Helicobacter pylori Eradication: Are there Alternatives to Antibiotics?

Alternative Medicine Review, August, 2001 by Alan R. Gaby

Abstract

It is now generally accepted that infection with Helicobacter pylori is an important cause of peptic ulcer disease and that eradication of this organism greatly reduces the recurrence rate of ulcers. H. pylori also can cause chronic gastritis and hypochlorhydria and is a risk factor for gastric cancer. Conventional eradication therapies, which consist of two antibiotics plus either a proton-pump inhibitor or a bismuth compound, are highly effective, but can cause significant side effects in some cases. Alternative methods of eradicating H. pylori are therefore being investigated. To date, the research in this area is still preliminary, and no treatment has emerged as a clear alternative to the conventional triple-therapy regimens.

(Altern Med Rev 2001;6(4):355-366)

Introduction

In the early 1980s, Warren and Marshall, two Australian physicians, reported the presence of an unidentified gram-negative curved and spiral-shaped bacillus in gastric epithelial tissue of patients with chronic gastritis. Originally called Campylobacter pylori, this organism was later renamed Helicobacter pylori when the organism was found to have characteristics that differed from those of true Campylobacters.

H. pylori and Peptic Ulcer

Marshall et al demonstrated that gastric antral mucosa can be present in the duodenum and that this tissue could also be infected with H. pylori. Although the medical community was initially skeptical, subsequent research strongly supports the proposition that H. pylori infection plays an etiologic role in both chronic gastritis and peptic ulcer (gastric and duodenal).

H. pylori infection is quite common, even among asymptomatic individuals. It occurs in about 10 percent of healthy individuals younger than age 30, and in nearly 60 percent of those over age 60. However, H. pylori is substantially more prevalent in people with peptic ulcer, occurring in virtually all patients with duodenal ulcer and about 80 percent of those with gastric ulcer.[1]

While some argue that H. pylori is merely an opportunistic organism that thrives on inflamed or ulcerated gastroduodenal tissue and plays little or no causative role in peptic ulcer,[2,3] clinical trials of H. pylori-eradication regimens indicate otherwise. A review of 60 studies that included a total of 4,329 patients demonstrated that H. pylori eradication accelerates the healing of peptic ulcers.[4] Even more important, appropriate antimicrobial therapy reduces the recurrence rate of the disease. Whereas 60-70 percent of H. pylori-infected ulcer patients develop a recurrence after initial healing, ulcers recur in only 5-10 percent of patients in whom H. pylori has been successfully eradicated.[5]

Because of strong evidence that H. pylori eradication facilitates ulcer healing and decreases recurrence rates, antibiotic therapy is now generally accepted as an important component of the overall treatment of peptic ulcer disease. Practice guidelines formulated by the American College of Gastroenterology state that, "antibiotic therapy is indicated for all H. pylori-infected ulcer patients."[6] This approach is widely considered to be a breakthrough in the treatment of peptic ulcer disease. However, the recommendation to administer antibiotics to all H. pylori-infected ulcer patients may be premature. There is a subset of ulcer patients -- those taking non-steroidal anti-inflammatory drags (NSAIDs) -- who may not benefit from antibiotic therapy. On the contrary, according to one study, H. pylori eradication in long-term NSAID users inhibited the healing of gastric ulcers.[7] However, with the exception of patients who are unable to discontinue NSAIDs, eradicating H. pylori infection appears to be an important goal in the treatment of peptic ulcer.

Other Gastrointestinal Conditions Associated with H. pylori

It is generally accepted that H. pylori infection causes chronic gastritis and is responsible for most cases of gastritis not associated with other known causes (e.g., autoimmune gastritis or eosinophilic gastritis). Virtually all people who harbor this organism acquire chronic superficial gastritis, which can persist for decades if left untreated. In most cases, however, the chronic gastritis causes no symptoms.

A condition that is related to and overlaps chronic gastritis is so-called "non-ulcer dyspepsia," which affects as much as 25 percent of the U.S. population. Non-ulcer dyspepsia is a syndrome characterized by recurrent upper abdominal pain or discomfort in the absence of definite gastrointestinal disease. Although some studies have shown that the prevalence of H. pylori infection is higher in patients with non-ulcer dyspepsia than in asymptomatic individuals, the potential benefit of curing the infection in such patients is questionable. While some studies have reported benefit,[8] three recent double-blind trials have failed to demonstrate any effect of eradication therapy on symptoms of non-ulcer dyspepsia.[9,10,11]

H. pylori infection is also a known risk factor for gastric cancer, although the disease develops in only one percent of infected individuals.[12] While the association between H. pylori and gastric cancer has not been proven to be causal, there is a theoretical mechanism by which the organism could be carcinogenic. It has been demonstrated that the concentration of vitamin C in gastric juice is significantly lower in patients with H. pylori infection than in healthy controls.[13] The reduction in gastric ascorbate concentrations appears to be due to inhibition by H. pylori of the secretion of vitamin C into gastric juice. When H. pylori was successfully eradicated, gastric-juice ascorbate concentrations increased; however, in patients in whom eradication therapy was unsuccessful, ascorbate concentrations did not increase.[14] As the presence of vitamin C in gastric juice is believed to prevent the development of gastric cancer (presumably by inhibiting the conversion of nitrites to carcinogenic nitrosamines),[15] the reduction in ascorbate levels by H. pylori infection may enhance carcinogenesis.