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.     

肝硬化门脉高压性胃病与幽门螺杆菌关系的探讨

目的探讨肝硬化门脉高压性胃病(PHG)与幽门螺杆菌(Hp)感染的关系及临床意义。方法对72例PHG和50例慢性胃炎患者进行了胃镜、病理检查和Hp检测,并进行对比分析。结果伴有PHG 的肝硬化门脉高压患者的Hp感染率为23.07%,不伴有PHG者为25.0%,两者差异无显著性(P>0.05), 轻度PHG患者Hp感染率为23.80%,重度为20.0%,差异无显著性(P>0.05)。门脉高压患者的Hp感染率显著低于慢性胃炎组(23.60%比72.0%,P<0.01),但门脉高压患者慢性活动性胃炎的发生与Hp的感染密切相关,活动性胃炎的Hp感染率(53.84%)比非活动性胃炎Hp感染率(16.94%)显著升高(P< 0.01)。结论肝硬化门脉高压性胃病的Hp感染率降低,可能与肝硬化患者胃内环境不适合Hp的生存有关。门脉高压患者胃黏膜的活动性炎症,可能是由Hp感染引起,与肝硬化门脉高压关系不大。     

一氧化氮与白介素2、8对肝硬化门脉系统血流量的影响

目的：探讨一氧化氮（ＮＯ）、白介素２（ＩＬ－２及白介素８（ＩＬ－８）对肝硬化门静脉系统血流量的影响。方法：应用ＭＴＴ法检测肝硬化患者血清ＩＬ－２活性;应用ＥＬＩＳＡ法测定血清ＩＬ－８含量;应用荧光比色法检测血清ＮＯ水平;应用多普勒超声检测门静脉系统血流量参数。结果：肝硬化患者血ＩＬ－２活性、血清ＩＬ－８与ＮＯ水平显著高于正常对照组,其脾静脉血流量（ＳＶＦ）与肠系膜上静脉血流量（ＳＭＶＦ）之和亦显著大于正常对照组的门静脉血流量（ＰＶＦ）。结论：肝硬化患者血ＩＬ－２、ＩＬ－８增加可能为ＮＯ增多的诱发因素;肝硬化患者存在内脏高动力循环状态,ＮＯ增加可能起重要作用。     

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.     

Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: the role of Helicobacter pylori infection and portal hypertensive gastropathy.

BACKGROUND & AIM: The relationship between Helicobacter pylori infection and peptic ulcer disease in cirrhosis remains controversial. The purpose of the present study was to investigate the role of H pylori infection and portal hypertension gastropathy in the prevalence of active peptic ulcer among dyspeptic patients with compensated hepatitis C virus (HCV)-related cirrhosis. METHODS: Patients undergoing upper endoscopy with compensated HCV-related cirrhosis were enrolled. Child-Pugh's score was determined at the entry. Variceal size was measured endoscopically and the severity of portal hypertensive gastropathy was graded. H pylori infection status was determined by urea breath testing and/or histology. RESULTS: A total of 178 patients positive for HCV (A and B Child-Pugh's score) were prospectively included. The prevalence of H pylori infection was 43%. An active peptic ulcer was found in 14 patients (8%) and was significantly more common among those with H pylori infection (16% versus 2% in H pylori uninfected patients, odds ratio: 8.0). No association was observed between H pylori infection and variceal size, or hypertensive gastropathy. CONCLUSIONS: Patients with compensated cirrhosis and H pylori infection showed higher risk of developing a peptic ulcer. Clinical relevance of this result would be that dyspeptic patients with HCV-related cirrhosis may benefit from preventive screening and eradication of H pylori, especially those with features of insufficient hemostasis.     

