血清腹水白蛋白梯度的临床应用进展

血清腹水白蛋白梯度(serum ascites albumin gradient,SAAG)是血清白蛋白与同日内测得的腹水白蛋白之间的差值,是间接反映门静脉压力的指标。以SAAG≥11 g/L和SAAG11 g/L将腹水分为门脉高压性和非门脉高压性,可用于腹水的病因诊断。近年来研究表明,SAAG在预测食管静脉曲张和肝性脑病的严重程度方面有一定的价值。     

血清-腹水白蛋白梯度与食管-胃底静脉曲张破裂出血的关系

目的 探讨血清-腹水白蛋白梯度（Serum-ascites albumin gradient,SAAG）与门脉高压的关系,评价SAAG对预测门脉高压性食管-胃底静脉曲张破裂出血的价值.方法 测定29例肝硬化腹水患者SAAG值并行胃镜检查以了解有无食管-胃底静脉曲张,以11 g/L为界将29例患者分为高SAAG组及低SAAG组,采用Pearson相关分析法分析SAAG与食管-胃底静脉曲张之间的关系.29例患者中并发食管-胃底静脉曲张破裂出血者8例,非出血者21例,测定两组患者的SAAG值并进行比较.结果 26例高SAAG患者中17例有食管-胃底静脉曲张,而3例低SAAG患者均无食管-胃底静脉曲张.SAAG与食管-胃底静脉曲张存在正相关关系（r=0.40,P＜0.05;r=0.84,P＜0.01）;8例出血组患者其SAAG值为（24.24±7.18）g/L,21例非出血组患者其SAAG值为（18.27±6.06）g/L,两组比较差异有显著性（P＜0.05）.结论 SAAG与门脉压力密切相关且对预测门脉相关性食管-胃底静脉出血有一定临床价值.     

血清腹水白蛋白梯度对食管胃底静脉曲张破裂出血的预测价值

目的 筛选食管胃底静脉曲张破裂出血的危险因素,为预测曲张静脉破裂出血提供更为经济且创伤更小的手段。方法 选取诊断明确的肝硬化腹水患者108例,肝硬化合并原发性肝癌患者60例。追踪随访1年,观察其发生食管胃底静脉曲张破裂出血的情况,并运用统计学方法进行分析。结果 单因素非条件Logistic回归分析显示腹水白蛋白、血清腹水白蛋白梯度(SAAG)、血小板、部分凝血活酶时间(APTT)、门静脉宽度、脾脏长度和厚度是危险因素,年龄和血白蛋白是保护因素。多因素分析显示SAAG、APTT和门静脉宽度是独立危险因素,OR值分别为3.559、2.468和2.608。构建受试者工作特征曲线后,SAAG取值18.50 g/L时为最佳临界值,敏感度和特异度分别为96.3％和56.3％。结论 SAAG对预测食管胃底静脉曲张破裂出血具有较好的价值。     

血清-腹水白蛋白梯度与肝硬化食管胃底静脉曲张破裂出血关系的Meta分析

目的探讨血清-腹水白蛋白梯度(SAAG)与肝硬化食管胃底静脉曲张破裂出血之间的关系。方法检索Pub Med、Embase、the Cochrane Library、万方、维普及CNKI数据库于2001年1月-2015年6月发表的所有有关SAAG与肝硬化食管胃底静脉曲张出血的中文文献,每篇文献均需设立出血组和未出血组。应用加强观察性流行病学研究报告质量为参考标准评价文献质量。合并各文献出血组和未出血组SAAG均数及标准差。采用Meta-Analyst软件计算每篇文献中出血组和未出血组SAAG标准化均值差(SMD)并进行Meta分析,多组间计数资料比较采用行×列χ2检验。结果共有13篇文献符合纳入标准。出血组SAAG为(22.54±4.69)g/L,未出血组SAAG为(15.91±4.20)g/L。异质性检验提示存在显著的异质性(Q=100.735,I2=89.065,P0.001),出血组SAAG值显著高于未出血组,两组SAAG值差异有统计学意义(SMD=1.970,95%可信区间:1.425~2.515,P0.001)。根据SAAG水平分为SAAG15 g/L、15 g/L≤SAAG≤19.9 g/L和SAAG≥20 g/L 3组,随着SAAG水平的升高,3组发生静脉曲张破裂出血者的比例也逐渐升高,且差异有统计学意义(χ2=111.702,P0.001)。结论 SAAG与肝硬化食管胃底静脉曲张破裂出血存在密切关系。出血组SAAG水平显著高于未出血组。SAAG有望成为预测肝硬化食管胃底静脉曲张破裂出血的一种有价值指标。     

