胃肌电图对胆道运动障碍性疾病的诊断价值

胆道系统疾病是内科的常见病,不少胆道系统疾病的发生和发展与胆道系统运动紊乱密切相关,因此对胆道系统运动的研究对胆道疾病的防治有重要意义。因此寻找简便易行,经济实用,易被患者所接受的检测胆道系统运动的方法,是非常迫切的临床需要,我们发现,许多胆道疾病患者表现为胃肌电图(Electrogastrogram,EGG)的异常,受EGG检测胃运动功能紊乱性疾病的启发,对26例胆道疾病患者在~(99m)Tc放射性核素胆囊排空运动序列成象证实伴有胆道运动障碍后检测EGG,并与15例经~(99m)Tc放射性核素胆囊排空运动检测无胆道运动障碍的胆道疾病患者和15例正常人进行对照比较。 1 材料和方法 1.1 材料经~(99m)Tc放射性核素胆囊排空动态成象证实伴有胆道运动障碍(~(99m)Tc放射性核素胆囊排空45min EF<25％定为胆道运动障碍)26例胆道疾病患者为1组,包括12例胆石     

酒精性肝硬化并发门静脉性胆道病致慢加急性肝衰竭行肝移植治疗1例报告

<正>酒精性肝病是由于大量饮酒摄入的乙醇损伤肝细胞,引起肝细胞脂肪变性,进而发展成伴有炎症反应的酒精性肝炎,甚至发生肝小叶结构破坏和假小叶形成引发肝纤维化和肝硬化~([1])。门静脉性胆道病(potal ductopathy,PD)是肝外门静脉阻塞所致的肝内外胆管、胆囊管和胆囊出现解剖学、形态学异常和功能异常~([2])。PD的发病因素较多,以肝硬化所致的门静脉高压为主。近年来,随着人们生活水平的提高,酒精性肝病屡见不鲜,而酒精性肝硬化基础上明确     

肝硬化并胆囊结石的临床特点与成因分析

目的:探讨肝硬化并胆囊结石的临床特点及其发病机制．方法:回顾性分析我院2003-2／2006-2住院的131例肝硬化患者,并以同期门诊行体检者790例作为对照组,分析的指标包括肝硬化并胆囊结石患者的性别差异、与对照组性别差异、肝病性胆囊改变在肝硬化胆囊结石发生中的作用、肝硬化并脾功能亢进在肝硬化胆囊结石发生中的作用．结果:肝硬化胆囊结石的发生率为41．22％,对照组胆结石的发生率为6．96％;肝硬化患者胆囊结石的发生率无性别差异(P>0．05);男性与女性肝硬化患者与对照组比较,胆囊结石发生率均有显著差异(39．58％vs 5％,P<0．05; 48．57％vs 10．53％,P<0．05);肝病性胆囊改变及肝硬化并脾功能亢进在胆囊结石发生中起着重要作用．肝病性胆囊改变患者胆囊结石发病率明显高于无肝病性胆囊改变者(48．39％vs 26．32％,P<0．05),肝硬化并脾功能亢进胆囊结石的发生率与对照组比较差异也有显著性(54．44％vs 6．96%,P<0．05)．结论:肝硬化患者易发生胆囊结石,与性别无关而与肝功能、胆囊运动功能障碍、脾功能亢进等有关．     

彩色多普勒超声显像对肝病患者胆囊运动功能的研究

慢性肝病、肝硬化是临床常见病，其对胆囊收缩功能的影响国内外已有报道。传统的概念认为胆囊的运动似一"慢泵"，最近国外学者提出胆囊在餐后和消化间期均有快速变换的储存和排空，类似"风箱样"运动，依据国外学者的观点，我们对２０例正常人和３０例慢性肝病、肝硬化病人进行脂餐前后胆囊运动的动态观察，结果表明，病理组和对照组脂餐前后分别对比Ｐ值均＜０．０５有明显差异。资料和方法３０例患者均系我院病人，实验室检查及肝组织活检明确诊断为慢肝、肝硬化，年龄３０－５５岁；男女各１５例。均有肝炎病史，３个月至５年不等。仪器采…     

