Our study shows that cervical length is comparable in nulliparous and multiparous women throughout pregnancy. In both groups, it actually shows a progressive, linear reduction between the 10th and 40th weeks. Reference ranges constructed for the whole gestational period might be more useful than a single cut-off value for more efficient prevention and management of preterm birth.
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%.
Gastric acid and pepsin secretion and serum gastrin concentrations were measured in nine patients with uncomplicated duodenal ulcer (DU) and 10 normal controls in the fasting state and in response to graded doses of bombesin, a tetradecapeptide gastrin releaser, and, for reference, synthetic gastrin G-17. Serum gastrin with bombesin stimulation was significantly greater in duodenal ulcer (maximum 467 pg/ml) than in controls (153 pg/ml), while in seven of the DU group tested gastrin levels after a meal were not different from that seen in five of the normal controls. Gastric acid concentrations and outputs were greater in duodenal ulcer with both stimuli. Secretory responses were then related to serum gastrin levels; despite increasing gastrin levels with bombesin stimulation, peak outputs achieved with bombesin were only 50% of G-17 maximum in normals and up to 90% of maximum in duodenal ulcer. Up to the point of peak response to bombesin, acid and pepsin outputs were the same with exogenous and endogenous gastrin, ie, bombesin acted only via G-17. Furthermore, in direct comparison of duodenal ulcer and normals with G-17 infusion, acid and pepsin outputs related to serum gastrin were congruent up to 75% of duodenal ulcer maximum, at which point normals reached their maximum level. These data have shown that duodenal ulcer patients are not more sensitive to either exogenous or endogenous gastrin; we have also shown regulatory defects in duodenal ulcer patients not previously described: an exaggerated release of gastrin with bombesin stimulation, and a defective inhibition of acid and pepsin secretion with higher doses of bombesin.
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