Helicobacter pylori Infection and Peptic Ulcer Disease in Cirrhosis

An increased frequency of peptic ulcer diseaseis noted in patients with cirrhosis, but the role of H.pylori in this disorder remains to be determined. Thediagnosis of cirrhosis was confirmed by a combination of clinical, biochemical, radiological, andhistological methods. The severity of cirrhosis wasassessed by Pugh's modification of Child's criteria.Upper gastrointestinal endoscopy was performedconsecutively to evaluate the presence of varices andgastroduodenal mucosa. H. pylori status was assessed byhistology, urease test, and serology. In all, 130patients with cirrhosis were recruited into the study;there were 86 males and 44 females with a mean (SD)age of 54.4 (12.7) years. The H. pylori prevalence was76.2% . There was no difference in age between the H.pylori-positive and -negative cirrhotics (P = 0.29). The H. pylori prevalence revealed no differenceamong cirrhotics with Child A (77.8%), Child B (72.9%),and Child C (78.6%) (P = 0.8), and neither was there adifference in H. pylori prevalence in cirrhotics with and without congestive gastropathy (77% vs73.7% , P = 0.84). The prevalence of H. pylori incirrhotics with and without varices did not show astatistical difference (75% vs 81.8%, P = 0.68). There also was no difference in the H. pyloriprevalence between cirrhotic patients with and withoutpeptic ulcers (84.4% vs 69.7% , P = 0.09). Inconclusion, the prevalence of H. pylori or peptic ulceris independent of the severity of cirrhotic liver disease. Theassociation between H. pylori infection and peptic ulcerdisease is weak in cirrhosis.     

Lack of association between seroprevalence of Helicobacter pylori infection and primary biliary cirrhosis

AIM: To determine the association between seroprevalence of Helicobacter pylori (H pylori) infection and primary biliary cirrhosis (PBC). METHODS: In this case-control study, 149 consecutive patients (10 males, 139 females, mean age 58.2+/-11 years, range 26-82 years) suffering from PBC and 619 consecutive healthy volunteer blood donors (523 males, 96 females, mean age 47+/-5.3 years, range 18-65 years) attending the Hospital Blood Bank and residing in the same area were recruited. A commercial enzyme linked immunosorbent assay was used to detect anti-H pylori (IgG) antibodies in serum. RESULTS: Antibodies to H pylori were present in 78 (52.3%) out of 149 PBC-patients and in 291 (47%) out of 619 volunteers (P = 0.24, OR 1.24, 95% CI 0.85-1.80). In the subjects less than 60 years old, the prevalence of H pylori infection among PBC-patients (40/79) was slightly higher than in controls (50.6% vs 46.2%) P = 0.46, OR = 1.19, 95% CI: 0.72-1.95). In those over 60 years, the prevalence of H pylori infection was similar between PBC-patients and controls (54.2% vs 57.8%, P = 0.7, OR 0.86, 95% CI 0.36-2.07). CONCLUSION: There is no association between seroprevalence of H pylori infection and primary biliary cirrhosis.     

内皮型一氧化氮合酶基因VNTR多态性与肝硬化门脉高压症的相关性研究

目的 探讨内皮型一氧化氮合酶(eudnthelial nitric oxide synthase,eNOS)基因第4内含子数目可变性串联重复序列(variable number of tandem repeats polymorphism VNTR) 态性与肝硬化门脉高压症的相关性。方法 采用病例对照和聚合酶链反应(PCR)及非变性聚丙烯酰胺凝胶电泳的方法,检测106例乙肝后肝硬化患者和108名健康对照者eNOS基因第4内含子的VNTR多态性及外周血NO2-/NO3-含量,并进行统计分析。结果 乙肝后肝硬化患者a等位基因频率高于对照组(13.21％VS 8.8％),但差异无显著性意义;然而,在门脉高压a等位基因频率明显高于对照组,差异有显著性意义(14.62％VS 8.8,P<0.05),相关分析呈正相关(r=0.16)。携带a等位基因者发生门脉高压症的危险性高于非a等位基因携带者1.2倍(OR=2.2)。结论 eNOS基因第4内含子的VNTR多态性与肝硬化门脉高压症形成相关,a等位基因可能是中国人群门脉高压症的遗传易感性的基因标志之一。     

