When to test for Helicobacter pylori and what to do with a positive test

Published on 13/02/2015 by admin

Filed under Gastroenterology and Hepatology

Last modified 13/02/2015

Print this page

This article have been viewed 1328 times

5 When to test for Helicobacter pylori and what to do with a positive test

Case

A 47-year-old executive consults you because his older brother, aged 61, has recently been diagnosed with gastric cancer. The patient advises you he wants to have testing for the stomach bacteria that causes gastric cancer. The patient is asymptomatic and in particular has no history of epigastric pain, fullness after meals, early satiety, vomiting, weight loss, dysphagia or gastrointestinal bleeding. He is a non-smoker. No other family members have been affected by gastric cancer to his knowledge. The patient was born in Australia to parents of British descent. The patient has been taking low-dose aspirin for cardiovascular health reasons, but has not been taking non-steroidal anti-inflammatory drugs. He has no known drug allergies. Physical examination is completely normal.

You counsel the patient that Helicobacter pylori is a known cause of gastric cancer and clusters in families. You further advise him that if testing is performed and infection is found, you would be obliged to advise treatment even though it is not certain in the current clinical situation whether the benefits of treating the infection outweigh the potential risks. You advise the patient the treatment of H. pylori infection can result in serious side effects, including, rarely, pseudomembraneous colitis.

After a full discussion, the patient still wishes to go ahead with testing.

A ¹³C urea breath test is performed and the patient returns with a positive result. You advise the patient he does have H. pylori gastritis, which has probably been present since childhood. As there are no alarm features, you do not recommend upper endoscopy although you discuss the pros and cons of the test. The patient is prescribed a course of triple therapy for 7 days (clarithromycin, amoxicillin and omeprazole twice daily). You advise the patient to take all of the medications as prescribed as otherwise treatment may fail, and to call you if he experiences any side effects. You further advise him to undergo a repeat urea breath 1 month after completing treatment to ensure the infection has been eradicated.

Introduction

H. pylori is a cause of peptic ulcer disease and gastric cancer, but most people who are infected are unaware of its presence and it usually causes no symptoms. Patients may present to the doctor’s office requesting testing for this stomach bacteria even if they have no symptoms. Some patients have a known history of peptic ulcer disease, but have not been tested for H. pylori as far as they know. Other patients present, worried because they have indigestion or one of their close family members has gastric cancer. What to do in these and related situations forms the basis of this chapter.

Pathogenesis

H. pylori is a spiral-shaped gram-negative rod with flagella at one end. The organism was first cultured by Barry Marshall after its existence in gastric biopsies was pointed out to him by a pathologist, Robin Warren. These Australians went on to describe the association of H. pylori with histological gastritis and peptic ulcer, and won the Nobel prize for their clinical research. H. pylori is associated with serious upper-gastrointestinal conditions including chronic gastritis, peptic ulcer disease, non-ulcer (functional) dyspepsia, and malignancy (gastric adenocarcinoma and mucosa associated lymphoid tissue—MALT—lymphoma).

H. pylori is most often acquired in childhood by close contact with other infected families and, once acquired, persists for life in most cases. The mode of transmission is probably oral (via saliva or vomit) and, in the developing world, faecal spread. Virtually 100% of infected individuals develop gastritis; the lifetime risk of peptic ulcer disease in those infected is approximately 20%.

In Western countries, approximately 20% of the population is infected, with older people and those from lower socioeconomic groups being more often infected. The higher prevalence with age reflects the higher infection rates in the past; the risk of adult acquisition is low (less than 1% per year). In developing countries (and in migrants from these countries), approximately 70% of adults are currently infected.

H. pylori is uniquely adapted to the gastric mucosal environment; for example, it produces the enzyme urease in very large amounts. It protects itself from gastric acid produced in the stomach by breaking down endogenous urea using urease to produce a protective ammonia cloud. The infection induces gastric inflammation characterised by mononuclear and polymorphonuclear cell infiltration of the mucosa; the inflammatory products provide nutrients for the bacteria. The stomach is functionally subdivided into the gastric antrum and the gastric body. With H. pylori infection the gastric antrum is predominantly inflamed in well-nourished individuals but the gastritis can involve the gastric body. The distribution of the bacteria determines the physiological effects.

Most duodenal ulcer patients (more than 90%) and many gastric ulcer patients (80%) have this infection. H. pylori causes an elevation in serum gastrin (because the antral gastritis reduces the D-cell function in the antrum that produces the inhibitory peptide somatostatin, disinhibiting antral G-cells that then secrete more gastrin). The elevated gastrin increases meal-related acid secretion from the gastric body (unless widespread inflammation in the gastric body impairs the acid output response). These changes in gastrin reverse with cure of the infection. Increased acid secretion damages the mucosa in the first part of the duodenum, leading to areas of gastric-type epithelium in the duodenum (called gastric metaplasia) that can be infected by H. pylori (note that these bacteria can live only on gastric epithelium). The localised inflammation in the duodenum caused by H. pylori (duodenitis) can progress to an ulcer in the presence of acid.

A duodenal ulcer will heal with acid suppression but usually recurs in H. pylori-infected patients (the duodenal ulcer diathesis). Cure of the infection leads to resolution of the gastritis (but not gastric metaplasia in the duodenum) and eliminates the ulcer diathesis (in both duodenal and gastric ulcers) when the ulcer is caused by the infection. Other factors, such as the virulence of H. pylori infection (based on the cytotoxin-associated gene pathogenicity island), smoking and host genetic factors, act as disease modulators.

Management Guidelines

Testing for H. pylori infection

Testing for H pylori infection should be performed only if the clinician plans to offer treatment to patients with a positive result (Box 5.1). The advantages and disadvantages of tests for H. pylori are summarised in Table 5.1.

Table 5.1 Tests for H pylori: advantages and disadvantages

Non-invasive (non-endoscopic) tests

Buy Membership for Gastroenterology and Hepatology Category to continue reading. Learn more here

Related

Clinical Gastroenterology