Background-Vitamin C may be protective against gastric cancer though infection with Helicobacter pylori is associated with a reduction in intragastric concentrations of vitamin C. Aims-To examine the eVects of H pylori infection, gastric juice pH, the severity and extent of gastric inflammation, and CagA antibody status of the individual on gastric juice and mucosal vitamin C concentrations. Patients-One hundred and fifteen patients undergoing routine gastroscopy for investigation of dyspepsia. Methods-High performance liquid chromatography was used to determine vitamin C concentrations. CagA antibody was detected by western blot analysis. Results-Gastric juice ascorbic acid concentration was significantly lower in patients infected with H pylori compared with those uninfected (19.3 µmol/l (interquartile range (IQR) 10.7-44.5) versus 66.9 µmol/l (IQR 24.4-94.2), p=0.003). The reduction in gastric juice ascorbic acid concentration was inversely related to the severity of gastritis (p=0.01). CagA positive patients had significantly lower gastric juice ascorbic acid concentrations than CagA negative ones (14.8 µmol/l (IQR 7.9-52.2) versus 39 µmol/l (IQR 19.9-142.2), p=0.05). Decreased gastric juice dehydroascorbic acid concentrations were observed in patients with gastric atrophy and intestinal metaplasia. Mucosal ascorbic acid concentrations were also significantly lower in infected patients than uninfected patients (p=0.04). Conclusions-The reduction in gastric vitamin C concentrations is related to gastric juice pH, the severity and extent of gastritis, the presence of H pylori, and the CagA antibody status of the individual. These findings may have implications in H pylori associated carcinogenesis. (Gut 1998;43:322-326)

SUMMARY Gastric juice from patients with peptic ulcer disease and from patients with no upper gastrointestinal abnormality was studied in order to assess its effect on a formed fibrin clot. In both groups of patients gastric juice caused a marked increase in fibrinolysis as evidenced by a shortening of the euglobulin clot lysis time. This plasmin mediated fibrinolytic activity was found to be heat labile and only present in an acid environment. Addition of tranexamic acid or sucralfate to gastric juice almost completely reversed this effect, whereas pepstatin was only partially effective. It is probable that acid dependant proteases other than pepsin are responsible for the marked fibrinolysis. The ulcer healing agent sucralfate might be useful in those patients at risk of bleeding or rebleeding from active peptic ulcer disease.Haemorrhage from active peptic ulcer disease remains a common and difficult therapeutic problem. Despite many new approaches in management, the mortality has changed little over the past 50 years. Approximately 10% of patients with acute upper gastrointestinal bleeding will die' and the mortality rate may rise to over 30% in that subgroup requiring emergency surgery."Th4 poor haemostatic response seen in the bleeding upper gastrointestinal tract has been variously ascribed to increased gastrointestinal motility during haemorrhage,' the marked vascularity and absence of autoregulation of local blood flow,' and the adverse effects of both acid and pepsin on the coagulation cascade.7 Moreover, dissolution of a formed fibrin clot is thought to be responsible for the very high incidence of rebleeding observed. Several investigators have identified fibrinolytic activity in gastric venous blood of patients with gastric haemorrhage`" and in gastric juice of patients with erosive gastroduodenitis."`R ecent work has suggested a beneficial effect of specific antifibrinolytic agents in preventing rebleeding in acute upper gastrointestinal haemorrhage."'" In the present study we have assessed the degree of fibriAddress for correspondencec: D P O'Donoghue,

The effect of age on the presentation, diagnosis, management and survival of patients with colorectal cancer was studied prospectively in 512 patients admitted to a single institution. In all, 225 patients were aged 70 years or more and 287 less than 70 years. Older patients had a significant excess of emergency presentations (18 versus 11 per cent). Methods of diagnosis, proportion of curative operations performed, stage and histological grade were similar in the two age groups. The postoperative mortality rate was 6 per cent in the elderly group and 3 per cent in younger patients. The postoperative mortality rate rose to 15 and 12 per cent respectively in those undergoing emergency surgery. The relative 5-year survival rate standardized for age and sex was 52 per cent for older patients and 45 per cent for younger patients; for those undergoing curative surgery it was 68 and 59 per cent respectively. The behaviour of colorectal carcinoma changes little with age and, allowing for population mortality, age has no effect on the long-term survival of elderly patients with large bowel cancer.

Helicobacter pylori is present in up to 87% of patients with nonulcer dyspepsia. This study assessed the effect of eradicating Helicobacter pylori infection on the symptoms of nonulcer dyspepsia at four weeks and one year after treatment. Dyspepsia was assessed on the frequency and severity of six symptoms [epigastric pain (night and day), nausea and vomiting, upper abdominal discomfort, and regurgitation] where each symptom was scored from 0 to 4. Helicobacter pylori status was assessed before treatment and four weeks after treatment with histology and microbiology, and at one year with a carbon-13 urea breath test. Eighty-three patients (23 males, 60 females; mean age 56.3 years; mean symptom duration 3.6 months) with nonulcer dyspepsia and Helicobacter pylori infection entered the study. Seventy-five were available at one year follow-up. Four weeks after treatment, the mean symptom score improved in those with eradication (6.95-2.3, P = 0.01, N = 41) or persistent infection (6.69-3.0, P = 0.015, N = 42). At one year, those with persistent Helicobacter pylori infection (N = 38, score 5.24) had a higher score than those remaining clear of infection (N = 24, score 1.4, P < 0.0001) and those with reinfection (N = 13, score 2.2, P < 0.0001). In addition, persistent Helicobacter pylori infection was associated with more additional treatments than those with eradication (34/38 versus 4/37, P < 0.001). These results suggest that Helicobacter pylori plays an important role in the symptoms of nonulcer dyspepsia.

Further study of prognostic indicators might result in an algorithm to distinguish Stage B cases at high risk of tumor recurrence and death. Such patients could be included in future trials of adjuvant therapies.

Inappropriate PPI therapy is still a problem in hospitals, though it appears to be at a lower level compared with previous studies. Awareness of evidence-based guidelines and targeted medicine reconciliation strategies are essential for cost-effective and safe use of these medications.

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EBL represents a safe and effective treatment for GAVE.