Nonsteroidal anti-inflammatory drug (NSAID) gastropathy is sufficiently important as to warrant co-administration of misoprostol, proton pump inhibitors (PPIs) or a switch to selective cyclooxygenase (COX)-2 inhibitors.
However, the serious ulcer outcome studies suggested that 40% of the clinically significant gastrointestinal bleeding originated more distally, presumably from NSAID enteropathy.
|The small bowel in 62% of patients on NSAIDs was abnormal|
|Clinical Gastroenterology and Hepatology|
Professor Ingvar Bjarnason and colleagues from England used capsule enteroscopy to study small-bowel damage in patients on long-term NSAIDs and COX-2-selective agents.
The team had 60 healthy volunteers act as controls.
The research team reported that 120 patients on long-term NSAIDs, and 40 on COX-2 selective agents underwent a capsule enteroscopy study.
Small-bowel damage was categorized and quantitated.
The researchers found that the small bowel in 62% of patients on conventional NSAIDs was abnormal, which differed significantly from controls.
The researchers noted that the main pathology related to reddened folds, denuded areas, and mucosal breaks.
About 2% had diaphragm-like strictures, and 3% had bleeding without an identifiable lesion.
The damage, seen in 50% of patients on selective COX-2 inhibitors, did not differ significantly from that seen with NSAIDs.
Dr Bjarnason's team concluded, "Long-term NSAIDs and COX-2-selective agents cause comparable small-bowel damage."
"This suggests an important role for COX-2 in the maintenance of small-bowel integrity."
"The results have implications for strategies that aim to minimize the gastrointestinal damage in patients requiring anti-inflammatory analgesics."