肝硬化患者胆囊和胃排空功能的研究

例肝硬化患者和10例健康对照者,禁食12小时后口服液体脂餐400ml,采用实时超声方法测定空腹及餐后90分钟内每15分钟胆囊及胃排空功能.结果显示:肝硬化患者胆囊最大排空率较对照组明显降低,胃半排空时间比对照组明显延长,提示肝硬化患者胆囊排空不足,胃排空延迟.肝硬化患者胃及胆囊排空曲线示胃排空延迟,胆囊再充盈迟缓.胆囊和胃排空曲线交点与对照组相似.提示肝硬化患者胆囊排空和胃排空可能有一定联系.结论:肝硬化患者存在胆囊和胃排空运动障碍,胆囊和胃排空之间可能存在一定联系.     

肝硬化病人胆囊运动功能与自主神经功能的关系

目的：为了解肝硬化病人胆囊运动功能与自主神经功能及二者的关系。方法：应用超声和心率变异分析技术，分别检测30例肝硬化病人的胆囊运动功能和自主神经功能．结果：与对照组相比：（1）肝硬化组空腹胆囊容积和剩余容积显著增大，胆囊排空时间明显延长，胆囊收缩频率减慢．（2）肝硬化组24小时总频谱功率、极低频频谱功率、低频频谱功率和高频频谱功率均明显降低。（3）肝硬化组高频频谱功率与空腹胆囊容积呈负相关，与胆囊收缩频率呈正相关．结论：肝硬化病人胆囊运动功能障碍可能与自主神经功能异常有关。     

胃肌肌电图对胆道运动障碍性疾病的诊断价值

胆道系统疾病是内科的常见病,不少胆道系统疾病的发生和发展与胆道系统运动紊乱密切相关,因此对胆道系统运动的研究对胆道疾病的防治有重要意义[1].因此寻找简便易行,经济实用,易被患者所接受的检测胆道系统运动的方法,是非常迫切的临床需要.我们发现,许多胆道疾病患者表现为胃肌电图(E1ectrogastrogram,EGG)的异常,受EGG检测胃运动功能紊乱性疾病的启发,对26例胆道疾病患者在99mTc放射性核素胆囊排空运动序列成象证实伴有胆道运动障碍后检测EGG,并与15例经99mTc放射性核素胆囊排空运动检测无胆道运动障碍的胆道疾病患者和15例正常人进行对照比较.     

吗丁啉促慢性肝病患者胆囊排空的疗效观察

目的：了解吗丁啉促进胆囊排空的疗效。方法：超声对比观察26例慢性肝病患者及22例正常对照者空腹胆囊大小及脂肪餐后胆囊收缩情况。20例有胆囊排空障碍的患者,给予吗丁啉,每次10mg,3次／d,治疗4周后复查。结果：正常对照组与慢性肝病组餐前胆囊面积及餐后胆囊收缩率差异均有非常显著性意义（均P＜0．01）。慢性肝炎组存在餐后胆囊排空障碍。20例有排空障碍的慢性肝病患者经吗丁啉治疗4周后,胆囊排空有显著改善。结论：慢性肝病患者常伴有胆囊排空运动障碍,吗丁啉有改善胆囊排空障碍的作用。     

ATP结合盒亚家族B成员4(ABCB4)基因突变相关性肝硬化合并胆囊结石1例报告

ATP结合盒亚家族B成员4(ABCB4)基因突变疾病谱涉及进行性家族性肝内胆汁淤积3型、胆石症、妊娠期肝内胆汁淤积症、门静脉高压、肝硬化,甚至原发性肝脏、胆道恶性肿瘤等多种疾病。本院肝胆内科收治1例青年男性患者,入院初步诊断为胆囊结石,计划腹腔镜胆囊切除术,术前检查发现该患者肝功能异常、肝硬化、脾大、食管静脉轻度曲张,后进一步行二代测序明确诊断为ABCB4基因突变相关性肝硬化合并胆囊结石,给予熊去氧胆酸胶囊利胆治疗后,肝功能逐渐恢复正常。     

