Peptic ulcer disease is a chronic illness manifested by recurrent ulcerations
in the stomach and proximal duodenum. Acid and pepsin are thought
to be crucial to ulcer development, but the great majority of peptic
ulcers are directly related to infection with Helicobacter
pylori or NSAID use.1,2 Gastritis is acute
or chronic inflammation of the gastric mucosa and has various etiologies. Dyspepsia is
continuous or recurrent upper abdominal pain or discomfort with
or without associated symptoms (nausea, bloating, etc.).3 Dyspepsia
may be caused by a number of diseases or may be functional.
About 500,000 new cases and about 4 million recurrent cases of peptic
ulcer disease are diagnosed each year in the U.S.4 Most
cases occur between the ages of 25 and 64 years.1 There
is a lifetime prevalence of peptic ulcer disease of between 8% and
14%, and an estimated U.S. $10 billion is spent
per year in total direct and indirect costs.1,4 H.
pylori infection is one of the most prevalent human infections
in the world, and approximately 30% to 40% of
the U.S. population is affected.5 The prevalence
of H. pylori infection is inversely related to
socioeconomic status and is particularly related to density of living
and household income during childhood.6 The age-adjusted
prevalence of H. pylori infection is decreasing
in industrialized countries, likely due to an improved standard
of living, especially during childhood, as well as spontaneous loss
of infection.5,6 This may explain the decreasing
incidence of peptic ulcer disease in the U.S., although increased
use of proton pump inhibitors (PPIs) may also be a factor.1 In
any given 6-month period about 40% of the population describes
some upper GI symptoms (including both dyspepsia and heartburn),
and investigation of these symptoms accounts for about 50% of
a gastroenterologist’s workload.7 The
point prevalence of dyspepsia alone is about 25%.3
Hydrochloric acid and pepsin destroy gastric and duodenal mucosa.
Mucus and bicarbonate ion secretions protect mucosa. Prostaglandins
protect mucosa by enhancing mucus and bicarbonate production and
by enhancing mucosal blood flow, thereby supporting metabolism.
The balance between these protective and destructive forces determines
whether peptic ulcer disease occurs. H. pylori infection
or NSAIDs are thought to be the causal agents of peptic ulcer disease
in almost all cases.2,8 H. pylori infection
is present in about 95% of patients who develop duodenal
ulcer and about 70% of those who develop gastric ulcer.9 Although
traditional treatment of peptic ulcers by various modalities heals
most ulcers, eradication of H. pylori reduces 1-year
recurrence rates from 35% to 2% for duodenal ulcers
and from 39% to 3% for gastric ulcers.5 H.
pylori is a spiral, gram-negative, urease-producing, flagellated
bacterium that is found living between the mucous gel and the mucosa.
The bacterium’s production of urease, cytotoxins, proteases,
and other compounds is thought to disturb the mucous gel and cause
tissue injury. In addition, increased gastrin levels and decreased
mucus and ...