Helicobacter pylori infection in hepatic encephalopathy: Relationship to plasma endotoxins and blood ammonia

Background/Aim: Hepatic encephalopathy (HE) is frequently observed in patients with advanced liver disease and manifests a wide variety of neuropsychiatric signs and symptoms. Ammonia toxicity and bacterial endotoxins have been suggested as key determinants of HE onset whereas a role for Helicobacter pylori infection has not been established. We investigated the correlation between H. pylori infection and HE severity (evaluated through functional tests) in 60 outpatients with established liver cirrhosis and 20 non-cirrhotic controls. Methods: Fasting arterial blood ammonia, plasma endotoxins, and H. pylori infection status were investigated in all subjects. Results: H. pylori infection was documented in 35/60 (58%) patients and in 6/20 (30%) controls (P = 0.039). Significant differences were observed between patients with and withoutHE for age, presence of ascites, fasting arterial blood ammonia, plasma endotoxin, and H. pylori infection. Further, a significant increase in fasting arterial blood ammonia and plasma endotoxin was associated with H. pylori infection in cirrhotic patients. Last, medical treatment of H. pylori infection led to a significant decrease in HE severity and fasting arterial blood ammonia levels. Conclusion: In conclusion, we submit that H. pylori infection might, in fact, play a role in increasing the circulating levels of ammonia and endotoxins in cirrhotic patients, thus facilitating the onset of HE.     

Nitric oxide synthase activity in the splanchnic vasculature of patients with cirrhosis: relationship with hemodynamic disturbances.

BACKGROUND/AIMS: It has been demonstrated that an overproduction of nitric oxide plays an important role in the pathogenesis of the hyperdynamic circulation exhibited by cirrhotic patients. Nevertheless, evidence is supported by studies performed in experimental models or by indirect measurements in humans. The purpose of this study has been to evaluate nitric oxide production in splanchnic vasculature of patients with cirrhosis and to investigate its possible relationship with systemic and splanchnic hemodynamics. METHODS: Nitric oxide synthase (NOS) activity was measured in hepatic artery and portal vein tissues of nine cirrhotic patients. Samples were obtained during liver transplantation. Control samples were obtained simultaneously from the corresponding tissues of the liver donors. Hemodynamic parameters were determined with Doppler ultrasonography. RESULTS: NOS activity was significantly higher in hepatic artery of cirrhotic patients than in controls (8.17 +/- 1.30 vs 4.57 +/- 0.61 pmoles/g of tissue/min, P < 0.05). Patients with ascites showed a higher hepatic artery NOS activity than patients without ascites. Highly significant correlation was observed between cardiac output and hepatic artery NOS activity as well as between portal blood flow and hepatic artery NOS activity. CONCLUSIONS: The present study demonstrates an enhanced production of nitric oxide in the splanchnic vasculature of patients with cirrhosis.     

Analysis of risk factors for chronic hepatic encephalopathy: the role of Helicobacter pylori infection

Objective: Elevated blood ammonia is an important pathogenic factor of hepatic encephalopathy. Although colonic bacteria are considered the main source of ammonia, the stomach in subjects with urease-producing Helicobacter pylori ( H. pylori ) is an alternative site. The objective of this study was to determine whether H. pylori is associated with this complication.
Methods: After assessing liver function and portal hypertension, 55 cirrhotics were evaluated for encephalopathy and H. pylori infection. Response to 2 weeks of amoxicillin (2 g/day) and omeprazole (40 mg/day) was then assessed in 17 (13 H. pylori -positive, four H. pylori -negative) encephalopathic subjects.
Results: H. pylori infection was more common (  67% vs 33%  ,   p = 0.004  ) among encephalopathic patients. Additional factors associated with encephalopathy included older age (  60.1 ± 1.5 vs 49.8 ± 2.4 yr  ,   p = 0.001  ), lower albumin (  3.17 ± 0.08 vs 3.69 ± 0.12 g/dl  ,   p = 0.001  ), higher total bilirubin (  2.24 ± 0.20 vs 1.53 ± 0.23 mg/dl  ,   p = 0.034  ), greater ascites score (  0.8 ± 0.1 vs 0.3 ± 0.1  ,   p = 0.01  ), greater diuretic score (  1.1 ± 0.1 vs 0.3 ± 0.1  ,   p = 0.002  ), and greater modified Child score (  6.7 ± 0.3 vs 5.1 ± 0.3  ,   p = 0.001  ). When adjusted for severity of cirrhosis and age, H. pylori continued to demonstrate a statistical association (   p = 0.039  ). After anti- H. pylori therapy, symptomatology in infected encephalopathic patients appeared to improve, whereas noninfected subjects were unaffected.
Conclusions: In cirrhotic patients, H. pylori infection is associated with hepatic encephalopathy, especially in younger patients with decompensated liver disease.     