肝硬化患者胆囊运动功能与胆结石形成的关系探讨

大量临床报道表明肝硬化患者并发胆结石的发生率明显高于非肝硬化群体，且肝硬化程度越重，胆结石发生率越高。本实验采用^99mcTc标记二乙基乙酰苯胺亚氨二醋酸（^99mTc-EHIDA）肝胆动态显像方法，系统研究了肝硬化患者胆囊运动功能受掼晴况，以及胆囊运动功能紊乱与胆结石形成之间的关系。     

Prolonged Q-T(c) interval in mild portal hypertensive cirrhosis

BACKGROUND/AIMS: The Q-T(c) interval is prolonged in a substantial fraction of patients with cirrhosis, thus indicating delayed repolarisation. However, no information is available in mild portal hypertensive patients. We therefore determined the Q-T(c) interval in cirrhotic patients with hepatic venous pressure gradient (HVPG) < 12 mmHg. METHODS: Forty-four patients with cirrhosis and HVPG < 12 mmHg underwent a haemodynamic study. They were compared with 36 cirrhotic patients with clinically significant portal hypertension (HVPG> or = 12 mmHg) and controls without liver disease. RESULTS: The fraction with prolonged Q-T(c) interval (> 0.440 s(1/2)) was similar in the two cirrhotic groups (49 vs 50%, ns) and significantly above that of the controls (5%, P < 0.005). Q-T(c) was normal in patients with normal HVPG. Likewise, mean Q-T(c) was 0.449 and 0.447 s(1/2) in the two cirrhotic groups (ns), values which are significantly above that of the controls (0.410 s(1/2), P < 0.01). In the mild portal hypertensive group, the Q-T(c) interval was inversely related to indicators of liver function, such as indocyanine green clearance (r = -0.34, P < 0.02). CONCLUSIONS: Delayed repolarisation of the myocardium already occurs in a substantial fraction of patients with cirrhosis with only a mild increase in portal pressure. The prolonged Q-T(c) interval may be related to liver dysfunction and to the presence of portal hypertension.     

Factors influencing the prevalence of gallstones in liver cirrhosis

BACKGROUND AND AIMS: To investigate the prevalence of gallstone disease in Chinese patients with liver cirrhosis and to identify risk factors for cholelithiasis. METHODS: Blood samples were tested and ultrasonographic examination of the upper abdomen was conducted to observe the prevalence of gallstones in 90 compensated cirrhotic patients (Child-Pugh A), 180 decompensated cirrhotic patients (Child-Pugh B, C) and 300 controls. Risk factors for gallstone formation (age, sex, pregnancy, family history) and the characteristics of liver cirrhosis (Child class, inside diameter of portal vein), and gallbladder (wall thickness) were assessed. RESULTS: Gallstones were found more often in cirrhotic patients (23.7%) than in controls (7.33%, P < 0.001). The prevalence of gallstones in decompensated cirrhotic patients was higher than that of the compensated cirrhotic patients (P < 0.001). Advanced age, female sex, family history of gallstones, gallbladder wall thickness 4 mm or greater and inside diameter of portal vein 13 mm or greater were significantly associated with gallstone disease in patients with liver cirrhosis. Multivariate analysis revealed that age (P < 0.001), sex (P = 0.0005) and thickness (4 mm or greater) of the gallbladder wall (P = 0.0064) were independently associated with gallstone disease in such patients. CONCLUSIONS: This study confirms the high prevalence of cholelithiasis in liver cirrhosis. Age and sex are risk factors for gallstones and gallbladder wall thickness could be an additional risk factor for the development of gallstone in patients with liver cirrhosis.     

