门脉高压性胃病患者幽门螺杆菌感染率调查

目的探讨幽门螺杆菌（Hp）与肝硬化并发胃和十二指肠病变的关系。方法采用快速尿素酶试验和改良的Giemsa染色法检测Hp感染。结果在264例肝硬化患者,Hp阳性183例（69．4％）,在262例慢性胃炎（EG）患者,Hp阳性172例（66．4％,19〉0．05）;在79例肝硬化伴有PHG患者,Hp阳性60例（75．9％）,在114例肝硬化不伴PHG患者,Hp阳性75例（65．8％）,在37例肝硬化伴轻型PHG患者,Hp阳性26例（70．2％）,在42例肝硬化伴重型PHG患者,Hp阳性34例（80．9％,P〉0．05）;在56例肝硬化伴十二指肠溃疡（DU）患者,Hp阳性48例（85．7％）,在109例肝硬化不伴消化性溃疡（Pu）患者,Hp阳性67例（61．4％,P〈0．05）;在125例DU患者,Hp阳性112例（89．6％）;在28例肝硬化伴胃溃疡（GU）患者,Hp阳性20例（71．4％）,在47例GU患者,Hp阳性43例（91．5％）。结论肝硬化伴DU患者Hp感染率较高。     

门脉高压性胃病与幽门螺杆菌相关性研究

为了解门脉高压性胃病(PHG)与幽门螺杆菌(HP)的关系,采用尿素酶试验、血清HP抗体检测和14C呼吸试验等方法检测50例肝硬化PHG患者HP的感染率,并与非PHG肝硬化(NPHG)、十二指肠球部溃疡(DU)、功能性消化不良(FD)三组患者比较.PHG组HP感染率为36%,与NPHG组(38%)、FD组(44%)分别比较差异无显著性(P＞0.05),与DU组(94%)比较差异有显著性(P＜0.01).说明HP感染对PHG发病影响不大.     

肝硬化并发消化性溃疡与Helicobacter pylori感染的临床相关性研究

目的探讨Helicobacter phylori(H.pylori)与肝硬化并发消化性溃疡的临床相关性。方法 H.pylori阳性患者1 887例和H.pylori阴性患者685例,采用Logistic回归分析计算其比值比(OR)和95%CI,以此确定H.pylori感染是否是肝硬化并发消化性溃疡的独立因素。结果 100例失代偿期肝硬化合并消化性溃疡患者,H.pylori阳性38例,H.pylori阴性62例。364例代偿期肝硬化并发消化性溃疡患者,H.pylori阳性195例,H.pylori阴性169例。非肝硬化患者消化性溃疡H.pylori阳性1 654例、H.pylori阴性454例。Logistic回归分析显示,失代偿期肝硬化患者(OR=0.25,P0.001)和代偿期肝硬化患者(OR=0.52,P0.001)H.pylori感染率较低。结论 H.pylori感染可能不是肝硬化合并消化性溃疡的主要病因。     

Helicobacter pylori seroprevalence in hepatitis C virus positive patients with cirrhosis

BACKGROUND/AIMS: Liver cirrhosis is a significant cause of death in Italy and one of the most frequent causes of hospitalization. Acute peptic ulcer and upper gastrointestinal bleeding reportedly occur in over one-third of cirrhotic patients. Since Helicobacter pylori (H. pylori) infection strongly correlates with peptic ulcer, we sought to ascertain the prevalence of H. pylori infection in cirrhotic patients. METHODS: In a case-control study, we examined 254 consecutive patients (127 male and 127 female, age range 30-82 years) suffering from hepatitis C virus (HCV)-related cirrhosis and 463 sex- and age-matched patients admitted to the Department of Emergency Care of our hospital (254 male, 209 female, age range 30-79 years) resident in the same area. RESULTS: Antibodies to H. pylori were present in 226/254 (89%) cirrhotic patients and in 275/463 (59%) controls (p<0.0001). The difference was significant both in males and in females. CONCLUSIONS: The very high prevalence of H. pylori infection may explain the frequent occurrence of gastroduodenal ulcer in cirrhotic patients and may possibly determine the prognosis of those who are also infected with HCV.     

