Background : One‐week triple therapy has been suggested to be superior to two‐week omeprazole‐clarithromycin therapy for the cure of Helicobacter pylori infection. However, direct comparisons of the two treatments are scarce. Aim : To compare triple with dual therapy for H. pylori infection in the primary care setting. Methods : One hundred and forty‐five patients with duodenal ulcer and H. pylori infection were randomized to receive omeprazole 20 mg b.d. and clarithromycin 500 mg t.d.s. for 14 days (OC14 group, 69 patients) or omeprazole 20 mg b.d., clarithromycin 500 mg b.d. and amoxycillin 1 g b.d. for 7 days (OCA7 group, 76 patients). Eradication was evaluated by the 13C‐urea breath‐test. Results : Intention‐to‐treat analysis showed a cure rate of 48% (95% CI: 36–60%) in the OC14 group, and 71% (95% CI: 59–80%) in the OCA7 group (P=0.0004). Per protocol analysis showed cure rates of 51% (95% CI: 38–63%, 33/65 patients) and 82% (95% CI: 70–90%, 54/66 patients), respectively (P=0.0001). There were no significant differences in compliance or side‐effects. Conclusion : One‐week twice‐daily triple therapy is superior to 2‐week dual therapy, but the cure rate in primary care was far below 90%.

The main determinants of mortality after burn injury that can be measured on admission include age, total burn size (% burn), and inhalation injury (INHAL). Other variables, measured during resuscitation, may provide additional information about injury severity. We assessed the utility of early arterial blood gas (ABG) data in predicting mortality after burn injury. Data were limited to samples obtained during the first 2 days after burn injury and to those obtained during high-frequency percussive ventilation. Mean values for each patient's ABG data were calculated; subsequent analysis used these derived variables. Logistic regression analysis (LRA) was used to generate a mortality predictor using burn, age (as a cubic age score, AGE), and INHAL. LRA was then repeated with the ABG variables. A total of 162 patients were included. By univariate analysis, death was associated with increased alveolar-arterial gradient (AaDO2), AGE, % burn, full-thickness burn size, INHAL, and with decreased pH and base excess. LRA of % burn, AGE, INHAL, and full-thickness burn size retained the first three variables. The addition of ABG data demonstrated that mean burn excess and mean AaDO2 also contributed independently to mortality. However, there was no difference in accuracy (86%) between the two equations. By Kaplan Meier analysis, AaDO2 but not BE predicted earlier death in those who died. Measured during resuscitation, metabolic acidosis (ie, a base deficit) and oxygenation failure (ie, increased AaDO2) contributed independently, but modestly, to ultimate mortality after burn injury. The inclusion of these variables did not improve predictive accuracy. Whether therapies targeted at these endpoints would improve outcome is unknown.

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