肝硬化患者血浆胃动素水平的动态观察

以放射免疫法检测35例肝硬化患者的血浆胃动素(MTL)水平。肝硬化组入院时血浆MTL水平显著高于对照组。待肝肾功能明显发转、腹水基本消退后,血浆MTL水平则较入院时显著降低。研究结果提示血浆MTL水平的动态变化可能与肝硬化的病理生理过程有密切关系。     

肝硬化腹水患者血浆N端B型脑钠肽前体水平变化及其临床意义

目的 观察肝硬化腹水患者血浆N端B型脑钠肽前体(NT-proBNP)水平的变化并探讨其临床意义.方法 将80例住院的肝硬化患者按腹水程度分成无腹水组、轻度腹水组、中度腹水组和大量腹水组4组,每组20例,选取20例健康体检者作为对照组.入选者分别行腹部超声检查,同时以ECLIA法检测血浆NT-proBNP水平.结果 肝硬化腹水患者血浆NT-proBNP水平显著高于对照组,各组间NT-proBNP水平比较差异有统计学意义(P＜0.05).结论 肝硬化腹水患者血浆NT-proBNP水平随着腹水严重程度的增加而升高,提示NT-proBNP在肝硬化腹水的病程中起着一定的作用.     

肝硬化患者血浆内皮素和一氧化氮水平及与肾功能状态的关系

测定不同阶段肝硬化患者血浆的NO、ET水平，探索它们对肝硬化腹水形成和肾功能损害所起的作用及其相互关系。测血浆NO的代谢产物NO2^-浓度（Griess法），ET-1浓度（放免法）及肾功能。1.血浆NO浓度在肝硬化各组均明显高于正常对照组，在肾衰组明显高于有腹水、无肾衰组。血浆ET浓度在肝硬化各组均明显高于正常对照组，肾衰组明显高于有腹水、无肾衰组。2.肝硬化患者血浆ET浓度与血肌酐呈正相关，与肌酐清除率、血钠、尿钠呈负相关。3.肝硬化患者血浆NO与ET水平呈正相关。血浆NO和ET升高可能在肝硬化病程进展中起了重要作用，是形成腹水和引起肾功损害的重要因素，二者相互依赖、相互影响的协同作用是肝硬化进展及出现并发症的重要机制之一。     

肝硬化患者血浆内皮素和胰高血糖素水平的变化及其临床意义

目的 研究肝硬化时血浆内皮素-1(ET-1)和胰高血糖素(GLU)水平的改变及其与肝功能损害和门脉高压形成的关系。方法 采用放射免疫分析法测定40例肝硬化患者和18例对照组空腹血浆ET-1和GLU水平。用彩色多普勒超声测定门静脉及脾静脉的直径、流速和流量。结果 肝硬化患者血浆ET-1和GLU水平显著高于对照组。按肝功能Child-Pugh分级将肝硬化患者分为A、B、C三组，各组血浆ET-1和GLU水平依次升高。合并腹水的肝硬化患者血浆ET-1和GLU水平显著高于未合并腹水者。血浆ET-1和GLU水平与门静脉和脾静脉的直径以及脾静脉的流量呈显著正相关。结论 肝硬化患者血浆ET-1及GIU水平升高反映了肝功能损害的严重程度，同时在门静脉高压的形成和发展过程中起着重要的作用。     

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。     

D-二聚体和肝纤维化Ⅰ类标志物在肝硬化患者血浆中的表达及其临床意义

目的 探讨血浆D-二聚体(D-dimer)和肝纤维化Ⅰ类标志物水平与肝硬化患者肝功能状况的关系.方法 检测198例研究对象(新诊断的肝硬化组80例、肝硬化治疗后组68例,对照组50例)血液中D-二聚体和肝纤维化Ⅰ类标志物水平.结果 与体检组和治疗后组比较,肝硬化组患者血浆D-二聚体和肝纤维化Ⅰ类标志物水平显著升高(P均＜0.05),对照组与治疗后组比较,差异无统计学意义(P均＞0.05),D-二聚体、肝纤维化Ⅰ类标志物水平与Child-Pugh肝功能分级密切相关.有腹水的肝硬化患者血浆D-二聚体和肝纤维化Ⅰ类标志物水高于无腹水的肝硬化患者;失代偿期的肝硬化患者血浆D-二聚体和肝纤维化Ⅰ类标志物水平显著高于代偿期的肝硬化患者;肝硬化患者血浆D-二聚体和肝纤维化Ⅰ类标志物水平与肝功能损害的严重程度呈正相关.结论 肝硬化患者血浆D-二聚体和肝纤维化Ⅰ类标志物的水平与肝硬化患者肝功能状况密切相关,是反映肝硬化患者肝功能状况的指标之一.     