血清-腹水白蛋白梯度对失代偿期乙型肝炎肝硬化患者发生EVB风险的预测价值

目的 研究血清-腹水白蛋白梯度(SAAG)预测失代偿期乙型肝炎肝硬化患者并发食管静脉曲张破裂出血(EVB)的临床价值.方法 2017年4月～2019年10月我院收治的失代偿期乙型肝炎肝硬化患者84例,根据是否发生EVB分组,计算SAAG和校正的SAAG值.采用Logistic多因素分析患者并发EVB的独立影响因素,采用...     

乙型肝炎肝硬化患者血清-腹水白蛋白梯度与食管静脉曲张程度的关系

目的探讨乙型肝炎肝硬化患者食管静脉曲张与血清-腹水白蛋白梯度(SAAG)的关系。方法检测67例乙型肝炎肝硬化患者SAAG和行内镜检查了解食道下段静脉曲张情况。结果 67例乙型肝炎肝硬化患者SAAG均大于11g/L,最高可达33g/L。根据SAAG水平,将患者分为11～l4.9g/L、15～19.9g/L和20g/L组,发现SAAG越高,其发生静脉曲张(x2=13.2,P0.01)的程度及出血(x2=6.7,P0.05)的风险就增加。结论 SAAG可以作为判定乙型肝炎肝硬化患者静脉曲张程度的指标。     

血清-腹水白蛋白梯度与门脉高压症关系的探讨

目的 探讨血清-腹水白蛋白梯度(SAAG)与门脉压力是否存在相关.方法28例肝硬化腹水行胃镜检查了解有无食管静脉曲张(EV)及其程度,并测定SAAG.SAAG=当日血清白蛋白-腹水白蛋白,以11g/L为界值分为高SAAG及低SAAG.采用Pearson相关分析SAAG与EV之间的关系.结果26例高SAAG中有22例有EV,而2例低SAAG均无EV.SAAG与EV存在相关(r=0.53,P＜0.01;r=0.55,P＜0.01),但高SAAG的水平与EV的程度并不相关(P＞0.05).结论SAAG与门脉压力密切相关.     

血清-腹水白蛋白梯度在腹水病因鉴别诊断中的价值

背景:血清-腹水白蛋白梯度(SAAG)是间接反映门静脉压力的指标。目的:探讨SAAG和其他实验室指标在腹水病因鉴别诊断中的价值。方法:回顾性分析以腹水待查入院的122例患者的病史,按出院诊断分为门静脉高压相关疾病组(68例)和非门静脉高压相关疾病组(54例);以同一天测定的血清白蛋白浓度和腹水白蛋白浓度计算SAAG,比较两组SAAG与诊断的关系。结果:门静脉高压相关疾病组的SAAG(18.5g/L±5.3g/L)显著高于非门静脉高压相关疾病组(7.0g/L±3.1g/L)(P<0.001)。以SAAG≥11g/L为界限值,诊断门静脉高压相关性腹水的敏感性为95.6%,特异性为98.1%,准确性为96.7%,阳性预期值98.5%,阴性预期值94.6%。结论:SAAG虽不能直接对腹水的病因做出诊断,但却能为进一步检查腹水病因提出方向。高SAAG腹水大都与门静脉高压有关,而低SAAG腹水患者,在排除结核性腹膜炎和自身免疫性疾病后,应尽力排查恶性肿瘤。     

门脉高压性胃病出血的诊断及治疗

门脉高压性胃病(portal Hypertensive Gastropathy PHG)是肝硬化失代偿期常见的并发症之一。在肝硬化门静脉高压(PHT）并发上消化道出血中，仅次于食道胃底静脉曲张破裂出血，其临床意义与食管胃底静脉曲张破裂出血同等重要。现就其研究现状综述如下。     