Helicobacter pylori is a risk factor for peptic ulcer disease in cirrhotic patients. A meta-analysis

BACKGROUND : Peptic ulcer disease is highly prevalent in cirrhosis, and ulcer complications are a major cause of morbidity in these patients. Helicobacter pylori infection is considered the chief aetiological factor of ulcer disease. However, in cirrhotic patients the role of H. pylori in the pathogenesis of peptic ulcer remains uncertain. AIM : To evaluate the evidence of the pathogenic role of H. pylori infection in peptic ulcer disease in patients with cirrhosis. MATERIALS AND METHODS : An extensive MEDLINE search of the literature was performed. Studies reporting the prevalence of H. pylori infection in cirrhotic patients with and without ulcers were selected. Meta-analysis was conducted using RevMan 4.0.3. Pooled odds ratios were calculated for each comparison, using a fixed model analysis. RESULTS : The search identified seven studies with a total of 976 patients with cirrhosis (275 cases with ulcer disease and 701 controls). The prevalence of H. pylori infection in patients with peptic ulcer disease was higher than in those without. The pooled odds ratio was 2.70 (95% CI, 1.91-3.82). H. pylori infection was associated more or less equally with duodenal and gastric ulcers. CONCLUSION: H. pylori infection increases the risk of peptic ulcer disease in patients with cirrhosis.     

Gastroduodenal ulcer and erosions are related to portal hypertensive gastropathy and recent alcohol intake in cirrhotic patients

Gastroduodenal ulcers and gastroduodenal erosions are particularly frequent in cirrhotic patients, but their precise cause is unclear. The aim of this study was to identify pathogenic factors associated with ulcers and erosions in patients with cirrhosis. We studied 64 consecutive patients with cirrhosis referred for gastroscopy. The severity of portal hypertensive gastropathy was graded with an endoscopic score. H. pylori status was determined by histological examination of gastric biopsy samples or by the [¹³C] urea breath test. The daily alcohol intake within the preceding week was recorded. The Child-Pugh score was determined. Fifteen patients had gastroduodenal ulcer and 20 had gastroduodenal erosions. Cirrhosis was related to alcohol in 44 patients and hepatitis B or C virus in 14 patients. The portal hypertensive gastropathy was graded as severe in 12 patients and mild in 25 patients. H. pylori infection, found in 37 patients, was not related to the gastroduodenal lesions. Univariate and multivariate analysis showed the links between gastroduodenal erosions and hypertensive gastropathy and recent heavy drinking. Gastroduodenal ulcer was independently associated only with the severity of the gastropathy. In conclusion, in these patients with cirrhosis, the presence of gastroduodenal ulcer was significantly related to hypertensive gastropathy but not to H. pylori infection. Recent alcohol intake favored the occurrence of gastroduodenal erosions.     

Prevalence of Helicobacter pylori infection and its effect on symptoms and non-steroidal anti-inflammatory drug induced gastrointestinal damage in patients with rheumatoid arthritis.

Non-steroidal anti-inflammatory drugs (NSAIDs) and Helicobacter (H pylori) are both associated with an increased risk of peptic ulceration and gastropathy. It is not known, however, if there is an interaction between these two agents, and thus whether or not screening for H pylori before NSAID treatment is of value. The aim of this study was to find out if H pylori potentiates the damaging effects of NSAIDs. Fifty two patients with rheumatoid arthritis requiring longterm NSAID treatment were studied. Dyspeptic symptoms were assessed according to a standardised questionnaire. Gastroscopy was performed after a one week washout period during which NSAIDs were discontinued. Gastric and duodenal mucosal damage was graded endoscopically. H pylori was identified by biopsy urease test and by histological tests. Investigations were repeated after one month's treatment with an NSAID. Patients with H pylori infection (n = 26) had a higher dyspeptic symptom score (p < 0.05). One patient with duodenal ulcer (H pylori +ve) and two with endoscopic gastritis (both H pylori +ve) were excluded from further study. Forty two subjects completed the study. After treatment there was a rise in the gastric damage score both in the H pylori +ve (p = 0.06) and the H pylori -ve (p < 0.005) groups. There was no difference in the extent of increase in grade or the final grade at the end of the treatment period between the H pylori +ve and -ve patients. It is concluded that H pylori infection is associated with increased dyspeptic symptoms in patients receiving NSAIDs but that it does not potentiate NSAID gastropathy.     

