幽门螺杆菌感染与肝性脑病的相关性

目的探讨肝硬化患者幽门螺杆菌（H．pylori）感染和肝性脑病（HE）发病的相关性。方法收集110例符合诊断标准的肝硬化患者,详细记录H．pylori检测结果、血氨水平、数字连接试验（NCT）结果、HE临床症状。其中71例H．pylori阳性者随机分为观察组和对照组,观察组予泮托拉唑钠肠溶胶囊＋克拉霉素缓释片＋奥硝唑胶囊进行根除治疗,1周后复查血氨。结果H．pylori阳性肝硬化患者的血氨水平及HE的发生率明显高于Hpylori阴性的肝硬化患者,两者差异有统计学意义（P〈0．05）;tt．pylori阳性者中观察组行H．pylori根除治疗,血氨下降明显优于对照组（P〈0．05）。结论H．pylori感染可使肝硬化患者血氨水平升高,根除H．pylori治疗对降低肝性脑病的发生有重要的临床意义。     

Hepatic encephalopathy: a review

Hepatic encephalopathy (HE) is a complication that presents in as many as 28% of patients with cirrhosis, and reported up to ten years after the diagnosis of cirrhosis. Commonly, it is observed in patients with severe hepatic failure and is characterized by neuropsychiatric manifestations that can range in severity from a mild alteration in mental state to a coma; additionally, some neuromuscular symptoms can be observed. This complication of either acute or chronic hepatic disease is the result of a diminished hepatic reservoir and inability to detoxify some toxins that originate in the bowel. Today, the role of astrocytes, specifically the Alzheimer type II cells, is known to be very important in the pathogenesis of the hepatic encephalopathy, and will be reviewed later. In conclusion, the objectives of this review are: To understand the pathogenesis of hepatic encephalopathy, To recognize the precipitating factors, as well as preventive measures for the development of the hepatic encephalopathy, To describe the new classification of hepatic encephalopathy and its clinical implications, To recognize the clinical manifestations and stages of the disease, To understand the main diagnostic tests used to detect the hepatic encephalopathy, To describe the main therapeutic treatments of hepatic encephalopathy.     

Helicobacter pylori is not a risk factor for hepatic encephalopathy.

BACKGROUND: Helicobacter pylori infection has been described as a risk factor for hepatic encephalopathy in patients with chronic liver disease although the topic remains controversial. AIMS: To determine whether Helicobacter pylori infection is an independent predictive factor for encephalopathy in patients with liver cirrhosis. METHODS: Clinical, epidemiological, analytical and nutritional parameters of 205 patients were collected. Helicobacter pylori infection was determined by serology. Encephalopathy (grade II or higher) was clinically assessed during follow-up. The relationship between each parameter and encephalopathy was analysed by Kaplan-Meier curves and the Log rank test. The most significant parameters underwent multivariate analysis by Cox regression. RESULTS: Twenty-five variables were related to encephalopathy in the bivariate analysis. Multivariate analysis selected five independent factors: previous bouts of encephalopathy (Odds ratio 3.79; 95% confidence interval 1.94-7.38), albumin (Odds ratio 0.86; 95% confidence interval 0.80-0.92), tricipital skin fold (Odds ratio 0.79; 95% confidence interval 0.66-0.95) chronic pulmonary disease (Odds ratio 2.78, 95% confidence interval; 1.31-5.92), and on-going alcoholism (Odds ratio 2.62; 95% confidence interval 1.16-5. BB). CONCLUSIONS: Helicobacter pylori is not an independent risk factor for hepatic encephalopathy.     

Rectal compliance: a critical reappraisal

Compliance is a widely measured parameter of rectal function. Its value is determined clinically by recording pressure changes associated with volume infusion into a rectal balloon. This paper examines the inherent assumptions of the rectal balloon technique and discusses several of its shortcomings. A stricter definition of rectal compliance is needed, and in vivo compliance should be correlated with the directly measured mechanical properties of the rectal wall.     