Helicobacter pylori infection and gastric emptying in cirrhotic patients with symptoms of dyspepsia

BACKGROUND/AIMS: Chronic gastric Helicobacter pylori infection is common in patients with dyspeptic symptoms. The effect of H. pylori infection on gastric emptying, in cirrhotic patients with dyspeptic symptoms, has never been studied. Therefore, we investigated the incidence of H. pylori infection and its relationship with gastric emptying in cirrhotic patients with dyspepsia. METHODOLOGY: A solid-phase gastric emptying study and 14C urea breath test were performed in 80 cirrhotic patients with dyspepsia. The severity of cirrhosis was assessed according to Child-Pugh's classification. RESULTS: The overall incidence of delayed gastric emptying was 75%. Delayed gastric emptying incidences according to severity of cirrhosis were 71.4% for Child-A, 73.1% for Child-B, and 80.8% for Child-C. The differences were not significant. The incidence of H. pylori infection was 52.5% overall. H. pylori infection rates were 46.4% for Child-A, 42.3% for Child-B, and 69.2% for Child-C. Although there was a tendency for the infection rate to increase with the severity of liver cirrhosis, the difference was not significant. In addition, there were no significant differences in the incidences of H. pylori infection among patients with normal and delayed gastric emptying. CONCLUSIONS: Delayed gastric emptying is common in cirrhotic patients with dyspepsia. However, the status of H. pylori infection does not seem to play a role in delayed gastric emptying in these patients.     

Effect of H pylori infection and its eradication on hyperammo-nemia and hepatic encephalopathy in cirrhotic patients

AIM: To investigate the relationship between H pylori infection, blood ammonia concentration and hepatic encephalopathy (HE), and the effect of H pylori eradication in cirrhotic patients.METHODS: From July 2003 to January 2005, 457 cirrhotic patients in five regions of Zhejiang Province were enrolled. Patients were evaluated for demographics, number connection test, H pylori infection, liver impairment, blood ammonia concentration and HE. Patients with H pylori infection were given 1 wk therapy with omeprazole plus clarithromycin and tinidazole. 14C urea breath test was performed and mental symptoms and blood ammonia level were reassessed after bacterium eradication.RESULTS: Overall H pylori infection rate was 60.6%, and HE occurred in 47.5% of cirrhotic patients. Subclinical HE (SHE) was detected in 55 of 117 cirrhotic patients. Blood ammonia concentration in H pylori negative (n = 180) and positive (n = 277) cirrhotic patients was 53.8 ± 51.4 and 78.4 ± 63.6 nmol/L, respectively (P < 0.01), which was significantly reduced to 53.5 ± 37.7 nmol/L after bacterium eradication (n = 126) (P < 0.01). Blood ammonia was 97.5 ± 81.0 nmol/L in H py/ori-positive cirrhotic patients, and this did not significantly change in those with persistent infection after H pylori eradication (n = 11). HE was more frequently observed in patients with H pylori infection than in those without (58.5% vs 30.6%, P < 0.01). HE rate significantly dropped to 34.1% after H pylori eradiation (P < 0.01). H pylori prevalence significantly differed among cirrhotic patients with HE (74.4%), SHE (69.1%), and those without HE (53.2%) (P < 0.05). Blood ammonia level was significantly different among cirrhotic patients with HE (94.5 ± 75.6 nmol/L), SHE (59.9 ± 49.2 nmol/L), and without HE (47.3 ± 33.5 nmol/L) (P < 0.05). Logistic regression analysis showed that blood ammonia concentration, Child-Pugh stage, upper gastrointestinal bleeding, electrolyte disturbance, and urea nitrogen were risk factors for HE.CONCLUSION: H pylori infection is an important factor for inducing high blood ammonia concentration and HE in cirrhotic patients. H pylori eradication may be helpful for treatment and prevention of HE.     

