In cirrhotics, Helicobacter pylori infection is the major cause of peptic lesions, which are an important cause of upper intestinal haemorrhage in these patients. However, some diagnostic methods are not accurate for H. pylori detection in cirrhotics.
The study assessed the accuracy of different diagnostic methods for H. pylori detection in cirrhotics with and without gastroduodenal lesions.
The study population comprised of 53 cirrhotics. All patients underwent upper endoscopy: three biopsies were taken in the antrum and three in the gastric body. Four biopsies were used for Giemsa staining, while two were used for a rapid urease test. A blood sample was obtained for serology using Western blotting, and a [13C]urea breath test was performed in all patients. Histological assessment was regarded as the gold standard for diagnosis of H. pylori infection.
H. pylori infection was detected at histological assessment in 28 (52.8%) patients. The [13C]urea breath test, rapid urease test, and serology were positive in 27 (51%) patients, 23 (43.4%) patients, and 34 (64.1%) patients, respectively. Sensitivity and specificity were 92.9 and 96% for the [13C]urea breath test, 78.6 and 96% for the rapid urease test, and 78.6 and 52% for serology.
The [13C]urea breath test is very accurate in cirrhotics, whilst both serology and the rapid urease test give disappointing results.
[Show abstract][Hide abstract] ABSTRACT: Introduction: Helicobacter pylori (H. pylori) infection could potentially contribute to the development and severity of hepatic encephalopathy due to strong urease activity in the stomach of H. pylori infected cirrhotic patients. Objectives: To assess the effect of triple eradication therapy for H. pylori on hepatic encephalopathy. Design: Open randomized controlled clinical trial with 4 arms. Setting: liver diseases unit in Suez Canal University Hospital – tertiary care. Patients and Maneuver: Forty four Hp+ (Group 1) and 44 Hp-patients (Group 2) [based on rapid urease test of gastric biopsy] with hepatic encephalopathy grade 1 – 3. Interventions: Triple eradication therapy for H. pylori versus standard treatment for hepatic encephalopathy in group 1 and antimicrobial therapy (without Omeprazole) versus standard treatment in group 2 for 14 days. Main Outcome Measures: Blind assessment of the grade of encephalopathy before and within three days from end of treatment. One grade improvement was considered treatment success. Results: Success rate was 18.2% in standard treatment and 63.6% in triple therapy (p< 0.001) in H pylori positive . While in H. pylori negative patients the success was 9.1% in standard treatment versus 59.1% (P< 0.001) in and antimicrobial therapy. Success rate was not significantly different between standard treatment or between triple therapy and antimicrobial therapy among both groups. Among other factors in logistic regression models both triple therapy (OR: 1.03<6.22<37.69, P= 0.047) and antimicrobial therapy (OR: 2.09<11.42<59.46, P= 0.02) were significant predictors of success in the respective groups. Conclusion: Both triple eradication therapy for H. pylori and antimicrobial therapy only, equally improve the outcome of management of hepatic encephalopathy. The improvement may be attributed to the effect of antimicrobial therapy on ammonia producing gut flora rather than H. pylori eradication. H pylori eradication therapy adds no benefit in hepatic encephalopathy.
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