Arterial-Venous Shunting in Liver Cirrhosis

Controversial data exist in the literature aboutthe presence and clinical relevance of hepaticarterial-venous shunting. An interesting opportunity forreconsidering the problem has been provided by the use, in the study of liver function, ofD-sorbitol, a substance whose first-pass hepaticextraction is very high in normal subjects, while beingdirectly related to circulatory alterations in livercirrhosis. Because of this property, the systemicbioavailability of D-sorbitol during hepatic arterialinfusion can be assumed to reflect arterial-venousshunting. Thirteen biopsy-proven cirrhotic patients(ages 35- 66 years), who required diagnostic arterialcatheterization, entered the study. Patients werestudied on two subsequent days, in which a sterilepyrogen-free solution (1.5%) of D-sorbitol wasadministered by direct low-rate infusion (15 mg/min for 20min) into the hepatic artery and the systemiccirculation, respectively. Urine samples werespontaneously collected for 8-hr periods before andduring/after each infusion. The hepatic arterialbioavailability of D-sorbitol was calculated as theratio between the net cumulative urinary outputs ofD-sorbitol after infusions into the hepatic artery andthe systemic vein. Observed values confirm the existence andthe large variability (0-88.7%) of hepaticarterial-venous shunting in cirrhoticpatients.     

Incidence of Gallstones in Liver Cirrhosis

We conducted a longitudinal follow-up of 72 patients with liver cirrhosis (LC) in order to assess gallstone (GS) incidence. The period of survey was 24.5 +/- 12.2 months. Patients were divided into two groups: group I--26 patients with ascites at the start or appearing during follow-up, and Group II--46 patients with compensated LC (no ascites) throughout the survey. During follow-up, 12 of 72 (16.6%) patients developed GS. The global cumulative incidence of GS was 5.5 cases/100 people/year. Age and sex had no influence on the incidence of GS in LC; neither had etiology or cirrhosis. On the contrary, the study revealed a significant increase in the incidence of GS in decompensated cirrhosis. In group I patients, GS appeared more frequently (34.6%) than in group II patients (6.5%) (chi 2 9.479; p less than 0.002). The cumulative incidence of GS was five times higher in decompensated versus compensated LC.     

Prevalence and Incidence of Gallstones in Liver Cirrhosis

Background: Our aim was to assess the prevalence and incidence of gallstone disease in patients with liver cirrhosis and to identify risk factors for cholecystolithiasis. Methods: We studied a cohort of 313 patients with liver cirrhosis confirmed by histology and/or laparoscopy and 357 patients free of liver disease, who had been referred for ultrasonographic examination of the upper abdomen. Hepatobiliary ultrasonography was performed when liver cirrhosis was diagnosed and every 6 months thereafter. Risk factors for cholelithiasis (age, gender, diet, pregnancy, diabetes, family history of cholelithiasis, etiology of cirrhosis, decompensated disease) were assessed. Results: The overall prevalence of gallstones in cirrhotic patients was 23.3%. In controls, the overall prevalence of cholecystolithiasis was 16.8%. After a median follow-up period of 65 months, 30 patients developed gallstones. The calculated annual incidence was 3.4%. Conclusions: Given that the prevalence of gallstone disease is higher in cirrhotics than in noncirrhotic patients, cirrhosis of the liver may be considered a risk factor for cholecystolithiasis.     

Muscle Biopsy Studies in Liver Cirrhosis

Some biochemical and histological findings in skeletal muscle tissue, obtained by needle biopsy from 22 patients with decompensated cirrhosis of the liver, are presented. Furthermore, the correlations between muscle composition analyses and electrolyte or acid-base balance are examined. Muscle analyses showed increased water, sodium, and chloride content; decreased potassium, magnesium, and protein nitrogen concentrations. No conclusive evidence of ‘true’ potassium depletion was found. However, a decrease in muscle potassium content was associated with extracellular metabolic alkalosis. Edema, nucleosis, and atrophy were the most common histological findings. They were in close agreement with the biochemical results of overhydration and decreased protein nitrogen content in muscle tissue.     

酒精性脂肪肝与肝硬化的超声诊断

本文报道经病理诊断的酒精性脂肪肝（ＡＦ）１０例，酒精性肝硬化（ＡＣ）１５例Ｂ超检查结果显示ＡＦ肝肿大，并有近场密集，远场衰减。ＡＣ示典型肝硬化表现。提出下列４点，有助于诊断ＡＦ与ＡＣ。①有明确嗜酒者，酒量＞１００ｇ／ｄ，５年以上；②ＡＦ者ＧＧＴ明显升高，ＡＣ轻度增高或正常；③Ｂ超结合病史有助于诊断ＡＦ及ＡＣ；④Ｂ超并可用于随访，ＡＦ戒酒后可完全恢复或明显好转。根据这些表现，作者认为Ｂ超是诊断ＡＦ与ＡＣ有价值的方法。     