Is Helicobacter pylori eradication indicated in cirrhotic patients with peptic ulcer disease?

INTRODUCTION: The association between H. pylori infection and peptic ulcer disease (PUD) and the efficacy of eradication of H. pylori in treating ulcer disease in cirrhotic patients remains controversial. This study was carried out to ascertain the prevalence and significance of H. pylori in cirrhotic patients with PUD and to assess the need for anti H. pylori thrapy METHODS: Three groups of patients were studied . These were patients with (A) cirrhosis and PUD, (B) uncomplicated PUD and (C) cirrhosis without PUD. H. pylori status was determined by endoscopic urease test . Eradication therapy was given with a four drug regimen and repeat endoscopy was done three months later to detect ulcer healing as well as H. pylori status with PUD in groups A and B. RESULTS: Cirrhotic patients with PUD had a significantly lesser prevalence of H. pylori compared to uncomplicated ulcer patients (46.9 % vs 80 %; p = 0.04). While H. pylori eradication rates were similar between cirrhotic and non cirrhotic patients, ulcer healing rate was significantly lesser in cirrhotic patients ( 48 % vs 80.9 %) . Majority of residual ulcers in cirrhotic patients were negative for H. pylori. CONCLUSION: Eradication of H. pylori does not reduce the residual ulcer rate indicating that H. pylori infection might not be a significant risk factor for PUD in cirrhotic patients. Hence, routine H. pylori eradication might not be warranted in patients with cirrhosis and peptic ulcer disease.     

慢性乙型肝炎病毒感染患者血清及肝组织中抗幽门螺杆菌抗体及特异性基因分析

目的 对慢性乙型肝炎病毒(HBV)感染患者血清抗幽门螺杆菌(Hp)IgG(抗Hp-IgG)阳性率进行流行病学调查,同时对患者肝组织进行Hp特异性基因检测,探讨Hp在肝病发生、发展中的作用.方法 病例对照研究中共纳入502例HBV感染患者和性别、年龄相匹配的429名健康对照者.应用酶联免疫吸附(ELISA)法进行血清抗Hp-IgG检测.同时用针对螺杆菌菌属特异性16S rRNA基因的通用引物对其中56例肝穿刺活检组织进行基因扩增,并对该基因阳性者进一步应用Hp cagA、vacA和glmM基因特异引物进行扩增.结果 HBV感染患者血清抗Hp-IgG阳性率为63.9%,显著高于健康对照者(43.4%,P<0.05),其中肝癌组的阳性率最高(29/36,80.6%),其次为肝硬化组(64/83,77.1%),两组均显著高于慢性乙型肝炎组(228/383,59.5%,P<0.01).56例行肝穿刺活检患者中,35例肝组织中发现螺杆菌菌属特异性16S rRNA基因,其中肝硬化组17例,肝癌组7例,慢性乙型肝炎组11例.进一步的扩增结果 证实35例中21例为Hp DNA.结论 HBV感染患者血清抗Hp-IgG阳性率显著高于健康对照者.HBV感染患者肝组织中除存在Hp DNA外,可能还存在其他螺杆菌DNA.螺杆菌在慢性乙型肝炎向肝硬化和肝癌的发展过程中可能发挥致病作用.     

