Prolonged Q-T interval predicts severe arrhythmias and sudden death, and has been shown to occur in alcoholic liver disease and cirrhotic patients who are candidates for liver transplantation. This study first evaluated the prevalence of prolonged Q-T interval in a large population of unselected patients with cirrhosis, and assessed the relationship between abnormal Q-T, etiology, and severity of liver disease and mortality of patients. Possible causes of Q-T abnormality were also explored. Ninety-four patients with cirrhosis without overt heart disease and 37 control subjects with mild chronic active hepatitis were enrolled. Rate-corrected Q-T interval (Q-T_c) was assessed along with routine liver tests, Child-Pugh score, serum bile salts, electrolytes and creatinine, plasma renin activity, aldosterone, norepinephrine, atrial natriuretic factor and, gonadal hormones. Q-T_c was longer in patients with cirrhosis than in controls (440.3 ± 3.2 vs. 393.6 ± 3.7 ms; P < .001) and prolonged (>440 ms) in 44 patients (46.8%) and 2 controls (5.4%; P < .001).Q-T_c length was not influenced by the etiology of cirrhosis and correlated with Child-Pugh score (r = .53; P < .001), liver tests such as prothrombin activity, and serum concentrations of albumin and bilirubin, plasma bile salts, and plasma norepinephrine. Multivariate analysis showed that only Child-Pugh score and plasma norepinephrine were independently correlated with Q-T_c duration. Over a median follow-up period of 19 months (range, 2-33 months), patients with Q-T_c longer than 440 ms had a significantly lower survival rate than those with normal Q-T_c. Q-T interval is frequently prolonged in patients with cirrhosis, regardless the etiology of the disease, worsens in parallel with the severity of the disease, and may have an important prognostic meaning. In addition to other undefined factors related to the severity of cirrhosis, sympathoadrenergic hyperactivity may play a pathogenetic role.

Background: Helicobacter pylori infection causes antral gastritis and is strongly associated with duodenal ulcer relapse. Eradication of H. pylori infection may be difficult to achieve due to antimicrobial resistance, side effects and poor patient compliance. Objective: To evaluate the efficacy, tolerability and patient compliance of short-term triple therapy with clarithromycin, omeprazole and tinidazole. Methods: Triple therapy, comprising clarithromycin 250 mg twice daily, omeprazole 20 mg once daily and tinidazole 500 mg twice daily, was administered to 65 patients with H. pylori gastritis for 1 week. H. pylori infection before and after treatment was determined by histology, the urease test and the ¹³C-urea breath test. Upper gastrointestinal endoscopy, during which four antral biopsy specimens were taken, and the ¹³C-urea breath test were performed in all patients before treatment and at 1 and 6 months after treatment. Drug tolerance was evaluated by patient interviews and compliance by counting returned pills at the end of treatment. Results: Sixty-three patients with H. pylori infection were studied. One month after treatment, on intent-to-treat analysis, H. pylori infection had been eradicated in 62 out of 65 patients (95.4%), confirmed by a negative urease test, ¹³C-urea breath test and histological examination of antral biopsy specimens. All patients were free of infection 6 months after treatment ended. All but one patient completed treatment and took more than 90% of the prescribed medication. There were no side effects except for one case of mild nausea (not severe enough to stop treatment) and one case of urticaria, following which treatment was withdrawn. Conclusions: Short-term, low-dose triple therapy with clarithromycin, omeprazole and tinidazole is highly effective for the eradication of H. pylori infection. The lack of side effects and good compliance are important for successful eradication.