Tu1592 Clinical Course of Patients With Aspirin-Induced Small Intestinal Ulcers Detected by Capsule Endoscopy

Many patients with cardiovasucular and/or cerebrovascular disease take low-dose aspirin for anti-platelet therapy. There is strong evidence that aspirin users tend to suffer more severe gastrointestinal bleeding than non-users. Recently, several studies have shown that low-dose aspirin induces small intestinal injury. However, there is no established treatment for aspirin-induced small intestinal injury. The purpose of this study was to clarify the clinical course of patients with aspirin-induced small intestinal ulcers undergoing a variety of treatments. Seventy-two patients on aspirin therapy were evaluated by capsule endoscopy to detect the source of obscure gastrointestinal bleeding (OGIB). Patients taking concurrent aspirin and NSAID medication were excluded. Small intestinal ulcers were defined as mucosal breaks with slough diameters measuring more than the combined widths of ten consecutive villi from the surrounding area. The ratio of OGIB patients with small intestinal ulcers was calculated for the group on aspirin medication. The clinical course of patients with small intestinal ulcers was also evaluated. Fifty-three small intestinal ulcers were detected in 19 patients (19/72: 26%). Among these patients, 14 patients (8 males; 6 females; mean age, 68 years) were followed-up for a mean interval of 15.4 months. Only one patient among the 14 patients took concomitant administration of clopidogrel before the onset of overt bleeding. All of the 14 patients stopped taking aspirin immediately after overt bleeding. Eleven patients with small intestinal ulcers resumed anti-platelet medication one or two weeks after the bleeding stopped. Out of 14 patients, six were taking clopidogrel (one with concomitant prostagrandin and rebamipide medication for intestinal protection), two were taking ticlopidine (one with rebamipide), one was taking cilostazol, two resumed aspirin medication (one along with misoprostol, the other with rebamipide). The remaining three patients stopped their anti-platelet therapy altogether. The hemoglobin concentrations of all 14 patients increased after diagnosis of aspirin-induced small intestinal ulcer, from 8.2g/dl before diagnosis to 12.2g/dl (p=0.001). The number of small intestinal ulcers decreased from a mean of 2.9 to 0.8 (p=0.024). Only one patient on clopidogrel medication experienced a new bleeding episode seven months later and was withdrawn from clopidogrel treatment. This last patient was examined by capsule endoscopy five weeks later where we found that fully-healed ulcer scars had formed. Although there was no consensus in treatment, all patients recovered from aspirin-induced small intestinal ulcers regardless of the treatment of choice.