Helicobacter pylori, hyperammonemia and subclinical portosystemic encephalopathy: effects of eradication

BACKGROUND/AIMS: An involvement of Helicobacter pylori in the development of hepatic encephalopathy in cirrhotic patients has been proposed, but data confirming such an association are lacking. This prospective study aimed to assess whether ammonia levels and indicators of subclinical portosystemic encephalopathy were influenced by H. pylori status in a series of 62 cirrhotic patients. The effects of H. pylori eradication on such parameters were also investigated. METHODS: Fasting blood ammonia levels, mental state, number connection test, flapping tremor, and EEG tracings were recorded at baseline, and in H. pylori-positive patients (as diagnosed by rapid urease test and 14C-urea breath test) these parameters were reassessed 2 months following eradication therapy. RESULTS: In this series of non-advanced cirrhotic patients, the prevalence of H. pylori infection was 52%. No significant differences were observed between H. pylori+ and H. pylori- cases with respect to fasting venous blood ammonia concentration (47+/-24 vs. 43+/-22 micromol/l) or to the remaining parameters assessing portosystemic encephalopathy. In addition, H. pylori eradication failed to induce any significant variation in either fasting blood ammonia levels (from 45+/-23 to 48+/-26 micromol/l) or neurologic disturbances. CONCLUSION: These results indicate that H. pylori infection is not a major contributing factor to either fasting blood ammonia levels or parameters assessing subclinical portosystemic encephalopathy in patients with non-advanced liver cirrhosis.     

Chlorpropamide-alcohol flush: a critical reappraisal

Conclusion Further progress can depend only on standardised testing to determine the response precisely, after consideration of known interacting factors (e. g. initial cheek temperature, plasma chlorpropamide concentration). Until liver biopsy to identify the alcohol dehydrogenase isoenzymes becomes harmless, further studies will perhaps reveal more about the extra-pancreatic effects of one sulphonylurea than about the aetiology of Type 2 diabetes and its complications.     

The eradication of Helicobacter pylori to prevent gastric cancer: a critical appraisal

Introduction: Gastric cancer is one of the top causes of cancer-related death worldwide. How to eliminate gastric cancer is an urgent public-health issue.

Areas covered: In this review, we present up-to-date results of studies on gastric cancer prevention through the eradication of Helicobacter pylori and discuss strategies and obstacles for the implementation of population-wide screening and treatment of this pathogen to prevent gastric cancer.

Expert commentary: Gastric cancer is an inflammation-associated cancer with multistep carcinogenesis. The process consists of H. pylori infection, ongoing inflammation, development of metaplastic epithelia and genetic instability eventuating in gastric cancer. H. pylori infection is critical for development of the disease and studies have consistently shown that H. pylori eradication results in a reduction in (a) gastric mucosal inflammation, (b) progression of histologic damage, (c) risk of peptic ulcers and ulcer recurrence, and (d) risk of gastric cancer. Compared with a large number of clinical trials evaluating chemopreventive approaches, studies of population-wide screening, and eradication of H. pylori have only recently begun and only in high-risk populations. To eliminate gastric cancer requires information on how to implement an effective program for screening and treatment of H. pylori taking into consideration the other health priorities in any specific population.     

Helicobacter pylori infection and extragastric disorders in children: A critical update

Helicobacter pylori(H. pylori) is a highly prevalent, serious and chronic infection that has been associated causally with a diverse spectrum of extragastric disorders including iron deficiency anemia, chronic idiopathic thrombocytopenic purpura, growth retardation, and diabetes mellitus. The inverse relation of H. pylori prevalence and the increase in allergies, as reported from epidemiological studies, has stimulated research for elucidating potential underlying pathophysiological mechanisms. Although H. pylori is most frequently acquired during childhood in both developed and developing countries, clinicians are less familiar with the pediatric literature in the field. A better understanding of the H. pylori disease spectrum in childhood should lead to clearer recommendations about testing for and treating H. pylori infection in children who are more likely to develop clinical sequelae. A further clinical challenge is whether the progressive decrease of H. pylori in thelast decades, abetted by modern clinical practices, may have other health consequences.     

