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Unusual causes of peptic ulcer disease

Section Editor
Mark Feldman, MD, MACP, AGAF, FACG
Deputy Editor
Shilpa Grover, MD, MPH, AGAF


Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) account for the large majority of cases of peptic ulcer disease (PUD) in Europe, Asia, Australia, and some populations in the United States. As the prevalence of H. pylori infection has decreased, NSAID-related ulceration is the major cause of ulcer disease in many parts of the United States. (See "Association between Helicobacter pylori infection and duodenal ulcer" and "NSAIDs (including aspirin): Pathogenesis of gastroduodenal toxicity".)

Several studies in the United States have shown that less than 75 percent of patients with duodenal ulcers (DUs) not associated with use of NSAIDs are related to H. pylori infection. In one study, after excluding NSAID use, 61 percent of DUs and 63 percent of gastric ulcers were H. pylori positive [1]. Only 52 percent of whites with DUs were H. pylori positive, compared with 85 percent of nonwhites, underscoring the importance of demographics. In a retrospective study conducted over five years in a large tertiary hospital in the United Kingdom, H. pylori-negative, NSAID-negative ulcers accounted for 12 percent of all ulcers [2]. The etiology of these ulcers remains uncertain. (See "Epidemiology and etiology of peptic ulcer disease".)

Before focusing on other etiologies of PUD, it is important to carefully exclude H. pylori infection and NSAID use (table 1). False negative H. pylori testing is commonly encountered, particularly with tests that depend upon the number of organisms (rapid urease testing on gastric mucosal biopsies, urea breath testing, histology, and stool antigen) when the patient has recently taken antibiotics, proton pump inhibitors, or bismuth. Several lines of evidence indicate that H. pylori is frequently missed [3]. For example, serology is positive in some ulcer patients when other tests are negative; although some of these results may be false positives, some are due to suppression of organisms or isolated duodenal colonization, as considered below (see "Indications and diagnostic tests for Helicobacter pylori infection"). In the United States, NSAIDs are so widely available, as over-the-counter medications that patients may not remember or report using them. Furthermore, approximately one-half of patients with aggressive ulcer disease attributable to aspirin deny taking aspirin [4]. Aspirin use has been detected in such patients by serum salicylate levels [4]. Given the rarity of other causes of peptic ulcer disease, the clinician should carefully assess the work-up for H. pylori and repeat it if necessary and re-evaluate the history of NSAID use before initiating a work-up for rare causes of ulcer disease.


Several factors and disorders have been implicated as causes of secondary peptic ulcer disease (PUD). A small proportion of acid hypersecretory and nonhypersecretory peptic ulcers remain at present in an idiopathic category; however, with careful evaluation (table 1), this idiopathic category is very small. It is important to exclude malignancy as the cause of gastric and, rarely, duodenal ulcers.

Drugs other than NSAIDs — There are a number of drugs that cause or exacerbate gastrointestinal (GI) bleeding, ulcer disease, or both, and the list is growing (table 2). The role of nonsteroidal anti-inflammatory drugs (NSAIDs) is well established (see "NSAIDs (including aspirin): Pathogenesis of gastroduodenal toxicity"). However, NSAIDs also appear to exacerbate the toxicity of several other drugs.


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Literature review current through: Apr 2017. | This topic last updated: May 22, 2017.
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