Prevalence of gastric ulcer in cirrhotic patients and its relation to portal hypertension

The prevalence of gastric ulcer and its relationship to the severity of cirrhosis and degree of portal hypertension was evaluated in 245 cirrhotic patients, and compared with 245 age- and sex-matched healthy subjects. Portal and systemic haemodynamic studies were performed in cirrhotic patients. The prevalence of gastric ulcer in cirrhotic patients was 20.8%, which was significantly higher than the 4.0% found in healthy controls. Using a multivariate logistic regression model, the hepatic venous pressure gradient was found to be the only predictor of the prevalence of gastric ulcer in cirrhotic patients to present with gastric ulcer. The hepatic venous pressure gradient was significantly higher in cirrhotic patients with gastric ulcer than in those without (17.3 ± 4.4 vs 15.5 ± 5.0 mmHg, P= 0.01). Other variables, including sex, smoking, cardiac output and severity or aetiology of cirrhosis did not show significant differences between the two patient groups. The prevalence of gastric ulcer in cirrhotic patients whose hepatic venous pressure gradient was below 12 mmHg (4.5%) was similar to that observed in the healthy controls (4.0%). However, when the hepatic venous pressure gradient was > 12 mmHg, the prevalence of gastric ulcer (24.4%) was significantly higher than that in control subjects. However, the incidence of gastric ulcer was not related to the degree of portal hypertension. In conclusion, the prevalence of gastric ulcer in cirrhotic patients was found to be significantly higher than in the age- and sex-matched healthy subjects. Portal hypertension with a hepatic venous pressure gradient > 12 mmHg may be an important factor contributing to the increased prevalence of gastric ulcer observed in patients with liver cirrhosis.     

Oxygen and bile acid content in the azygos blood. Clues to the azygos derivation in patients with portal hypertension

In patients with cirrhosis, elevation of azygos blood flow has been attributed on indirect grounds to cephalad portosystemic collaterals. To gather more information on the origin of the azygos blood, we studied the oxygen and bile acid content of the azygos and mixed venous blood in patients with portal hypertension. Azygos oxygen saturation was 59.6 +/- 6.0% in 8 controls, and significantly higher in 35 patients with cirrhosis (76.7 +/- 7.6%; P less than 0.01) as well as in 6 patients with noncirrhotic portal hypertension (84.0 +/- 8.2%; P less than 0.01). High oxygen saturation, however, was not correlated to azygos blood flow in patients with cirrhosis. In cirrhotic patients, total bile acid concentrations were 28.1 +/- 20.4 mumol/l in the pulmonary artery and 25.9 +/- 17.6 mumol/l in the azygos vein, giving an azygos to mixed venous ratio of 0.95 +/- 0.18. These results provide new evidence that elevated azygos blood flow in patients with portal hypertension is derived from the portal system, and perhaps predominantly from the splenic territory.     

Evaluation of Gallbladder Motility in Patients with Liver Cirrhosis

To investigate the postprandial gallbladder motility, including emptying and refilling, in cirrhotic patients and to evaluate the relationship to the presence of gallstones and various humoral mediators, 82 patients with liver cirrhosis and 40 age- and sex-matched healthy subjects were enrolled into this study. Postprandial gallbladder volumes were measured with ultrasonography every 15 min for 2 hr. Plasma levels of estradiol, testosterone, substance P, and nitrate/nitrite were also measured. Cirrhotic patients showed a higher prevalence of gallstones than healthy subjects (41% vs 15%, P = 0.003), and the prevalence increased with the progression of liver cirrhosis (Child-Pugh class A: 26%, B: 44%, and C: 65%, P = 0.02). Plasma levels of estradiol, testosterone, and substance P, and nitrate/nitrite and estradiol/testosterone ratios were not different between cirrhotic patients with and without gallstones. However, postprandial refilling of the gallbladders was significantly impaired in patients with cirrhosis, especially in those combined with gallstones. There was no significant difference in the postprandial gallbladder motility between cirrhotic patients with and without elevated plasma levels of estradiol, testosterone, and substance P and nitrate/nitrite, and estradiol/testosterone ratios. Gallstones were common in patients with liver cirrhosis and the prevalence increased with the progression of liver diseases. Sex hormones, substance P, and nitrate/nitrite did not play major roles in the formation of gallstones in cirrhotic patients. Refilling of the gallbladder was significantly impaired in patients with liver cirrhosis, especially in those with gallstones, and may play an important role in the pathogenesis of gallstones.     