肾素、血管紧张素Ⅱ及抗利尿激素与肝硬化腹水形成的关系

目的肾素-血管紧张素-醛固酮系统（RAAS）、抗利尿激素（ADH）与腹水的形成有着密切的关系，本研究旨在通过观察肝硬化患者血浆肾素活性（PRA）、血管紧张素Ⅱ（AngⅡ）以及ADH水平，探讨PRA、AngⅡ及ADH与肝硬化患者腹水形成的关系。方法选择47例肝硬化患者，其中Child—Pugh分级A级13例，B级19例，c级15例，肝硬化无腹水13例，腹水伴肝肾综合征（hepatorenal syndrome，HRS）8例，腹水无HRS26例，应用放射免疫方法分别检测其血浆PRA、AngⅡ及ADH表达水平进行检测，并以30例健康人为对照组进行比较。结果（肝功能）Child—PughB级及C级患者PRAAngⅡ及ADH水平均明显高于对照组与A级组，肝硬化患者在未合并腹水时PRA、AngⅡ及ADH水平与对照组比较无显著差异，在出现腹水后，与对照组比较差异有显著意义（P〈0．01）。腹水伴HRS组与腹水无HRS组比较，有显著差异（P〈0．05）。结论肝硬化患者血浆PRA、AngⅡ及ADH与肝硬化腹水的形成密切相关。     

肝硬化腹水并发HRS和低钠血症患者综合护理干预效果分析

目的评估综合护理干预对肝硬化腹水并发HRS和低钠血症患者的临床效果。方法选取2015年3月至2017年6月在我院住院治疗的肝硬化腹水并发肝肾综合征低钠血症患者88例,随机分为观察组和对照组,各44例。观察组给予综合护理,对照组给予常规护理,对比分析两组患者的临床效果。结果在经过药物治疗和不同的护理干预后,观察组血清钠和GFR水平明显高于对照组(P0.05),但两组的肝功能Child-Pugh分级评分无统计学差异(P0.05)。观察组临床总有效率明显高于对照组(P0.05)。结论综合护理干预提升了肝硬化腹水并发肝肾综合征低钠血症患者的临床疗效,效果确切,值得推广。     

血浆内源性阿片肽升高与实验性肝硬化高动力循环状态及腹水形成的关系

目的:通过检测实验性肝硬化各阶段3种内源性阿片肽(EOP)血浆浓度变化,探讨其与肝硬化高动力循环状态及腹水形成的关系.方法:应用放射免疫法测定了四氯化碳(CCl_4)诱发大鼠肝硬化过程中血浆3种EOP的含量变化.结果显示:肝硬化腹水组及肝硬化无腹水组血浆亮啡肽(L-ENK)、强啡肽(Dyn Al-13)的含量均显著高于正常对照组(P<0.01,P<0.05),而且升高的水平与肝功能损害的程度呈显著正相关,但血浆β内啡肽(β-EP)的含量在3组中无显著差异(P>0.05).提示肝脏灭活功能受损导致大鼠血浆小分子阿片肽含量升高,后者又是引起实验性肝硬化高动力循环状态及腹水形成的原因之一.     

肝硬化伴自发性细菌性腹膜炎患者血浆及腹水降钙素原检测临床意义

探讨血浆及腹水降钙素原 (Procalcitonin ,PCT)检测在肝硬化伴自发性细菌性腹膜炎 (SBP)患者临床意义。采用免疫发光法测定 6 2例肝硬化腹水患者 (SBP 4 1例、非SBP 2 1例 )血浆及腹水PCT水平 ,并与TNF -α、IL - 6水平比较。SBP组血浆及腹水PCT、TNF -α和IL - 6水平均显著高于非SBP组 (P <0 0 1)。均以非SBP组均数加 2倍标准差为阳性判断值时 ,血浆PCT对SBP诊断阳性预测值最高 ,腹水IL - 6阴性预测值最高。死亡组入院时血浆PCT、TNF -α和IL - 6水平均显著高于同期存活组水平 ,腹水各项指标测定价值有限。血浆PCT水平是诊断肝硬化伴SBP和预后判断的有效指标。     

