Dysfunction in gastric myoelectric and motor activity in Helicobacter pylori positive gastritis patients with non-ulcer dyspesia.

Helicobacter pylori (Hp) infection has been shown to affect gastric acid secretion and the somatostatin-gastrin ratio but its effects on gastric motility have not been evaluated. This study was carried out in 12 patients (10 males and 2 females, mean age 33 +/- 6 yrs) who underwent endoscopy and Campylobacter-like Organism (CLO)-test. All patients were found initially to be Hp positive according to CLO-test. Gastric emptying was evaluated by measuring antral diameter with ultrasonography (Hitachi EUB 240) in fasted and fed patients. Electrogastrography (EGG) with antral manometry were done 5 h before and 4 h after a meal before the therapy and one month after the eradication with triple therapy (lanzoprazole 30 mg daily- 2 x 250 mg clarithromycin 500 mg t.i.d.-3 x 500 mg and metronidazole 500 mg b.i.d.-2 x 500 mg). In Hp positive patients before the triple therapy the mean fasted antral diameter was 4.3 cm2, initial EGG showed significant dysrhythmia of electrical control activity (ECA) with tachygastria up to 25% of recording time in 9 of 12 Hp positive patients without normal increase of the power of signal in any of tested subjects. In 7 Hp positive fasted antral manometry failed to exhibit gastric phases III of the migrating motor complex (MMC). Hp eradication was accomplished in 10 of 12 examined patients and this was followed by a decrease in tachygastria to 3 cpm rhythm with an increase of the ECA power after meal. Phase III of MMC was observed again in 7 Hp negative patients with a decrease of fasted antral diameter (p < 0.05). Fasted and fed antral motility pattern increased after eradication. Two patients remained Hp positive after standard therapy. We conclude that most symptomatic non ulcer dyspeptic Hp positive patients show changes in ECA and antral hypomotility that are associated with Hp infections.