Helicobacter pylori infection in dyspeptic cirrhotic patients

BACKGROUND/AIMS: To date, few studies have focused on the role of Helicobacter pylori (H. pylori) in cirrhotic patients with gastroduodenal disease and reported results are conflicting. The aim of this study was to assess the H. pylori infection rate in dyspeptic cirrhotic patients with or without gastroduodenal lesions at endoscopy. METHODOLOGY: In a prospective study, 226 consecutive dyspeptic cirrhotic patients were enrolled in the study upon assessment of H. pylori infection. Two-hundred dyspeptic non-cirrhotic patients were also included as controls. The presence of H. pylori was detected by rapid urease test and histology (Giemsa staining) in 3 biopsy specimens from the antrum and 3 from the gastric body. RESULTS: H. pylori infection was found in 135 (59.7%) cirrhotics and in 121 (60.5%) controls (p = NS). The prevalence of gastric ulcer was higher in cirrhotics than in controls (16% vs. 2.5%, p = 0.0001), while the prevalence of duodenal ulcer was similar (11% vs. 12%, respectively). The H. pylori infection rate was similar between cirrhotics and controls, both with gastric (83% vs. 80%) and with duodenal (88% vs. 96%) ulcers. Moreover, in our study, a H. pylori-related peptic lesion was the cause of previous gastroduodenal bleeding in 6 of 50 (12%) cirrhotic patients. CONCLUSIONS: Our results indicated that H. pylori infection is implicated in the pathogenesis of peptic ulcer in cirrhotic patients, similar to findings in non-cirrhotic patients.     

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.     

High Prevalence of Helicobacter pylori in Liver Cirrhosis (Relationship with Clinical and Endoscopic Features and the Risk of Peptic Ulcer)

In 153 consecutive patients with cirrhosis weassessed: (1) the prevalence of IgG to Helicobacterpylori and compared it with that found in 1010 blooddonors resident in the same area; and (2) therelationships of IgG to Helicobacter pylori with clinical andendoscopic features and with the risk of peptic ulcer.The IgG to Helicobacter pylori prevalence of cirrhoticswas significantly higher than in blood donors (76.5% vs 41.8%; P < 0.0005) and was notassociated with sex, cirrhosis etiology, Child class,gammaglobulins and hypertensive gastropathy. In bothgroups, the prevalence of IgG to Helicobacter pylori was significantly higher in subjects over 40. Amongpatients with cirrhosis a significantly higherprevalence of Helicobacter pylori was found in patientswith previous hospital admission (P = 0.02) and/or upper gastrointestinal endoscopy (P = 0.01) andpatients with peptic ulcer (P = 0.0004). Multivariateanalysis identified increasing age and male sex as riskfactors for a positive Helicobacter pylori serology and no independent risk factors for pepticulcer. The high prevalence of Helicobacterpylori-positive serology found in the present series isrelated to age and sex and might also be explained byprevious hospital admissions and/or uppergastrointestinal endoscopy. Our results do not confirmthe role of Helicobacter pylori as risk factor forpeptic ulcer in patients with liver cirrhosis.     

Hepatic venous pressure gradient determination in patients with hepatitis C virus-related and alcoholic cirrhosis

OBJECTIVES: Few data exist regarding the degree of portal hypertension in hepatitis C virus (HCV)-related cirrhosis, as the majority of studies have included mainly patients with alcoholic cirrhosis. This study was aimed at comparing the severity of portal hypertension in patients with HCV-related or alcoholic cirrhosis. METHODS: In total, 59 cirrhotic patients with portal hypertension (HCV-related in 34 cases and alcoholic in 25) underwent main right hepatic vein catheterization, with determination of the wedged and free hepatic venous pressures, and of hepatic venous pressure gradient (HVPG). RESULTS: HVPG values did not differ between the two groups of patients (19.4 +/- 6.0 mmHg vs 18.5 +/- 3.5 mmHg; P = 0.51). The prevalence and degree of oesophageal and gastric varices and portal hypertensive gastropathy did not correlate with the aetiology. Patients with viral cirrhosis had a lower prevalence of previous bleeding than those with alcoholic cirrhosis, despite a similar proportion of large varices in the two groups and similar HVPG levels. In both groups of patients, HVPG did not differ between patients with previous bleeds and those without. CONCLUSIONS: The degree of portal hypertension in cirrhotic patients does not correlate with the cause of the disease. Thus, current statements on the management of portal hypertension, although based upon studies including mainly patients with alcoholic cirrhosis, can be applied also to patients with viral-related cirrhosis.     

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.     

肝硬化患者中幽门螺杆菌感染的研究

目的 研究幽门螺杆菌（Hp)在肝硬化患者中的感染情况。方法 肝硬化组656例，对照组600例，接受胃镜检查，采用血清学方法，快速尿素酶试验，组织学染色进行Hp检测。结果 肝硬化组Hp感染率为70％，对照组为71％。两者比较无显著性差异，而在肝硬化组中Hp阳性患者的消化性溃疡发生率，门脉高压性胃病发生率及严重程度，上消化道出血率均高于Hp阴性组。结论 在肝硬化患者中Hp感染可能与消化性溃疡，门 脉高压性胃病及上消化道出血的发生相关。     

The Helicobacter pylori breath test: a surrogate marker for peptic ulcer disease in dyspeptic patients.

