Histopathological aspects of mucosal injury related to non-steroidal anti-inflammatory drugs

As the majority of patients with chronic arthritis are treated, for many years, with non-steroidal anti-inflammatory drugs (NSAID), it is only natural to expect the long-term use of these agents to be associated with a range of oesophago-gastro-duodenal histopathological changes. We have demonstrated that oesophagitis (defined as basis of papillary length, basal cell hyperplasia and inflammatory cell infiltration) is less prevalent in patients taking NSAID. This phenomenon can be utilised in the treatment of certain conditions such as post-irradiation oesophagitis and Barrett's oesophagitis. It also implies that NSAID-related oesophageal ulceration is due to lodging of tablets in the oesophagus and is, in turn, preventable by swallowing of some fluids or solids after taking NSAID. In the stomach, long-term use of NSAID is associated with a specific entity known as chemical or reactive gastritis in about 25% of cases. This is frequently associated with ulceration. Chronic active superficial gastritis, in the presence of Helicobacter pylori, can be found in about 70% of cases. Not unlike oesophagitis, the prevalence of active duodenitis is low in chronic NSAID users. Local ulceration still takes place. This implies that duodenitis is not required in at least some cases of NSAID-related duodenal ulcers, and demonstrates the multi-factorial nature of the pathogenesis of mucosal damage in long-term users of a NSAID.