Role of Helicobacter pylori infection and its eradication in patients with subclinical hepatic encephalopathy

AIMS: Helicobacter pylori infection in cirrhotic patients has been associated with episodes of hepatic encephalopathy (HE), although conclusive data are still lacking. This prospective study has evaluated the prevalence of H. pylori infection in 37 patients with advanced cirrhosis of the liver and subclinical hepatic encephalopathy (SHE), diagnosed by changes in psychometric tests and/or electrophysiological tests, as well as the repercussion of H. pylori eradication on ammonaemia and the evolution of this disorder. RESULTS: A positive result for H. pylori infection was obtained in 22/37 (59%) patients. Initial fasting blood levels of ammonia were high in both groups. Infected and non-infected patients showed similar levels (62.05 mmol/l v. 62.5 mmol/l), which were lowered by the standard diet, although statistical significance was only reached in the infected patient group (53.05 +/- 26 mmol/l; P < 0.05). Infection was eradicated in 19 patients, but no reduction of blood levels of ammonia was observed after H. pylori eradication among infected patients (52.37 +/- 29 mmol/l). No change has been found in either group after the administration of diet or antimicrobials with regard to psychometric and/or electrophysiological tests. CONCLUSIONS: H. pylori infection does not contribute significantly to high blood levels of ammonia in patients with advanced cirrhosis and SHE. Likewise, H. pylori eradication does not induce any improvement in the psychometric and/or electrophysiological tests used to define SHE.     

Role of Helicobacter pylori infection in hyperammonemia and subclinical hepatic encephalopathy in cirrhosis of liver.

INTRODUCTION: Gastric Helicobacter pylori infection is believed to be associated with a higher risk of hepatic encephalopathy among patients with cirrhosis of liver. However, the role of this infection in causation of subclinical hepatic encephalopathy has not been studied in detail. METHODS: Patients with cirrhosis of liver but no hepatic encephalopathy underwent venous blood ammonia measurement, psychometric tests (number connection tests [NCT] and figure connection tests [FCT]), and gastric biopsies for presence of H. pylori infection. The results of blood ammonia and psychometric tests in the H. pylori-positive and -negative study subjects were compared. RESULTS: Of 58 patients with liver cirrhosis studied, 31 had evidence of gastric H. pylori infection. Venous blood ammonia levels were comparable in patients with (median 29 mmol/L; range 18-47) and without (34 [15-48] mmol/L; p=ns) H. pylori infection. The time taken to complete NCT trail A (median 37 s [range 25-69] versus 36.5 [26-62]), NCT trail B (64 s [48-91] versus 63.5 [42-88]), FCT trail A (59 s [31-115] versus 58 [38-590]) and FCT trail B (76 s [55-187] versus 82 [36-125]) were similar in those with and those without H. pylori infection. For each of the four tests, the proportion of subjects with abnormal test results was similar among H. pylori-positive and -negative subjects. CONCLUSION: Presence of H. pylori infection among patients with cirrhosis of liver but no overt hepatic encephalopathy is not associated with increase in blood ammonia concentration or deterioration in psychomotor function.     

Long-term effects of Helicobacter pylori eradication in Mongolian gerbils

Background: In this study, to clarify whether Helicobacter pylori eradication alters the course of the development of gastric mucosal changes in the stomach, we examined the long-term effects of H. pylori eradication on H. pylori-inoculated gerbils. Methods: A total of 40 H. pylori-inoculated gerbils were randomized and subjected, at 22 months after inoculation, to eradication treatment with dual therapy of omeprazole plus clarithromycin, or with therapy with a novel quinolone compound, Y-34867, alone. The animals were killed at the start of administration (control group) or at 8 months after the completion of therapy (vehicle or eradication-treatment groups). Results: Severe histopathological changes in the gastric mucosa were observed in all H. pylori-inoculated gerbils at the start of administration. At 8 months after completion of therapy, the frequency of gastritis, erosion, intestinal metaplasia, and gastric carcinoid in the eradication therapy groups was markedly reduced compared with that in the control and vehicle groups. Values for anti-H. pylori IgG titer, bacterial counts, and gastrin also decreased significantly. Conclusions: These results suggest that H. pylori eradication may have had a therapeutic effect not only on gastritis, erosion, and gastric ulcer but also on glandular atrophy, intestinal metaplasia, and gastric carcinoid. Received: November 8, 2001 / Accepted: May 31, 2002 Reprint requests to: F. Hirayama     