D-二聚体在肝硬化中的临床意义

目的探讨D-二聚体在肝硬化中的临床意义。方法检测A组(肝硬化组)及B组(健康体检组)D-二聚体含量,并分析A组(肝硬化组)中Child-Pugh评分与D-二聚体含量的相关性。结果 A组D-二聚体含量高于B组,差异具有统计学意义(P<0.01)。A组(肝硬化组)中Child评分与D-二聚体含量呈正相关(P=0.37)。结论 D-二聚体可作为肝硬化病情判断的参考指标之一。     

Anti-T Agglutinin in Cirrhosis of the Liver

Abstract. Anti-T agglutinin has been studied in 44 cases of liver cirrhosis and 2 of chronic active hepatitis. The antibody titre was significantly higher than in normal controls. No correlation was found between anti-T titre and γ-globulin level or clinical conditions.     

肝硬化的临床流行病学分析

采用x、x^2及P值统计学方法观察一组大样本肝硬化住院病例的主要临床流行病学指标。结果显示临床发病构成比为1．39％,占全部肝病住院病例之51．07％。病死率为11．79％。病因学分析表明88％病例与HBV感染相关,主要HBV标记组合形式为HBsAg 抗HBe 抗HBc及HBsAg 抗HBc,单项抗HBc及并抗HBe和(或)抗HBs者亦非少数。直接死因以上消化道出血为最主要(80．42％),伴脑病肝衰竭次之。由于肝硬化以与HBV相关者为最多,故其预防当从防治乙型肝炎入手。     

酒精性肝硬化的临床特点

目的：分析酒精性肝硬化的临床特点。方法：以１９９０年１月～１９９９年３月间在我院住院的４５８例肝炎后肝化为对照,对同期住院的６７例酒精性肝硬化进行了分析。结果：酒精性和肝为后肝硬化的主要症状均为腹胀、纳差、乏力,两者之间没有差异：与肝炎后肝硬化相比,酒精性肝硬化的蜘蛛痣、肝掌、男性乳房发育、肝大是非常常见的,两者这间黄疸、腹水、脾大的发生情况没有差异：酒精性肝硬化的ＡＳＴ／ＡＬＴ、γ－ＧＴ、ＡＬＰ     

Nitric Oxide Metabolites in Decompensated Liver Cirrhosis

High levels of nitric oxide are thought to bethe cause of some of the complications associated withdecompensated end-stage liver disease. To assess nitricoxide metabolism in cirrhotic patients, we measured the levels of nitric oxide metabolites(nitrosohemoglobin, methemoglobin, nitrate, and nitrite)in normal subjects, in patients with decompensatedcirrhosis, in patients with renal failure (model forimpaired NO metabolites excretion), and in patients withmononitrates-treated anginal syndrome (model forexogenous nitric oxide). When compared to controls,patients with decompensated cirrhosis exhibited elevated levels of nitrate only. A significant increaseof nitrate was also noted in patients receivingexogenous nitrates, whereas patients with impairedexcretion had significantly elevated levels of bothnitrite and nitrate. In conclusion, nitric oxidemetabolism in patients with decompensated cirrhosis issimilar to that of patients receiving nitric oxide froman exogenous source. Renal impairment, whether alone or associated with cirrhosis, causes a changein nitric oxide metabolism. These findings may haveclinical implications for nitrates treatment in patientswith decompensated cirrhosis.     

内毒素受体、内毒素血症与肝硬化

内毒素在肝脏内可激活Kupffer细胞,合成和释放多种细胞因子和炎症介质,使肝细胞受损,其作用机制主要是通过Kupffer细胞上的内毒素受体启动宿主免疫反应和效应功能。肝硬化患者因多种原因引起肠道菌群生长过度和菌群易位,可导致内毒素血症;反之,内毒素本身又可加重肝脏损伤。因此,通过改变肝硬化患者的肠道微生态,调节肠道菌群,可减少肠道内毒素的产生,防止内毒素血症的发生,减轻肝脏损伤,延缓肝硬化的进程。     

Esophageal Varices in Rat Models of Liver Cirrhosis

Animal models resembling the human situation arevery useful to investigate human disease. However, therehas been no evidence of esophageal varices in rats withliver cirrhosis. In the present study, to determine whether intrahepatic portalhypertension produced by liver cirrhosis inducesesophageal varices in rats, the esophagus was examinedendoscopically in rat models of liver cirrhosis. Allrats given carbon tetrachloride or thioacetamide and sixof seven rats given a choline-deficient diet hadesophageal varices or venous dilatation after 16 weeksof treatment, although the varices in one rat given carbon tetrachloride and in two rats given acholine-deficient diet were reduced from weeks 16 to 18.These findings suggest that timing is important whenstudying esophageal varices in rat models of liver cirrhosis. It is concluded that certain modelsof liver cirrhosis in rats could be used as models ofesophageal varices due to intrahepatic portalhypertension.