Nitric oxide synthase 1 is partly compensating for nitric oxide synthase 3 deficiency in nitric oxide synthase 3 knock-out mice and is elevated in murine and human cirrhosis.

BACKGROUND: The role of endothelial nitric oxide synthase 3 (NOS-3) in the hyperdynamic circulation associated with cirrhosis is established but not that of the neuronal (NOS-1) isoform. We therefore investigated aortic NOS-1 levels in NOS-3 knock-out (KO) and wildtype (WT) mice and in hepatic arteries of patients. METHODS: Mice rendered cirrhotic by bile duct ligation (BDL) were compared with sham-operated controls. Hepatic arteries of cirrhotic patients were collected during liver transplantation; donor vessels served as controls. mRNA levels were quantified by real-time PCR, protein levels by Western blotting and NO production by Nomega-nitro-L-arginine methyl ester inhibitable arginine-citrulline assay. RESULTS: Aortae of NOS-3 KO mice exhibited higher NOS-1mRNA (5.6-fold, P < 0.004) and protein levels (8.8-fold) compared with WT. NO production in aortae of NOS-3 KO mice was 52% compared with WT (P = 0.002). BDL increased NOS-1 mRNA (2.4-fold, P = 0.01) and protein (7.1-fold) levels in aortae of WT, but no further in the NOS-3 KO mice. Hepatic artery NOS-1 mRNA levels in cirrhotic patients were markedly increased compared with controls (24.5-fold, P = 0.0007). CONCLUSIONS: Increased NOS-1 mRNA and protein levels and partially maintained in vitro NO-production in aortae of NOS-3 KO mice suggest that NOS-1 may partially compensate for NOS-3 deficiency. BDL-induced increase in aortic NOS-1 mRNA and protein levels hint that not only NOS-3, but also NOS-1 may be involved in the regulation of systemic hyperdynamic circulation and portal hypertension. Upregulation of NOS-1 mRNA levels in hepatic arteries of portal hypertensive patients suggests possible clinical significance for these experimental findings.     

Hyperglobulinemia in alcoholic cirrhosis

The relative importance of portal hypertension and intrahepatic portal-systemic shunting in the pathogenesis of hyperglobulinemia is examined in 31 alcoholic cirrhotic patients and 6 patients with idiopathic portal hypertension. The degree of portal hypertension was evaluated by combined umbilicoportal and hepatic vein catheterization and the intrahepatic portal-systemic shunting was assessed by the Kupffer uptake of [¹²⁵I]albumin microaggregates during a single passage through the liver. All patients had comparable severe portal hypertension and most had bled from ruptured varices; however, no demonstrable relationship could be found between portal hypertension and hyperglobulinemia. Elevated levels of serum gammaglobulins and immunoglobulins (mainly IgG) were observed only in cirrhotic patients, particularly those with markedly altered Kupffer cell uptake. It is concluded that intrahepatic portal systemic shunting as evaluated by the Kupffer cell uptake is more important than the collateral circulation secondary to portal hypertension in the pathogenesis of hyperglobulinemia in alcoholic cirrhotic patients.     