Effect of H pylori infection and its eradication on hyperammo-nemia and hepatic encephalopathy in cirrhotic patients

AIM： To investigate the relationship between H pylori infection, blood ammonia concentration and hepatic encephalopathy （HE）, and the effect of Hpylori eradication in cirrhotic patients. METHODS： From July 2003 to January 2005, 457 cirrhotic patients in five regions of Zhejiang Province were enrolled. Patients were evaluated for demographics, number connection test, Hpylori infection, liver impairment, blood ammonia concentration and HE. Patients with Hpylori infection were given I wk therapy with omeprazole plus clarithromycin and tinidazole. ^14C urea breath test was performed and mental symptoms and blood ammonia level were reassessed after RESULTS： Overall H pylori infection rate was 60.6%, and HE occurred in 47.5% of cirrhotic patients. Subclinical HE （SHE） was detected in 55 of 117 cirrhotic patients. Blood ammonia concentration in H pylori negative （n = 180） and positive （n = 277） cirrhotic patients was 53.8 ± 51.4 and 78.4 ± 63.6 μmol/L, respectively （P 〈 0.01）, which was significantly reduced to 53.5 ± 37.7 μmol/L after bacterium eradication （n = 126） （P 〈 0.01）. Blood ammonia was 97.5 ± 81.0 μmol/L in H pylori-positive cirrhotic patients, and this did not significantly change in those with persistent infection after Hpylori eradication （n = 11）. HE was more frequently observed in patients with H pylori infection than in those without （58.5% vs 30.6%, P 〈 0.01）. HE rate significantly dropped to 34.1% after H pylori eradiation （P 〈 0.01）. H pylori prevalence significantly differed among cirrhotic patients with HE （74.4%）, SHE （69.1%）, and those without HE （53.2%） （P 〈 0.05）. Blood ammonia level was significantly different among cirrhotic patients with HE （94.5 ± 75.6 μmol/L）, SHE （59.9 ± 49.2 μmol/L）, and without HE （47.3 ± 33.5 μmol/L） （P 〈 0.05）. Logistic regression analysis showed that blood ammonia concentration, Child-Pugh stage, upper gastrointestinal bleeding, electrolyte disturbance, and urea nit     

Dyssynchronous electrical and mechanical systole in patients with cirrhosis

BACKGROUND/AIMS: Previous investigations have shown a prolonged QT interval in some patients with cirrhosis. The aim of this study was to investigate the relation between electrical and mechanical systole in patients with different degrees of severity of cirrhosis. METHODS: Forty-eight patients with cirrhosis and portal hypertension, studied during a haemodynamic investigation, were compared to 17 controls. RESULTS: A prolonged QTc (above 0.440 s(1/2)) was found in 37% of the cirrhotic patients vs. 5.9% in the controls (P=0.03), and there was a correlation to liver dysfunction (P<0.02). A direct relation between QT and time of mechanical systole (tS) was observed in controls (r=0.58, P<0.01), and cirrhotic patients (r=0.44, P<0.002). In patients with a prolonged QTc interval, the difference between electrical and mechanical systole time was substantially longer than in patients with a normal QTc interval (0.078 vs. 0.031 s, P<0.005). The QT values were related to markers of hyperdynamic circulation (r=-0.48 to 0.56, P<0.05-0.001). CONCLUSIONS; Prolonged repolarization, as evidenced by prolonged QTc, is related to both impaired liver function and systemic circulatory dysfunction. In addition these patients have alterations in the cardiac excitation-contraction relation with compromised association between electrical and mechanical function.     