肝硬化患者肾血流及内皮素变化的临床研究

目的 研究肝硬化患者肾脏血液动力学的变化。 方法 对49例肝硬化患者,采用彩色多普勒超声测定肾叶间动脉及弓形动脉搏动指数(PI)、阻力指数(RI)、收缩期最高峰值(PS)、舒张期最低峰值(PD)及收缩期最高峰值/舒张期最低峰值(PS/PD)等指数,并同时监测患者的血内皮素情况。 结果 PI和RI随肝功能损伤加重而增高,尤以RI为著。肝功能Child分级A、B、C,RI值分别为0.60±0.09、0.66±0.06、0.72±0.07,F=10.005,P<0.01;随腹水量的增加,PI、RI等亦有明显增高:少量、中—大量、顽固性腹水组PI分别为1.14±0.20、1.31±0.29、1.42±0.36,F=28.747,P<0.05。RI分别为0.61±0.09、0.68±0.07、0.77±0.05,F=17.250,P<0.01。肝硬化患者血内皮素值增高为(1.26±0.27)ng/L,且与PI及RI增高呈正相关(相关系数分别为0.556、0.576)。 结论 肝硬化患者肾血流PI和RI的变化与肝功能及腹水的加重有密切相关。内皮素可能是参与肝硬化患者肾血管收缩的重要活性因子。     

Vasodilatory State of Decompensated Cirrhosis: Relation to Hepatic Dysfunction, Ascites, and Vasoactive Substances

The objective of this study was to determine the relations between the hallmark circulatory finding of decompensated cirrhosis, a reduced systemic vascular resistance (SVR), and the indices of hepatic decompensation, the accumulation of ascites, and the concentrations of various vasoactive substances. At a university-affiliated teaching hospital, eighteen hospitalized patients with cirrhosis and 18 age- and sex-matched healthy subjects were used. This was a case-control study. Measurements included cardiac dimensions and indices derived from echocardiograms and Doppler studies, abdominal ultrasound estimates of ascites, indices of hepatic function, and various serum (S) and urinary (U) substances. Results showed that cirrhotics had increased left atrial and left ventricular dimensions, left ventricular mass, heart rate, cardiac output (CO), transvalvular velocities, and a decreased SVR. SVR was related to hepatic dysfunction, as reflected by an abnormal prothrombin time ratio (r= -0.64, p= 0.006), and also related to overall severity of liver disease as estimated by the Child-Pugh score (r= -0.53, p = 0.044). Although cirrhotics with ascites generally had a reduced SVR, estimates of ascites were directly related to SVR (r = 0.57, p = 0.03) and inversely related to CO (r= -0.53, p= 0.04). Concentrations of S and U digoxin-like immunoreactive substance (DLIS) were also increased, but the concentrations of S glucagon and estradiol were not elevated. The accumulations of S and U DLIS, S glucagon, and S estradiol were all related to hepatic dysfunction. S estradiol was also related to SVR (r = -0.55, p= 0.04), but this was only evident with S estradiol expressed as a logarithm and did not emerge as significant on a multivariate analysis. The reduced SVR observed in decompensated cirrhosis is related to various indices of hepatic dysfunction. Certain substances that accumulate in cirrhosis (such as DLIS, glucagon, and estradiol) do not explain the vasodilatation observed. Although ascites in decompensated cirrhosis generally signifies a vasodilated state, a reduced SVR may be found even before ascites is clinically evident, and tense ascites may actually obscure this finding.     

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.     

Circulating endogenous cannabinoid anandamide and portal, systemic and renal hemodynamics in cirrhosis.