Hyperglucagonaemia in cirrhosis

Summary Plasma glucagon and growth hormone concentrations were measured fasting and after oral glucose in 19 patients with portal vein block with extensive portal-systemic shunting but minimal liver cell damage, 11 cirrhotic patients and 12 matched control subjects. Portal vein block patients and controls had similar fasting glucose and glucagon levels (glucose 3.8 ±0.1 mmol/l vs control 3.4±0.1 mmol/l (mean±SEM); glucagon 57.5 ±9.1 pg/ml vs control 51.3±7.8 pg/ml). Cirrhotic patients were hyperglycaemic (cirrhosis 4.3±0.2 mmol/l vs control 3.4 ±0.1 mmol/l, p < 0.01) with significantly elevated glucagon levels (167.3±61.1 pg/ml vs control 51.3 ±7.8 pg/ml, p < 0.05), which suppressed towards control values after oral glucose. There was no correlation between fasting plasma glucagon levels and the degree of portal-systemic shunting in cirrhotic patients. There was a strong correlation between fasting plasma glucagon concentrations and aspartate transaminase levels (r = 0.68; p < 0.01) in cirrhotic and portal vein block patients. Significant elevations of growth hormone were seen only in cirrhotic patients. It is concluded that hyperglucagonaemia is a feature of hepatocellular damage rather than portalsystemic shunting but the relationship between elevated glucagon and growth hormone concentrations and carbohydrate intolerance in cirrhosis remains unclear.     

Correlation between hemodynamic parameters of the portal circulation in cirrhotic patients

The aim was to study the relationships between portal hemodynamic parameters in cirrhotic patients. Portal hemodynamics was assessed by scintisplenoportography and sonography, and the measurement of portohepatic gradient. Gradient between wedged and free hepatic venous pressures was 2.71 +/- 0.90 kPa (SD), and extrahepatic shunting was 49 +/- 31 p. 100 (SD) in 27 cirrhotic patients. Intrahepatic shunting was present in 17 p. 100 out of 23 cirrhotics. Portal blood flow was 0.582 +/- 0.196 l/min (SD) and hepatic resistance to portal blood flow was 4.84 +/- 2.62 kPa/l/min (SD). Portal blood flow correlated neither with the pressure gradient, nor with portosystemic shunting. The pressure gradient was significantly correlated with portal systemic shunting (r = 0.64, p less than 0.001). Hepatic resistance to portal blood flow was significantly (p less than 0.05) correlated with portal systemic shunting, however the value of the correlation coefficient was low (r = 0.433). The pressure gradient and portosystemic shunting were higher in patients with large esophageal varices than in those with small ones (respectively t = 2.665, p less than 0.02 and t = 3.00, p less than 0.01). Hemodynamic pattern was not correlated with the degree of hepatocellular failure, as assessed by the Child-Pugh index. In conclusion this study provides further evidence for the forward theory of portal hypertension in human liver cirrhosis.     

The impact of chronic hepatitis B viral infection on gastrointestinal motility

OBJECTIVES: Disturbed gastrointestinal (GI) motility probably exists in alcoholic cirrhotic patients; however, the influence of chronic hepatitis B virus (HBV) infection on GI motility remains unknown. The purpose of this prospective study was to determine the impact of chronic HBV infection on human GI transit, and to explore the possible patient factors modulating GI motility. METHODS: We used a non-invasive hydrogen breath test measuring the oro-caecal transit time (OCTT) to assess the GI motility in 45 asymptomatic HBV carriers, 26 patients with chronic hepatitis B, 23 patients with HBV-related liver cirrhosis, and 45 age- and sex-matched healthy volunteers. Their clinical symptoms and various blood parameters, such as platelet count, prothrombin time, etc. were recorded. Plasma substance P, nitrate/nitrite and endothelin-1 levels were also measured. RESULTS: The OCTTs in controls, HBV carriers, chronic hepatitis B and liver cirrhosis patients were (mean +/- SEM) 78.4 +/- 5.8, 80.9 +/- 4.2, 93.9 +/- 8.8 and 106.5 +/- 12.4 min, respectively. The OCTT was delayed in patients with HBV-related liver cirrhosis compared to that of controls (P=0.039). Among the cirrhotic patients, presentation with ascites delayed OCTT (145.7 +/- 27.2 versus 91.3 +/- 11.9 min, P=0.039). Neither Child- Pugh grade, portal hypertension, various blood parameters, plasma substance P, nitrate/nitrite or endothelin-1 levels had any influence on OCTT. CONCLUSIONS: HBV infection alone does not alter GI motility, whereas the patients with liver cirrhosis may have delayed GI motility. Ascites is most likely a factor responsible for the delayed GI transit among chronic HBV-infected subjects.