H. pylori eradication may not be enough
A mucosa-protective agent may be needed to decrease chronic gastritis
The antimicrobial treatment for Helicobacter pylori in peptic- ulcer disease and gastric-mucosa-associated lymphoid-tissue (MALT) lymphoma was considered a landmark in the management of gastroduodenal diseases in the past decade. But with recent studies, "it appears that this treatment is not the panacea," said Prof. Francis Megraud of the University of Bordeaux II. "There is room for other complementary or alternative treatments."
Speaking in a symposium organized by Otsuka Philippines in October 2004, Mégraud, who also heads the pediatric bacteriology unit of Bordeaux's Hôpital Pellegrin, said that some studies show that symptoms may actually continue in 30 percent of patients despite successful
H. pylori eradication, and that increased mucosal permeability to food antigens maintaining inflammation may be the culprit.
He explained: "When [the] bacteria arise in the stomach [they] induce chronic gastritis and can stay for months, years, even [throughout] life if there's no eradication treatment. Fortunately, there are no symptoms occurring in 90 percent of the cases. But in five to 10 percent of the cases, it leads to peptic ulcer, with probably less than one percent eventually leading to adenocarcinoma."
H. pylori eradication
The impact of
H. pylori eradication on healing and recurrence of duodenal ulcer was reviewed in a large metaanalysis by Ford et al. (2004) involving cases from 1966-2003. Healing was significantly improved from 41 percent with no treatment to 76 percent with
H. pylori eradication. Recurrence decreased within the year to 14 and 16 percent with eradication treatment and maintenance, compared with a high 64 percent without.
With gastric ulcer, there were significant reductions in recurrence rates--12 percent in those with
H. pylori treatment, against 40 percent in those without. However, the apparent success of eradication treatment came with some notable complications. A low eradication rate was noted with the one-week proton-pump inhibitor (PPI) and clarithromycin-based triple therapies because of increased
H. pylori resistance to antibiotics. Some patients also continued to manifest symptoms even after successful eradication.
Jonas et al. (1999) surveyed long-term results after successful eradication (one to seven years after; mean = 3.8 years) in Belgium. Sixty-seven percent of the respondents reported that they were still symptomatic and even underwent further endoscopy during the period; half still needed medication, mainly PPIs. A third did not report a perceived improvement in their quality of life. Bretagne et al. (1998) made a follow-up study of duodenal-ulcer patients who had been successfully cured of
H. pylori infection. Thirty-six percent of the respondents reported symptoms one year after eradication.
"[The recurrence rates are high] because after eradication, inflammation is still present during the first few months and even sometimes a few years," explained Mégraud. "After the cure, it takes a long time before the recovery to the normal status of the gastric mucosa."
Restoring mucosal integrity
Using Western Blot technique against cytokine antigens, prospective risk studies by Forman et al. (2004) showed significant correlation of noncardiac gastric carcinoma with
H. pylori infection. Wong et al. (2004) in a seven-year randomized controlled trial on the impact of
H. pylori treatment in the development of gastric carcinoma also showed decreased incidence with eradication versus placebo (0.86 percent v. 1.38 percent; p = 0.02).
Given these findings, Correa noted that a cascade of events leading to adenocarcinoma may be influenced by
H. pylori infection as it causes chronic gastritis, eventually giving rise to atrophy, intestinal metaplasia, and subsequent dysplasia. "In the future, it may help to use antiinflammatory drugs because the [whole] point is still inflammation [of the mucosa] that...remain[s] during the months and years [after eradication]," said Mégraud.
Restoration of mucosal integrity necessitates successful
H. pylori eradication. However, destruction of the offending organism does not immediately result in regeneration of the mucosa. A mucosa-protective agent like rebamipide may be necessary to decrease the intensity of chronic gastritis and proctitis.
Naito et al. (1998) documented the beneficial effects of rebamipide in decreasing the symptoms of indomethacin-induced gastric-mucosal injury (43 percent v. 80 percent placebo), while actively reducing gastric lesions (14 percent v. 70 percent placebo).
Said Mégraud: "Rebamipide (Mucosta) is a cytoprotective drug that decreases gastritis by scavenging oxygen-free radicals and decreasing cytokine production and neutrophil activity. It also increases prostaglandin synthesis and the expression of epidermal growth factor. All are positive effects that are of value in gastric-mucosal regeneration."
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