Helicobacter pylori and Other Gastritides

Fig. 27.1
Chronic H. pylori gastritis. The arrow points to the chronic inflammatory exudate. Courtesy of Timothy Wallace, MD


Fig. 27.2
H. pylori gastritis: immunological stain for H. pylori. The arrow points to H. pylori organisms. Courtesy of Timothy Wallace, MD


Fig. 27.3
Chronic H. pylori gastritis with intestinal metaplasia. Arrow points to metaplastic cells. Courtesy of Timothy Wallace, MD

Pathogenesis of H. pylori Gastritis

H. pylori is an organism that is uniquely equipped to deal with the harsh environment of the stomach. H. pylori has very strong urease activity, which allows it to adjust the acidity of its microenvironment.

The fecal-oral route of transmission is the most well documented method of transmission but there are reports of gastric-oral and oral-oral infection [5]. Children have been shown to transmit the infection by emesis in day care settings and H. pylori has been shown to exist in dental plaque. The risk of acquiring H. pylori is increased by the presence of infected parents and siblings [6]. Crowded living conditions, poor sanitation, and poor hygiene are risk factors for transmission.

Evolution of Gastritis and Pathogenesis

Infection with H. pylori causes a transient acute gastritis after which the infection may resolve or may go on to become chronic. Acute gastritis is associated with a neutrophilic infiltrate and a transient hypochlorhydria [2]. If the organism colonizes the stomach successfully, an antrum-predominant gastritis develops (Figs. 27.1, 27.2). This form of gastritis is associated with reduced somatostatin production, enhanced gastrin production, and increased gastric acid secretion. The increased acid is delivered into the proximal duodenum and can cause ulcers in some cases. As the infection proceeds progressive inflammation causes a loss of gastrin producing cells and acid production falls. This is accompanied by changes of atrophy on biopsy and intestinal metaplasia develops in some cases. As the environment becomes more alkaline, the infection moves into the corpus of the stomach where continuing inflammation causes a loss of gastric glands and further decreases in acid secretion. Gastric cancer is associated with extensive corpus gastritis, atrophy, and extensive intestinal metaplasia [2] (Fig. 27.4).


Fig. 27.4
Treatment regimens for H. pylori

Symptoms of Gastritis

Gastritis may be asymptomatic or may be associated with mild dyspeptic symptoms. In other patients, symptoms resembling peptic ulcer disease may be present, including epigastric burning pain and postprandial distress. None of these symptoms is diagnostic of the pathological condition of gastritis but clinicians often use the term gastritis to describe this constellation of symptoms although this use of the term has no specific pathological correlation.

Diagnostic Testing

Several tests are available to check for H. pylori infection, including noninvasive and invasive approaches. Endoscopy with biopsy is the only way to demonstrate gastritis but the presence of infection can be determined by noninvasive tests.


Serologic tests for H. pylori are an indirect test of H. pylori infection [7]. Serologic tests are no longer useful for clinical testing in most countries because of the high rate of false positives.

Stool Antigen Test

The fecal antigen test is an accurate test for use both before and after treatment of H. pylori infection [8]. The sensitivity and specificity of the monoclonal stool antigen test is better than 90% and it is comparable in efficacy to the urea breath test. As with the urea breath test the accuracy of the stool antigen test can be impaired by the recent or current use of PPIs or antibiotics [9]. PPIs should be discontinued for approximately 2 weeks before the fecal antigen test, to allow time for the organism to repopulate the stomach.

Urea Breath Test

Another noninvasive, accurate testing option for H. pylori is the urea breath test, which is approved for use before and after treatment [10]. The normal human stomach lacks urease activity. H. pylori has strong urease activity and therefore evidence of urease activity is diagnostic of H. pylori infection. Radiolabeled urea is administered orally. If the stomach is infected, the urea is broken down. The urea breath test is affected by proton pump inhibitors much as the stool antigen test [11].

Treatment of Gastritis Caused by H. pylori

Anti-microbial therapy is required to eradicate H. pylori and this results in a gradual improvement in gastritis. Eradication of H. pylori reduces recurrences of peptic ulcer disease and can be curative of early MALT lymphoma and prevent recurrent gastric cancers in patients who have a resection of an early gastric cancer. The recently published guidelines of the Maastricht IV consensus suggest that standard triple therapy may be used in parts of the world where clarithromycin resistance is less than 15% [12]. Doses and durations are listed in Fig. 27.2. In patients with amoxicillin resistance, metronidazole may be substituted. Bismuth-based quadruple therapy is recommended in areas with high clarithromycin resistance. Second-line therapy recommended by the Maastricht group is levofloxacin-based triple therapy [12]. If second-line therapy fails, culture and sensitivity testing are recommended if available. High dose PPI therapy with amoxicillin and rifabutin triple therapy are alternatives when culture and sensitivity testing is not available.

Disease Associations with H. pylori Gastritis

Peptic Ulcer Disease

In developing countries 90% of duodenal ulcers and 80% of gastric ulcers are caused by H. pylori infection and eradication prevents relapse [1315]. In developed countries, H. pylori infection causes fewer duodenal and gastric ulcers because nonsteroidal anti-inflammatory drugs are a more frequent cause of ulceration than in developing countries.

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Jan 31, 2018 | Posted by in ABDOMINAL MEDICINE | Comments Off on Helicobacter pylori and Other Gastritides

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