BACKGROUND: There is interest in noninvasive H pylori testing as a means of predicting diagnosis and determining management in dyspeptic patients. AIMS: To assess the value of the 14C urea breath test as a predictor of peptic ulcer disease in patients presenting with dyspepsia. PATIENTS AND METHODS: 327 consecutive patients referred for investigation of dyspepsia had a 14C urea breath test performed before endoscopy. Patients were not included if they had previously confirmed ulcer disease, previous gastric surgery, or were taking non-steroidal anti-inflammatory drugs. RESULTS: Of the 182 patients with a positive 14C urea breath test, duodenal and/or gastric ulcers were present in 45% and erosive duodenitis in a further 2%. Oesophagitis was present in 12% of the breath test positive patients with two thirds of the oesophagitis patients having co-existent ulcer disease. The prevalence of ulcer disease in the H pylori positive dyspeptic patients was independently related to smoking and previous investigation status. If previously uninvestigated, the prevalence of ulcers was 67% in smokers and 46% in non-smokers. If previous upper gastrointestinal investigations were negative, the prevalence of ulcers was 53% in smokers and 28% in non-smokers. Of the 136 patients with a negative breath test, only 5% had peptic ulcers. The most frequent endoscopic finding in these H pylori negative subjects was oesophagitis, being present in 17%. CONCLUSIONS: This study demonstrates that a positive H pylori test is a powerful predictor of the presence of underlying ulcer disease in dyspeptic patients, especially if smokers, and that a negative H pylori test is a powerful predictor of the absence of ulcer disease. It also indicates that a negative upper gastrointestinal investigation does not preclude subsequent presentation with ulcer disease.     

Epidemiology of Helicobacter pylori and peptic ulcer in India

BACKGROUND: There is a wide variation in the prevalence of peptic ulcer in India both before and since the use of endoscopy. We studied the prevalence of peptic ulcer disease in a community in northern India and its relationship with Helicobacter pylori infection. METHODS: A house-to-house survey of residents aged 15 years or above in a sub-sector of Chandigarh was performed as part of a pilot survey. Subsequently, the study randomly covered all sectors of Chandigarh and we screened 2649 persons. A questionnaire was administered to each subject by trained staff. All individuals with history of peptic ulcer/dyspepsia and an equal number of asymptomatic individuals were asked to attend the outpatient department of the Institute. Diagnosis of peptic ulcer was based on endoscopy or history of previous ulcer surgery. RESULTS: Two hundred and fifty-four individuals attended the outpatient department at the Institute and 147 underwent endoscopy, biopsy for histology and rapid urease test, and blood was collected for H. pylori serology. There were 80 symptomatic and 67 asymptomatic individuals. Helicobacter pylori was positive in 38 (56.7%) asymptomatic and 49 (61.3%) symptomatic individuals (P > 0.05). The point prevalence of active peptic ulcer was 3.4% and the lifetime prevalence was 8.8%. The duodenal-to-gastric ulcer ratio was 12:1. Helicobacter pylori was present in 11/13 (84.6%) subjects with peptic ulcer. Peptic ulcer was more common in elderly and dyspeptic individuals and there was no effect of sex or socioeconomic status. Helicobacter pylori was associated with age only and did not depend on sex, socioeconomic status or dyspepsia. Of the 38 asymptomatic persons having H. pylori infection, none had active peptic ulcer. CONCLUSIONS: This study demonstrates frequent occurrence of peptic ulcer and H. pylori in this part of the country. Peptic ulcer was more prevalent in the elderly and dyspeptic subjects. Helicobacter pylori was not associated with dyspepsia, and was more prevalent in elderly subjects. There was a low prevalence of peptic ulcer in asymptomatic H. pylori-infected persons in this community.     

Dyspepsia, Helicobacter pylori, and peptic ulcer in a randomly selected population in India.