幽门螺杆菌感染与肝硬化患者的高氨血症

一、背景———问题的提出氨的来源有外源性与内源性之分。内源性氨是体内蛋白质分解生成 ,对外源性氨来源的认识经历了一个较长的过程。早期认为是存在于消化道粘膜尿素酶分解由血液弥散到消化道的尿素生成 ,但 1976年Ｍｅｙ ｅｒｓ等[1] 发现氨苄青霉素及新霉素可使胃液内氨浓度下降 ,提示胃内尿素酶活性并非来源于粘膜本身而是来源于细菌 ,至此外源性氨的生成有了较一致的意见即肠菌丛 (主要是大肠杆菌 )分解由血液弥散到消化道的尿素以及食物蛋白质分解产物氨基酸而生成。这便是长期以来一致公认的氨的肠源性学说。但自 1983年Ｍａｒｓ…     

共同治疗策略对根除幽门螺杆菌的影响

[目的]研究存在幽门螺杆菌(Hp)感染家庭聚集的感染患者Hp根除治疗后复发情况,探讨共同根除治疗策略对远期根除Hp的影响。[方法]通过对内镜检查确诊的195例Hp感染患者的家庭成员采用13碳呼气试验进行Hp感染调查,筛选有家庭成员Hp感染的患者140例。按照对Hp感染家庭成员有无根除治疗,将140例随机分成家庭成员共同根治组和单独根治组,每组70例。治疗后每月随访患者感染复发情况,观察不同根治策略对Hp根除的影响。[结果]134例患者参与根治后4、6、12、18、24个月随访,其中家庭成员共同根除治疗患者68例,Hp感染复发患者分别为0、1、2、4、5例,累积复发率为7.4%,平均复发时间为(12.6±6.1)个月;而66例单独根治患者复发者则分别为3、5、9、11、13例,累积复发率为19.7%,平均复发时间为(11.1±6.3)个月。χ2检验分析发现,在根除治疗后4、6个月时,2组复发率比较差异无统计学意义(P0.05);随着时间推移,治疗后12、18、24个月,共同根治组患者Hp感染再发率显著少于单独根治组(P0.05)。[结论]从远期观察,对于存在Hp感染家庭聚集的Hp感染患者,Hp感染成员共同根除治疗可有效降低根治后感染再发。     

Helicobacter pylori: factors affecting eradication and recurrence

Proton pump inhibitors play an important role in increasing the bioavailability of antibiotics in the gastric mucus by altering gastric volumes and increasing the stability of some antibiotics, e.g., clarithromycin. Increasing the doses of potent proton pump inhibitors has small effects on eradication rates but there may be differences between proton pump inhibitors that need further study.     

Economics of Helicobacter pylori eradication therapy

The annual incidence of peptic ulcer disease in developed countries is around one to three per thousand inhabitants. Since the introduction of acid-secretion inhibitors, the indirect costs of this disease, which has a high rate of relapse, have steadily decreased, although direct costs have been increasing. The possibility of healing the patient through Helicobacter pylori eradication has the potential for a huge economic impact considering the long-term cost: benefit ratio. A recent study has shown that H. pylori eradication therapy can save between US$750,000 and US$1,000,000 per year per million inhabitants in western Europe compared to maintenance or episodic therapy. This paper reviews the cost implications of various management strategies for peptic ulcer disease, comparing the cost: benefit ratios of five different treatment regimens.     

Helicobacter pylori eradication therapy in Korea

Helicobacter pylori (H. pylori) is known to be associated with many gastrointestinal diseases including peptic ulcer. In Korea, eradication of H. pylori is recommended for peptic ulcer disease, low grade gastric mucosa-associated lymphoid tissue lymphoma, and early gastric cancer. Standard triple therapy using proton pump inhibitor, clarithromycin, and amoxicillin and bismuth-containing quadruple therapy have been the main first-line and second-line therapy for H. pylori in Korea. Although eradication rate of second-line quadruple therapy remains similar to that of the past, the success rate of eradication with triple therapy has decreased with increasing antimicrobial resistance to H. pylori. There is no standard third-line therapy, and some regimens that incorporate levofloxacin, moxifloxacin, and rifabutin can be used. New regimens such as sequential or concomitant therapy are suggested as alternative treatment for H. pylori. We need more well designed randomized controlled studies to choose proper treatment for H. pylori infection.