BACKGROUND: Endocannabinoids may participate in the homeostasis of arterial pressure. Recently, anandamide, the most extensively studied endocannabinoid, has been proposed as a key mediator in the peripheral arterial vasodilation of cirrhosis. OBJECTIVES: To determine if circulating levels of anandamide are related to the extent of the peripheral arterial vasodilation, the severity of portal hypertension and the degree of liver and renal dysfunction of patients with cirrhosis. METHODS: Plasma levels of anandamide and several systemic, portal and renal hemodynamic parameters were determined in 18 patients with cirrhosis and eight healthy subjects (control group). RESULTS: Plasma levels of anandamide were elevated in patients compared to the control group (P<0.05), nevertheless, no differences between patients with ascites and well-compensated patients were found. There was no correlation between anandamide concentration and arterial pressure, cardiac output and systemic vascular resistance, Child-Pugh's score, portal pressure, renal vascular resistance, plasma renin activity or plasma aldosterone concentration. CONCLUSIONS: Circulating levels of anandamide are increased in cirrhotic patients. However, this elevation was unrelated to the extent of arterial vasodilation, the severity of portal hypertension or the degree of hepatic and renal dysfunction. Although a local hormonal action cannot be excluded, our results do not support a relevant contribution of this system in the hemodynamic disturbance of cirrhosis.     

Renal diseases and the liver

Many liver diseases coexist with chronic renal disease, because many systemic conditions affect both the liver and the kidneys. Certain liver diseases are also common in patients with chronic renal disease, especially viral hepatitis, either because the renal disease occurs as a complication of viral hepatitis, or the viral hepatitis is acquired as a result of dialysis. Renal tubular dysfunction is also frequently observed with cholestasis. However, liver complications of renal diseases are extremely uncommon, notable examples include nephrogenic ascites and nephrogenic hepatic dysfunction. Nephrogenic ascites can mimic liver cirrhosis with ascites, and it improves with renal transplantation. Nephrogenic hepatic dysfunction is a manifestation of renal cell carcinoma, which settles with the removal of the renal cell carcinoma, but returns with the recurrence of the tumor. In general, the presence of liver disease in patients with chronic renal disease makes management of both conditions more challenging. Viral hepatitis should be treated, if possible, before renal transplant. If cirrhosis is present, renal transplant alone is contraindicated; combined liver and kidney transplantation is indicated in patients with end-stage renal disease and advanced cirrhosis.     

Cimetidine kinetics and dynamics in patients with severe liver disease

Following cimetidine administration, 60% of the dose is excreted as unchanged drug in the urine, and 40% is eliminated by metabolism. We evaluated the effect of liver disease on cimetidine disposition by comparing its kinetics in 7 healthy subjects and 8 patients with alcoholic cirrhosis. Cirrhotic patients had severe liver disease as evidenced by the presence of ascites, hepatic encephalopathy, jaundice, muscle wasting, and low serum albumin, but serum creatinine and creatinine clearance did not differ significantly between controls and cirrhotics. Following intravenous administration, cimetidine systemic clearance was decreased by 56% in cirrhotics. This reduction was due in major part to an impairment of the renal clearance of unchanged drug. The ratio of cimetidine to creatinine clearance was 3.71 +/- 0.63 in controls, indicating active tubular secretion, and was decreased in cirrhotics (1.22 +/- 0.09, p less than 0.05). The volume of distribution of cimetidine was also decreased by 39% in cirrhotics. To verify whether these findings observed after a single dose could be extended to patients receiving chronic cimetidine treatment, cimetidine trough (predose) plasma levels were measured in an additional group of 56 subjects receiving continuous cimetidine therapy (15 controls and 41 cirrhotics). Trough plasma levels did not differ significantly in controls and patients with compensated liver disease, but were elevated in patients with moderate and severe hepatic dysfunction. It is concluded that cimetidine clearance is decreased in patients with severe liver disease, mostly due to an impairment of the tubular secretion of unchanged drug, and that a reduction of cimetidine dosage is warranted in these patients, even in the presence of a normal creatinine clearance.     

Elevated carboxy terminal cross linked telopeptide of type I collagen in alcoholic cirrhosis: relation to liver and kidney function and bone metabolism

