| セッション情報 |
International Forum 1(Gastrointestinal tract) 5.Diagnosis and prevention of NSAIDs-enteropathy
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| タイトル |
IF1-5-II (Keynote lecture) Video Capsule Endoscopy Diagnosis of NSAID-enteropathy
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| 演者 |
Laurence Maiden（University HospitalLewishamLondonUK） |
| 共同演者 |
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| 抄録 |
Background & Aims ：Undoubtedlythe major limitation on the use of non-steroidal anti-inflammatory drugs （NSAIDs） is theirserious gastrointestinal （GI） side effectsnamely dyspepsia （which is the most common reason for discon-tinuing NSAIDs）ulcerationbleedingperforation and obstruction． Worldwidethe prevalence of NSAID-associated gastric and duodenal ulcers ranges from 9% to 22% with severe haemorrhage or perforationoccurring in less than 1% annually． Much more is known of the gastroduodenal toxicity of aspirinNSAIDs and cyclooxygenase-2 inhibitors than their small bowel effects because of the severity ofandgreater accessibility tothese proximal lesions． Case reports have linked NSAIDs to a variety of lesions inthe sma11 and large bowel including bleedingprotein lossstricturesincreased intestinal permeability andhence-called NSAID-enteropathy． Diagnosis is largely based on assay of surrogate markers of infiamma-tion in stool such as faecal calprotectin． However stool markers are not widely available and the precisenature of this inflammation is uncertain． We used wireless capsule endoscopy to quantitate and assess thenature of the small bowel damage caused by NSAIDs when taken short-term and in patients on long-term NSAIDs and COX-2 inhibitors．Methods ：Forty healthy volunteers underwent a baseline capsule endoscopy． After taking diclofenac slow-release75mg twice a day（with omeprazole 20mg twice a day for gastroprotection）for a total of 14 days both in-vestigations were repeated． A further 120 patients on long-term NSAIDs （more than 3 months） and 40 onCOX-2 inhibitors underwent a capsule endoscopy study． Sixty healthy patients acted as controls． Smallbowel damage was categorised and quantitated．Results ：Short-term diclofenac ： Capsule endoscopy demonstrate d new pathology in 27 （68%） of subj ects． Thecommonest lesions were mucosal breaksseen in 16 （40%）which were seen to be bleeding in 2 （5%） ； red-dened folds in 14 （35%）；petechiae or red spots in 13 （33%）；denuded mucosa in 8 （20%） and blood inthe lumen without a visualised source in 3 （8%） ． Fifteen of the 27 subj ects had more than 1 lesion concur-rently．Long-term NSAID : 62% of patients on conventional NSAIDs were abnormal which differed signifi-cantly （p < 0.001） from controls． The main pathology related to reddened folds （13%）denuded areas（39%） and mucosal breaks （29%）． 2% had diaphragm-like strictures and 3% had bleeding without anidentifiable lesion． The damageseen in 50% of patients on selective COX-2 inhibitors （reddened folds（8%）denuded areas （18%） and mucosal breaks （22%）） did not differ significantly （p < 0.5） from thatseen with NSAIDs．Conclusion ：Capsule endoscopy demonstrates evidence of macroscopic injury to the small intestinein up to 68% ofvolunteersresulting from 2 weeks ingestion of slow-release diclofenac． Long-term NSAIDs and COX-2inhibitors cause comparable small bowel damage （50 to 62%）． Sma11 bowel ulceration is seen on capsuleendoscopy in 30-40％ of patients and should not be underestimated with respect to gastroduodenal pa-thology． This also suggests an important role for COX-2 in maintenance of small bowel integrity． The re-sults have implications for strategies that aim to minimise the gastrointestinal damage in patients requir-ing anti-infiammatory analgesics． |
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