Colonization by Helicobacter pylori and its relationship to histological changes in the gastric mucosa in portal hypertension

Abstract In order to investigate the relationship between Helicobacter pylori infection of the gastric mucosa and mucosal changes in portal hypertension, gastric fundic and antral biopsies were obtained from 66 patients with portal hypertension and 49 controls with non-ulcer dyspepsia (NUD). Gastric mucosa from portal hypertensive patients exhibited typical vascular dilatation and congestion, while mild dilatation of lamina propria blood vessels was not uncommon in NUD patients with histological evidence of gastritis. Colonization of the gastric mucosa by H. pylori infection was significantly less in portal hyptertension (51.5%) compared to controls (75.5%; P <0.01). The difference was more apparent in patients with marked vascular dilatation (18.8% colonization) compared to patients with minimal vascular dilatation (66.7%). H. pylori infection was significantly associated with active superficial gastritis ( P <0.001), and with atrophic gastritis ( P <0.001), in both study groups. H. pylori -negative superficial gastritis was significantly more common in portal hypertension (25/66 patients) than in controls (7/49; P <0.05). H. pylori infection was not more common in patients who had undergone repeated sclerotherapy. The results suggest that the gastric mucosa of portal hypertension does not provide a hospitable environment for H. pylori colonization, particularly when mucosal congestion is marked. H. pylori infection does not add significantly to the gastropathy of portal hypertension.     

Brain natriuretic peptide and severity of disease in non-alcoholic cirrhotic patients

BACKGROUND: Cirrhotic patients have a hyperdynamic systemic circulation. They have insidious cardiac problems besides well-known complications. Brain natriuretic peptide (BNP) relaxes vascular smooth muscle and has a portal hypotensive action. The relations between BNP levels and severity of disease, cardiac dysfunction and esophageal varices were studied in non-alcoholic cirrhotic patients. METHODS: Fifty-two non-alcoholic cirrhotic patients were evaluated for decompensation component of cirrhosis. The BNP concentration of echocardiographically examined patients was determined. RESULTS: The BNP levels were significantly higher in ascites, spontaneous bacterial peritonitis and hepatic encephalopathy history group (P = 0.033, P < 0.001, P = 0.014, respectively), but no significant difference were observed for presence of esophageal varices and bleeding history (P = 0.267, P = 0.429). A significant correlation was observed between BNP concentration and Child score (r = 0.427, P = 0.012), interventricular septal thickness (r = 0.497, P < 0.001) and left ventricular posterior wall thickness (r = 0.526, P < 0.001). According to Child-Pugh classification there were no significant difference between groups for echocardiographic measurements and blood pressure (P > 0.05), but plasma BNP levels were significantly higher in Child class B and C patients compared with class A patients (P < 0.05). CONCLUSION: Increased levels of BNP are more likely related to the severity of disease in non-alcoholic cirrhotic patients. The advanced cirrhosis is associated with more advanced cardiac dysfunction and BNP has prognostic value in progression of cirrhosis.     

Lipoic acid prevents development of the hyperdynamic circulation in anesthetized rats with biliary cirrhosis

Chronic bile duct ligation is associated with the development of oxidant injury, biliary cirrhosis, portal hypertension, and a hyperdynamic circulation. We have previously demonstrated that the hyperdynamic circulation in the partial portal vein-ligated rat can be prevented by the administration of N-acetylcysteine. To extend these findings, we have examined the effect of lipoic acid, a thiol-containing antioxidant, on hemodynamics, oxidative stress, and nitric oxide (NO) production in bile duct-ligated (BDL) cirrhotic rats. Lipoic acid was given continuously in drinking water to normal and BDL rats; control rats received ordinary drinking water, and animals were studied at 24 days following surgery. Lipoic acid prevented the development of the hyperdynamic circulation (cardiac index [CI]: 15.7 +/- 2.0 vs. 29.5 +/- 2.1 mL x min-1 x 100 g-1; P <. 05) and significantly attenuated the rise in portal pressure (PP) (12.7 +/- 0.8 vs. 15.2 +/- 0.5 mm Hg; P <.05). Hepatic nitric oxide synthase (NOS) activity and plasma nitrite/nitrate concentration increased significantly following bile duct ligation, and both of these were prevented by lipoic acid. Lipoic acid had no effect on the biochemical or histological parameters of liver function in the cirrhotic group. We conclude that lipoic acid prevents the development of the hyperdynamic circulation in the rat model of biliary cirrhosis, and that this is associated with decreased synthesis of NO.