There seems to be a worldwide geographic variation in the prevalence of peptic ulcer disease, although there are few reliable population based studies. This study aimed to determine the prevalence of peptic ulcer disease in a community in southern India and to evaluate the relationship between dyspeptic symptoms, Helicobacter pylori infection, gastritis, and peptic ulcer disease. A sample population was selected randomly from a rural monastic settlement in southern India. Subjects were interviewed using a standardised symptom and demography questionnaire then underwent upper endoscopy and antral biopsy for histology and CLO rapid urease test. Altogether 197 subjects from a population of 1499 (13.1%) were studied. All were male monks and ethnically Tibetan. The median age was 28 years (range: 21-81). None smoked or took NSAIDs. The six month period prevalence of dyspeptic symptoms was 68.5%. Current symptoms were present in 58.9% of subjects. Dyspepsia was more common in subjects aged 40 years or younger (p < 0.0001). H pylori was detected in 77.2% subjects. There was no association between dyspepsia and the presence of H pylori or histological gastritis, although there was a strong correlation between symptoms and ulcer (p < 0.003). The point prevalence of active peptic ulcer was 6.6% (13/197). All ulcers detected were either prepyloric or pyloroduodenal in location. A further 6.6% of subjects had definite evidence of scarring or deformity indicative of ulceration in the past. Subjects with past or present ulcers comprised 17.8% of dyspeptic subjects. H pylori was present in all subjects with active ulcers and in 12/13 of those with scarring. Dyspepsia, H pylori infection, gastritis, and peptic ulcer are all more common in this population than in those from developed countries. Ulcer disease, however, accounts for only a small proportion of subjects with symptoms and neither H pylori infection nor gastritis are significantly associated with the presence of dyspepsia.     

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。     

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.     

Helicobacter pylori density and cagA status in cirrhotic patients: a case-control study

BACKGROUND AND AIM: Despite a similar Helicobacter pylori prevalence, peptic ulcer is more frequent in cirrhotic patients than in controls. We evaluated whether cirrhotic patients had an increased bacterial density and/or a higher prevalence of H. pylori cagA-positive strains than controls. METHODS: A total of 36 dyspeptic cirrhotic patients with H. pylori infection and 72 matched controls were enrolled. H. pylori infection was detected at histology on Giemsa staining, bacterial density was assessed using difference over baseline (DOB) values at 13C urea breath test, and cagA status was established at serology. RESULTS: Overall, both DOB values and prevalence of cagA did not significantly differ between cirrhotic patients and controls. However, peptic ulcer controls showed significantly higher DOB value (27.9 +/- 17.4 vs 19.4 +/- 9.3, respectively; P = 0.009) and cagA positive rate (85%vs 48%; P = 0.01) than non-ulcer dyspepsia patients. Although not statistically significant, a similar trend was observed in cirrhotic patients with peptic ulcer for DOB values (26.5 +/- 16.3 vs 18.3/1000 +/- 9.2, respectively; P = 0.07), whereas the cagA-positive rate was similar between peptic ulcer and non-ulcer dyspepsia patients (60%vs 50%; P = 0.30). CONCLUSIONS: The present data showed that both bacterial density and cagA prevalence did not differ between cirrhotic patients and controls.     

Scoring system has better discriminative value than Helicobacter pylori testing in patients with dyspepsia in a setting with high prevalence of infection

OBJECTIVE: To prospectively assess the accuracy of a scoring system to predict organic diseases in dyspeptic patients in an area of South Europe, and to compare it with that of Helicobacter pylori testing in patients with dyspepsia in an environment with high prevalence of H. pylori infection. METHODS: Symptoms and demographic data were recorded in 501 consecutive dyspeptic patients referred to an outpatient gastroenterology clinic. A simple scoring system was constructed from the predictive factors obtained in a multi-variate logistic regression analysis. Overall predictive accuracy was assessed with the c statistic. The model was validated using bootstrap techniques. The accuracy of clinical judgement and H. pylori testing to predict endoscopic diagnosis was also assessed. RESULTS: Organic dyspepsia (peptic ulcer, oesophagitis or malignancies) was diagnosed in 45% of the patients. The test for H. pylori was positive in 68%, and 29% of infected patients had an ulcer. The organic dyspepsia predictive model had an accuracy of 0.79, which decreased to 0.77 after validation adjustment. The predictive accuracies for clinical judgement and H. pylori testing were 0.69 and 0.61, respectively. The addition of H. pylori testing to the scoring system resulted in a minor improvement of the predictive accuracy. CONCLUSION: In an environment with a high rate of H. pylori infection and a low prevalence of peptic ulcer among infected patients, a scoring system has higher predictive accuracy for the diagnosis of organic disease than H. pylori testing. Moreover, in this setting, H. pylori testing adds a minimum value to the predictive capability of the scoring system.