BACKGROUND: The carboxy terminal cross linked telopeptide of type I collagen (ICTP) has been put forward as a marker of bone resorption. Patients with alcoholic liver disease may have osteodystrophy. AIMS: To assess circulating and regional concentrations of ICTP in relation to liver dysfunction, bone metabolism, and fibrosis. METHODS: In 15 patients with alcoholic cirrhosis and 20 controls, hepatic venous, renal venous, and femoral arterial concentrations of ICTP, and bone mass and metabolism were measured. RESULTS: Circulating ICTP was higher in patients with cirrhosis than in controls. No overall significant hepatic disposal or production was found in the patient or control groups but slightly increased production was found in a subset of patients with advanced disease. Significant renal extraction was observed in the controls, whereas only a borderline significant extraction was observed in the patients. Measurements of bone mass and metabolism indicated only a mild degree of osteodystrophy in the patients with cirrhosis. ICTP correlated significantly in the cirrhotic patients with hepatic and renal dysfunction and fibrosis, but not with measurements of bone mass or metabolism. CONCLUSIONS: ICTP is highly elevated in patients with cirrhosis, with no detectable hepatic net production or disposal. No relation between ICTP and markers of bone metabolism was identified, but there was a relation to indicators of liver dysfunction and fibrosis. As the cirrhotic patients conceivably only had mild osteopenia, the elevated ICTP in cirrhosis may therefore primarily reflect liver failure and hepatic fibrosis.     

Serum uric acid levels in patients with cirrhosis: a reevaluation.

It has been reported that the serum uric acid levels in patients with cirrhosis were decreased compared with healthy subjects. These studies suggested that the lower serum uric acid levels in cirrhotic patients were attributed mainly to an increased effective vascular volume, and consequently to an excessive renal clearance of uric acid. However, the previous observations are challenged by a recent hypothesis for the pathogenesis of hyperdynamic circulation and formation of ascites in cirrhosis. The current study was undertaken to reevaluate serum uric acid levels in patients with cirrhosis. Ninety-eight cirrhotic patients with normal renal functions were included in this study. All biochemical and hemodynamic data were utilized for analysis. The mean serum uric acid level (mean, 6.1+/-1.2 mg/dL; range, 2.7-9.1 mg/dL) was higher than that of the age- and sex-matched healthy control subjects (mean, 5.5+/-1.3 mg/dL; range, 2.9-8.1 mg/dL; p = 0.018). Using multiple regression analysis it was determined that the serum uric acid level was not related to the severity of liver disease, cardiac index, systemic vascular resistance, and hepatic venous pressure gradient but was related closely to age (r = 0.210, p = 0.026) and effective renal plasma flow (r = -0.677, p < 0.0001). Compared with cirrhotic patients without ascites, those with ascites had a significantly higher serum uric acid level (6.7+/-1.6 mg/dL vs. 5.6+/-1.7 mg/dL, p < 0.05) and lower effective renal plasma flow (396+/-125 mL/min vs. 445+/-149 mL/min, p < 0.05). In conclusion, for cirrhotic patients with normal serum creatinine levels, the current study shows that the mean serum uric acid level is higher than that of healthy control subjects. It is not related to the severity of liver failure and systemic and portal hemodynamics, but is related closely to renal functions, especially the renal plasma flow.     

Increased plasma levels of neuropeptide Y in hepatorenal syndrome

BACKGROUND/AIMS: To investigate the relationship between neuropeptide Y (NPY), a potent renal vasoconstrictor peptide released upon marked stimulations of sympathetic nervous system (SNS), and renal and circulatory function in cirrhosis. METHODS: Plasma levels of NPY (radioimmunoassay) and norepinephrine and renal function parameters were determined in 17 healthy controls, nine patients with cirrhosis without ascites, and 37 patients with cirrhosis and ascites, of whom 12 had hepatorenal syndrome (HRS). RESULTS: Patients with ascites showed circulating levels of NPY similar to those of patients without ascites and controls (73+/-4, +/-4 and 68+/-4 pmol/l, respectively; NS). However, patients with HRS had significantly increased levels of NPY with respect to the other groups (110+/-6 pmol/l; P<0.001). NPY levels correlated inversely with renal plasma flow and glomerular filtration rate and directly with norepinephrine. In patients with HRS (n=6) treatment with terlipressin and albumin was associated with a marked improvement in circulatory and renal function and marked suppression of NPY and norepinephrine levels. CONCLUSIONS: Patients with HRS have increased levels of NPY which are related to circulatory dysfunction and SNS activation and may contribute to renal vasoconstriction.     

Doppler study of hepatic vein in cirrhotic patients： Correlation with liver dysfunction and hepatic hemodynamics

INTRODUCTIONThere are many studies on inflow to the liver in liver cirrhosis (LC) in relation to hepatic dysfunction and portal hypertension. In LC, there are changes in liver parenchyma as well as alteration of hepatic vasculature, including morphologica…