度过高或过低均不利于肝素的结合。     

肿瘤标志物和血清腹水白蛋白梯度在恶性腹水诊断中的价值

目的 探讨肿瘤标志物和血清腹水白蛋白梯度(SAAG)在恶性腹水诊断中的应用价值.方法 回顾性研究2005年1月至2008年1月收治的114例腹水患者,根据腹水病因分为恶性腹水组39例和良性腹水组105例(其中结核性腹水12例、无菌性肝硬化腹水93例).分析腹水和血清癌胚抗原(CEA)、糖链抗原(cA)19-9、CA125和SAAG在良、恶性腹水中分布的差异,并构建受试者工作(ROC)曲线.结果 在恶性和良性腹水患者中均检出肿瘤标志物.恶性腹水患者的血清CEA和CA19-9、腹水CEA和CA19-9均明显高于良性腹水患者(P<0.05).恶性腹水患者的SAAG明显低于肝硬化腹水患者(P<0.05),而与结核性腹水患者差异无统计学意义(P>0.05).恶性腹水患者的血清和腹水CA125与良性腹水患者差异均无统计学意义(P>0.05).腹水CEA、CA19-9和SAAG的曲线下面积分别为0.79、0.82和0.85;准确度最高的临界值分别是1.45 U/L、19.50 U/L和13.50 g/L,敏感度和特异度分别是66.7%和78.1%、74.4%和84.8%及82.9%和84.6%.联合检测价值最好的组合为SAAG和腹水CA19-9,其敏感度和特异度为61.54%和97.14%.结论 通过ROC曲线寻找最佳的生化指标组合鉴别良、恶性腹水是可行的.     

Elevation of serum and ascites cancer antigen 125 levels in patients with liver cirrhosis

BACKGROUND AND AIM: Serum cancer antigen (CA) 125 elevation has been reported in patients with liver disease, but it is poorly characterized. The present study aimed to evaluate the range of serum and ascitic CA 125 levels in patients with liver cirrhosis and to explore possible factors associated with CA 125 elevation. METHODS: A total of 70 patients were studied. Group I consisted of 30 patients with liver cirrhosis with or without ascites. Group II consisted of 30 patients with digestive malignant tumors with or without ascites. Group III consisted of 10 patients with benign ascites. The CA 125 levels were measured in the serum of all patients and also simultaneously in the ascitic fluid of 15 patients. RESULTS: Serum CA125 levels in 80% of (24/30) patients from group I were elevated, particularly in those with ascites, irrespective of the etiology of cirrhosis. Serum CA 125 levels were correlated with Child-Pugh scores (r = 0.38), but not significantly (P = 0.06). All patients from group II with ascites and from group III had elevated serum CA 125 levels, but there was no difference in the serum CA 125 levels between patients with ascites from group I (275 +/- 175 U/mL), group II (368 +/- 190 U/mL) or group III (396 +/- 287 U/mL), nor was there a significant difference in ascitic CA 125 levels (P > 0.05). The levels of serum CA 125 (198 +/- 108 U/mL) were lower than, but correlated with that of ascites (460 +/- 234 U/mL, r = 0.58, P = 0.026). The elevation of serum CA 125 accompanied by abnormalities of other tumor markers was more common in malignant ascites than in benign ascites (90% compared with 6%, P < 0.05). CONCLUSION: The elevation of serum CA 125 is common in patients with liver cirrhosis. It is related to the presence of ascites, and possibly to the insufficiency of liver function, but not the etiology of cirrhosis and ascites. Serum CA 125 probably comes from ascites. It usually predicts benign disease if the elevation of serum or ascites CA 125 is not accompanied by the abnormalities of other tumor markers.     

Cancer antigen 125: a sensitive marker of ascites in patients with liver cirrhosis

OBJECTIVE: Cancer antigen 125 (CA 125) is a high molecular mass glycoprotein, usually used for monitoring the course of epithelial ovarian cancer. Recently it has been shown that liver cirrhosis is associated with increased levels of CA 125, particularly in the presence of ascites. The aim of this study was to evaluate CA 125 as a marker for the detection of ascites in patients with chronic liver disease. METHODS: A total of 170 patients were studied. All had ultrasound scanning for detection of ascites. Group I consisted of 123 patients with chronic liver disease without ascites; whereas group II consisted of 47 patients with chronic liver disease with ascites. CA 125 levels were measured in all patients and also simultaneously in the ascitic fluid of 31 patients from group II. RESULTS: Of 47 patients, 46 (97.8%) of group II had elevated serum levels of CA 125 (mean 321 +/- 283 U/ml) as compared with only nine of 123 (7.3%) patients of group I [mean 13 +/- 15 U/ml]), p < 0.001. The mean CA 125 concentration in the ascitic fluid of 31 cirrhotic patients (group II) was 624 +/- 397 U/ml and was always higher than corresponding serum levels (p < 0.01). Serum CA 125 levels correlated with the amount of ascitic fluid (r = 0.78). A profound decrease in serum CA 125 concentration was noted 2-3 and 10 days after large volume paracentesis. CA 125 was more sensitive and preceded ultrasonography in detection of ascites in few cirrhotic patients. CONCLUSIONS: CA 125 is a highly sensitive marker to detect ascites in patients with liver cirrhosis. This marker may be useful to detect small to moderate amounts of ascitic fluid in cirrhotic patients when physical examination is difficult or equivocal for ascites.     

Endotoxin-induced ascites formation in the rat: partial mediation by platelet-activating factor

Systemic endotoxemia has been observed in patients with acute and chronic liver failure, and bacterial endotoxin is known to increase vascular permeability. We investigated in the normal rat the effects of intraportal endotoxin administration and the possible mediation of these effects by platelet-activating factor. Injection of endotoxin lipopolysaccharide (10 and 25 mg per kg) in the rat resulted in rapid ascites formation, as well as systemic hypotension, hemoconcentration and acute erosions of the gastrointestinal mucosa. These effects were significantly attenuated by pretreatment with L652,731 and CF-3988, specific platelet-activating factor antagonists. Administration of 25 mg per kg endotoxin also resulted in significant elevations of platelet-activating factor biosynthesis in vitro by samples of duodenum, liver and lung. The effects of endotoxin were mimicked by intraportal infusion of platelet-activating factor (50 ng per kg per min), which induced ascites and gastrointestinal lesions. Platelet-activating factor reduced circulating plasma volume and increased peritoneal permeability to albumin as assessed by the ascites to plasma ratio of labeled albumin. These results, therefore, support a role for platelet-activating factor in mediating endotoxin-induced ascites and gastrointestinal erosions.