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.     

Targeting portal pressure measurements: a critical reappraisal

Many of the complications of cirrhosis reflect the presence of portal hypertension, which is commonly expressed as the hepatic venous pressure gradient (HVPG). Baseline and repeat measurements of HVPG have been recommended for the management of patients with cirrhosis in the setting of pharmacologic prophylaxis of variceal bleeding and for gaining information about prognosis. However, published studies have demonstrated problems with the interpretation of the data on HVPG monitoring, making its use controversial. We view the current data as insufficient evidence to support the monitoring of a targeted reduction of HVPG as routine clinical practice. We recommend the performance of new prospective studies to establish the clinical importance of HVPG measurements.     

Surveillance in Barrett's oesophagus: a critical reappraisal

BACKGROUND: Current recommendations are for endoscopic surveillance of patients with Barrett's oesophagus to detect dysplasia and to diagnose carcinoma at an early and possibly treatable stage. However, observations suggest that these current practice guidelines are thwarted by many factors often not taken into account. These observations stem from general surveillance aspects as well from specific data on Barrett's oesophagus. This review therefore aims at discussing data on the current surveillance strategy in conjunction with general surveillance aspects relevant for their interpretation. METHODS: Literature survey of published articles. RESULTS: A critical reappraisal of the literature shows that the current surveillance strategy is hampered by multiple problems with the marker dysplasia, cost-ineffectiveness, an overrated cancer risk and an astonishing lack of prospective, randomized data showing a clear benefit in terms of a greater life expectancy. Moreover, the decisive study is unlikely ever to be performed because of the large number of patients needed and the required length of follow-up. As a result, protocols are being carried out that have never been critically tested prior to large-scale clinical implementation. CONCLUSIONS: Although these findings should not lead to therapeutic nihilism, the data raise the issue of whether or not surveillance protocols should be restricted to specialized referral centres with particular research efforts aimed at improving existing and developing new techniques that lack most of the described pitfalls and problems. Since it is foreseen that matters will not change rapidly in the (near) future, the clinician has no other choice than to rely on individually tailored arguments to survey taking into account for example family history, age and anxiety about potential long-term effects.     

Association of Helicobacter pylori with the Risk of Hepatic Encephalopathy

Digestive Diseases and Sciences - Hepatic encephalopathy is the common manifestation of decompensated cirrhosis. The association between Helicobacter pylori (H. pylori) infection and hepatic...     

Gallstones in cystic fibrosis: a critical reappraisal

Radiolucent gallstones are common in young adults with cystic fibrosis. In the mid-1970s, it was suggested that gallstones are made of cholesterol, but this hypothesis has never been tested. Several recent studies have shown that the detection of cholesterol monohydrate crystals in bile has high sensitivity and specificity for the diagnosis of cholesterol gallstones. We therefore used this approach to study 17 young adults with cystic fibrosis, 10 of whom had radiolucent gallstones. The two groups of patients were comparable in age and gender (all patients but one were male). Duodenal bile was obtained after gallbladder contraction with intravenous cerulein; it was used for lipid and protein chemistry studies and for polarizing microscopy. The latter was performed both in whole bile and in the postultracentrifugation (100,000 g) sediment. Bile cholesterol saturation did not significantly differ between patients with (1.21 +/- 0.28) or without gallstones (0.99 +/- 0.54). Slight cholesterol supersaturation was found in 7 of 10 gallstone and three of seven nongallstone patients. At no time were cholesterol crystals detected in either the group, even after bile ultracentrifugation. Two more cystic fibrosis patients with gallstones died of severe bronchopneumopathy, and small pigment gallstones were obtained at autopsy. At stone analysis, cholesterol content was 44% and 28% of dry weight, respectively. Infrared spectroscopy of stone powder was compatible with the presence of calcium bilirubinate and proteins as major components. We conclude that radiolucent gallstones of cystic fibrosis are not of the conventional cholesterol type.