The histopathology of non-steroidal anti-inflammatory drug induced gastroduodenal damage: correlation with Helicobacter pylori, ulcers, and haemorrhagic events

Abstract

Aims-The spectrum of microscopic lesions resulting from the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), known as chemical gastritis, remains unclear, and the variable prevalence reported in diVerent studies makes this issue a matter of lively debate. The aim of this study was to evaluate the prevalence and importance of chemical gastritis in patients regularly taking NSAIDs. Owing to the high prevalence of Helicobacter pylori infection, particularly in subjects over 60 years of age, and in view of a possible association with damage, the presence of H pylori infection in the same tissue sample was also determined in all patients. Methods-One hundred and ninety seven subjects were enrolled, 118 of whom were receiving chronic treatment with NSAIDs and 79 of whom were controls, pair matched for age, sex, and clinical symptoms (ulcer-like dyspepsia or upper digestive tract haemorrhage). Antral biopsies taken during upper gastroduodenal endoscopy were assessed for chemical gastritis according to a modified version of Dixon's score, and for helicobacter correlated chronic active gastritis, according to the updated Sydney system. Results-Chemical gastritis was identified in 11 patients taking NSAIDs (9%) and in four controls (5%) (p < 0.05). Helicobacter pylori was detected in 53 patients taking NSAIDs (45%) and in 34 controls (43%). Patients taking NSAIDs had a significantly higher number of erosions and ulcers and worse endoscores than controls. The presence of H pylori did not appear to increase histological damage, ulcer prevalence, or haemorrhagic events. Conclusions-Chemicalgastritis is present in a limited number of patients regularly taking NSAIDs, and is not strongly correlated with NSAID induced damage. In many cases of peptic ulcer or upper gastrointestinal bleeding in patients taking NSAIDs, the presence of chemical gastritis or H pylori infection cannot solely account for the development of mucosal damage. The chronic use of non-steroidal antiinflammatory drugs (NSAIDs) is a common cause of gastroduodenal erosions and peptic ulcers resulting, in many cases, in fatal haemorrhage.

Gastritis and Carditis

“…Interestingly, it appears that NSAIDs are not a risk factor for classical peptic duodenal ulceration (70,72,73). There seems to be some agreement that the risk of gastric mucosal injury with NSAIDs is compounded by H. pylori (68,69), although this association has been denied by other investigators (75). Unless complications are present (erosions or ulcers), reactive gastropathy appears to be an asymptomatic lesion (71).…”

“…Unless complications are present (erosions or ulcers), reactive gastropathy appears to be an asymptomatic lesion (71). The prevalence of reactive gastropathy in patients taking NSAIDs has been estimated to be between 34 and 45% (69,70,75).…”

Assessing the efficacy of famotidine and rebamipide in the treatment of gastric mucosal lesions in patients receiving long-term NSAID therapy (FORCE—famotidine or rebamipide in comparison by endoscopy)

“…5 Other mechanisms, however, are also considered to play a role in NSAID-associated gastric mucosal lesions. 6,7 NSAIDs may cause gastric mucosal lesions by reducing gastric mucosal blood flow. 8 As with other peptic ulcers, the involvement of gastric acid in NSAID-associated gastric mucosal lesions is important.…”

How to Interpret Biopsies for “Gastritis”

“…Occasionally there is focal edema in the lamina propria, and a predominantly acute but also a sparse chronic inflammatory infiltrate, and over time there is also foveolar hyperplasia, proliferation of smooth muscle and congestion. 12,13 Chemotherapy and radiation can cause both gastritis and stomach ulcers. The pathology is similar to that seen in chemical/reactive gastropathy with glandular atypia, increased apoptosis, and abnormal mitosis.…”