肝硬化食管胃静脉曲张破裂出血的相关危险因素分析

目的探讨可以评估肝硬化患者食管胃静脉曲张破裂出血风险的临床指标。方法回顾性分析572例合并食管胃静脉曲张破裂出血的肝硬化患者(观察组)及704例未发生出血的肝硬化患者(对照组)的临床资料,对两组间存在差异性的指标运用单因素和多因素Logistic回归模型进行分析。结果两组在肝功能分级状况(P0.05)、血清白蛋白(t=5.05,P=0.000)、凝血酶原时间(t=-2.80,P=0.005)、门静脉内径(t=-2.28,P=0.006)、脾脏厚度(t=-2.73,P=0.006)方面比较,差异有统计学意义。单因素非条件Logistic回归分析显示白蛋白(OR=0.944,P=0.000)、凝血酶原时间(OR=1.067,P=0.007)、门静脉内径(OR=3.423,P=0.007)、脾脏厚度(OR=1.276,P=0.007)与出血存在相关性,进一步多因素非条件Logistic回归分析提示白蛋白(OR=0.936,P=0.000)、门静脉内径(OR=4.098,P=0.013)、脾脏厚度(OR=1.275,P=0.007)是出血的独立危险因素。结论白蛋白、门静脉内径、脾脏厚度是肝硬化并发食管胃静脉曲张破裂出血的独立危险因素,对预测食管胃静脉曲张破裂出血的发生有重要的临床价值,改善白蛋白可在一定程度上减少肝硬化并发食管胃静脉曲张破裂出血的风险。     

Optimal management of ascites

Ascites is the most common complication of cirrhosis, which develops in 5%‐10% of patients per year. Its management is based on symptomatic measures including restriction of sodium intake, diuretics and paracentesis. Underlying liver disease must always be treated and may improve ascites. In some patients, ascites is not controlled by medical therapies and has a major impact on quality of life and survival. TIPS placement and liver transplantation must therefore be discussed. More recently, repeated albumin infusions and Alfapump^® have emerged as new therapies in ascites. In this review, the current data on these different options are analysed and an algorithm to help the physician make clinical decisions is suggested.     

Treatment for cirrhotic ascites

Common complications of decompensated liver cirrhosis are esophageal varices, hepatic encephalopathy and ascites. After the onset of complications, the prognosis worsens. In patients with ascites, the 5‐year mortality rate is 44%. Furthermore, hyponatremia, spontaneous bacterial translocation and hepatorenal syndrome also greatly worsen the prognosis. Effective treatment of cirrhotic ascites improves the quality of life and survival rate. Recently, the newly produced diuretic, tolvaptan (vasopressin V2 receptor antagonist), was reported to be effective in the treatment of refractory ascites in liver cirrhosis; however, there has not been an associated positive effect on the prognosis. There are various types of treatment for ascites, such as large‐volume paracenteses, a cell‐free and concentrated ascites reinfusion therapy, a transjugular intrahepatic portosystemic shunt, and a peritoneo‐venous shunt. Although they improve the prognosis, liver transplantation remains the ultimate form of treatment. The present article discusses the therapeutic management of cirrhotic ascites.     

Chylous ascites after liver transplantation with mesentero-portal jump graft

Chylous effusions and lymphatic leaks occur after trauma, malignant disease, primary lymphatic disorders, and parasitosis, and rarely after abdominal surgery. Chylous ascites after orthotopic liver transplantation is a rare complication. We report a case of chylous ascites occurring after hepatic transplantation with a mesentero‐portal venous jump graft, successfully treated with conservative management.     

Management of ascites in cirrhosis

Ascites is one of the earliest and most common complications of patients with cirrhosis. A typical circulatory dysfunction characterized by arterial vasodilation, high cardiac output and stimulation of vasoactive systems is commonly present in these patients and is associated with a poor prognosis. The treatment of ascites has been based on the combination of a low-sodium diet and the administration of diuretics. The reintroduction of paracentesis and the recent introduction of the transjugular intrahepatic portosystemic shunt (TIPS) are the most relevant innovations in the treatment of ascites during the past two decades, although controlled trials in large series of patients are needed to delineate whether TIPS is a safe and useful treatment for these patients.     

