MORE ABOUT HELICOBACTER PYLORI AND GASTRODUODENAL MOTLITY
JOS O HELICOBACTERu PYLORI I GASTRODUODENALNOM MOTILITETU
Rational management of functional dyspepsia and peptic ulcer disease has become a major challenge in health care. In the January issue of Archives of Gastroenterohepatology, Ugljesic et Perisic discussed gastrointestinal motility disturbance and its role in peptic ulcer disease, minimizing the role of Helicobacter pylori. Helicobacter pylori role in pathogenesis of secretory abnormalities is very well understood, but the data concerning influence on gastroduodenal motor activity are still missing. Although studies denying Helicobacter pylori influence on gastroduodenal motility overcome ones in favor, there are few to be mentioned.
In the study of Testoni et al. (1) absence of phase III in dyspeptic patients was significantly associated with higher prevalence of Helicobacter pylori infection. If proved, prolonged MMC phase 2 and specially phase 3 among Helicobacter pylori positive patients, could induce more HCL, pepsin and bile acid impact on stomach mucosa (2).
In another study, there was no difference observed between Helicobacter pylori positive and negative patients in respect to the duration of phases I and II of the MMC, but the eradication of bacteria, however, normalized the duration of MMC phases (3).
Interesting study was conducted by Konturek et al. (4) in which gastric emptying rate, postprandial motility index (MI= number of contractions x mmHg/min) significantly improved as well as amplitude of postprandial gastric electric activity six weeks after the eradication of Helicobacter pylori infection.
Helicobacter pylori is associated with increased production of neuropeptides such as somatostatin and substance P. There is also increased production of some cytokines, including tumor necrosis factor alpha, interleukin 8 (IL-8) and IL-1 and nitric oxide (NO) in both, ulcer disease and non-ulcer dyspepsia. IL-1, for example, has been shown to increase enteric neural sensitivity mediating through increased prostaglandin E2 level. (5). Nitric oxid also acts as an inhibitory neurotransmitter.
From the above, there are some reasons to suggest that a chronic inflammation affecting the gastric mucosa might alter enteric neuromuscular function. It is possible, therefore, that Helicobacter pylori infection is associated with changes in upper gastrointestinal sensory and motor function, but these changes are obscured by considerable individual variations. The changes in function produced by infection and inflammation could become evident only if patients were compared before and after resolution of the underlying inflammatory process. In this case, the symptoms may persist for months and even for years, analogous to the prolonged persistence of symptoms in the post-infectious form of irritable bowel syndrome. Also it would be interesting to observe whether in the presence of ulcer-like symptoms of functional dyspepsia and present Helicobacter pylori infection, prokinetic agents would diminish symptoms and prevent ulcer formation.
References:
1.Testoni PA, Bagnolo F, Colombo E, Bonassi U, Tosi T. The correlation in dyspeptic patients of Helicobacter pylori infection with changes in interdigestive gastroduodenal motility patterns but not in gastric emptying. Helicobacter 1996; 4 (1): 229- 237.
2.Minocha A, Mokshagundam S, Gallo SH, Rahal PS. Alterations in upper gastrointestinal motility in Helicobacter pylori-positive non-ulcer dyspepsia. Am J Gastroenterol 1994; 89:1797-1800.
3.Qvist N, Rasmussen L, Axelsson CK. Heliobacter pylori associated gastritis and dyspepsia. The influence on migrating motor complexes. Scand J Gastroenterol 1996; 29:133- 7.
4.Konturek JW, Fischer H, Reimann B, Domschke W. Effect of eradication of Helicobacter pylori on gastric secretory and motor function in patients with non-ulcer dyspepsia. Gastroenterology 1997; 112:A181.
5.Noach LA, Bosma NB, Jansen J, Hoek FJ, van Deventer SJH, Tytgat GNJ. Mucosal tumor necrosis factor-alpha, interleukin 1 beta, and interleukin 8 production in patients with Helicobacter pylori infection. Scand J Gastroenterol 1994; 29:425-9.
Dr Ivan Jovanovic, MD. M.Sc.
Institute of Digestive Diseases,
Clinical Center of Serbia¸
6 Koste Todorovic Street
Yu-11 000 Belgrade¸ Yugoslavia
FAX ( 381 11 ) 361 54 32
E-mail: ivangastro a beotel.yu
REPLAY
We are very aware as Dr Jovanovic about the quoted literature data about the possible role of H.pylori and gastroduodenal motility changes. But this do permit us only to presume what Dr Jovanovic suggest. Interesingly Dr Jovanovic in his comment did not discuss very recent
references from 1998 and 1999 about this matter. It appears from this literature data that still there is no established definite casual relationship between H.pylori infection and motlity disturbances.
M.Ugljesic
V.Perisic