Management of ascites in cirrhosis

Ascites is a common complication of liver cirrhosis associated with a poor prognosis. The treatment of ascites requires dietary sodium restriction and the judicious use of distal and loop diuretics, sequential at an earlier stage of ascites, and a combination at a later stage of ascites. The diagnosis of refractory ascites requires the demonstration of diuretic non-responsiveness, despite dietary sodium restriction, or the presence of diuretic-related complications. Patients with refractory ascites require second-line treatments of repeat large-volume paracentesis (LVP) or the insertion of a transjugular intrahepatic portosystemic shunt (TIPS), and assessment for liver transplantation. Careful patient selection is paramount for TIPS to be successful as a treatment for ascites. Patients not suitable for TIPS insertion should receive LVP. The use of albumin as a volume expander is recommended for LVP of >5-6 L to prevent the development of circulatory dysfunction, although the clinical significance of post-paracentesis circulatory dysfunction is still debated. Significant mortality is still being observed in cirrhotic patients with ascites and relatively preserved liver and renal function, as indicated by a lower Model for End-Stage Liver Disease (MELD) score. It is proposed that patients with lower MELD scores and ascites should receive additional points in calculating their priority for liver transplantation. Potential new treatment options for ascites include the use of various vasoconstrictors, vasopressin V(2) receptor antagonists, or the insertion of a peritoneo-vesical shunt, all of which could possibly improve the management of ascites.     

Chylous ascites caused by portal vein thrombosis treated with octreotide

Chylous ascites is an uncommon entity with variable causes and rarely arises from portal vein thrombosis. This is a case report of chylous ascites caused by idiopathic portal vein thrombosis that was refractory to medical therapy and shunt surgery, which showed an impressive response to treatment with subcutaneous octreotide. We review the literature on chylous ascites with particular reference to the role of somatostatin analogs in the management of this rare condition.     

A hyperdynamic portal syndrome with ascites after endoscopic laser treatment

Received: November 17, 2000 / Accepted: June 22, 2001     

Management of portal hypertension and ascites in polycystic liver disease

Patients suffering from polycystic liver disease may develop Hepatic Venous Outflow Obstruction, Portal Vein Obstruction and/or Inferior Caval Vein Syndrome because of cystic mass effect. This can cause portal hypertension, leading to ascites, variceal haemorrhage or splenomegaly. For this review, we evaluate the evidence to provide clinical guidance for physicians faced with this complication. Diagnosis is made with imaging such as ultrasound, computed tomography or magnetic resonance imaging. Therapy includes conventional therapy with diuretics and paracentesis, and medical therapy using somatostatin analogues. Based on disease phenotype various (non‐)surgical liver‐volume reducing therapies, hepatic or portal venous stenting, transjugular intrahepatic portosystemic shunts and liver transplantation may be considered. Because of complicated anatomy, use of high‐risk interventions and lack of empirical evidence, patients should be treated in expert centres.     

Management of refractory ascites and hepatorenal syndrome

Refractory ascites and hepatorenal syndrome (HRS) are the late complications of the terminal stages of cirrhosis. The definitions of refractory ascites and HRS proposed by the International Ascites Club in 1996 are now widely accepted, and are useful in diagnosis, treatment and research in this field. In both conditions, the only treatment of proven value for improved survival is liver transplantation. However, because of better understanding about the pathophysiology of HRS, including the roles of portal hypertension, ascites formation and hemodynamic derangements, treatments such as transjugular intrahepatic portasystemic shunt (TIPS) and new pharmacological agents may be considered to alleviate the problem prior to transplantation. Symptomatic treatment of refractory ascites includes TIPS and repeated large volume paracentesis. Transjugular intrahepatic portasystemic shunt can improve survival while waiting for liver transplantation. Practical management guidelines for TIPS and large volume paracentesis, including the prevention and management of further complications, are considered in this review.