Low-dose aspirin affects the small bowel mucosa: results of a pilot study with a multidimensional assessment.

BACKGROUND & AIMS: Whether low-dose aspirin (acetylsalicylic acid [ASA]) produces intestinal damage is controversial. Our aim was to determine whether the small bowel is damaged by low-dose ASA on a short-term basis. METHODS: Twenty healthy volunteers (age range, 19-64 years) underwent video capsule endoscopy (VCE), fecal calprotectin, and permeability tests (sucrose and lactulose/mannitol [lac/man] ratio) before and after ingestion of 100 mg of enteric-coated ASA daily for 14 days. Video capsule images were assessed by 2 independent expert endoscopists, fully blinded to the treatment group, by using an endoscopic scale. RESULTS: Post-ASA VCE detected 10 cases (50%) with mucosal damage not apparent in baseline studies (6 cases had petechiae, 3 had erosions, and 1 had bleeding stigmata in 2 ulcers). The median baseline lac/man ratio (0.021; range, 0.011-0.045) increased after ASA use (0.036; range, 0.007-0.258; P = .08), and the post-ASA lac/man ratio was above the upper end of normal (>0.025) in 10 of 20 volunteers (vs baseline, P < .02). The median baseline fecal calprotectin concentration (6.05 microg/g; range, 1.9-79.2) also increased significantly after ASA use (23.9 microg/g; range, 3.1-75.3; P < .0005), with 3 patients having values above the cutoff (>50 microg/g). Five of 10 subjects with abnormal findings at VCE also had lac/man ratios above the cutoff. Median baseline sucrose urinary excretion (70.0 mg; range, 11.8-151.3) increased significantly after ASA administration (107.0 mg; range, 22.9-411.3; P < .05). CONCLUSIONS: The short-term administration of low-dose ASA is associated with mucosal abnormalities of the small bowel mucosa, which might have implications in clinical practice.

[Chemoprevention in adenocarcinoma of the esophagus]. / Quimioprevención en adenocarcinoma de esófago.

The incidence of the adenocarcinoma of the esophagus (ACE) has dramatically for the last decades in western countries, which has been associated with a parallel increase in the incidence and prevalence of symptoms associated with gastroesophageal reflux diseases (GERD) and Barrett's esophagus (BE). Both conditions are now considered risk factors for ACE. Different pathways, including overexpression of cyclooxygenase (COX) isoenzymes, has been proposed to explain the carcinogenic process leading from normal esophagus to esophagitis, BE and ACE. The survival rate in patients with ACE is very low because of the poor outcomes of surgery and the limited benefits obtained with concomitant chemo-radiotherapy Several strategies based on early detection and surveillance of preneoplastic lessions have failed to have a global and significant impact on the prognosis of the ACE. Recent epidemiological and experimental studies suggest that chemoprevention could be useful in the management of patients with GERD and especially in those with BE. The current therapy with protom pump inhibitors (PPI) is effective to reduce the esophageal acid exposure, to improve reflux symptoms, and to heal inflammatory injuries, but probably is not enough to avoid the dysplastic progression of the metaplastic epithelium. Regular use of COX inhibitors (aspirin and other non steroid antiinflamatory drugs) has been associated with reduction of the risk of ACE and to decrease the incidence of ACE in animal models. In humans, the association of PPI with COX inhibitors could be a cost-effectiveness strategy but direct evidence is lacking. Other potential agents that have shown some chemoprevention potential include troglitazone, free radical scavengers, tamoxifen or prostaglandin receptor blockers, but the available scientific evidence is still poor and not ready to be tested in humans.

[Prevention and treatment of non-steroidal anti-inflammatory drug gastroenteropathy]. / Prevención y tratamiento de la gastroenteropatía por antiinflamatorios no esteroideos.

Nonsteroidal anti-inflammatory drug (NSAID) use is associated with both upper and lower gastrointestinal tract complications in 1 to 2% of patients using these drugs for 6 to 12 months. Gastroduodenal ulcers are also present in 30 to 50% of patients using NSAID. Dyspepsia is another frequent side effect that may or may not be associated with mucosal lesions. Main risk factors for NSAID-associated gastrointestinal complications include age > 60 years, ulcer history, high dose of NSAID, and concomitant use of anticoagulants, aspirin, or corticosteroids. Patients with risk factors that need NSAIDs should receive gastroprotection with proton pump inhibitors or misoprostol. Another gastrointestinal safer option is use of COX-2 selective NSAIDs (coxibs). Increased cardiovascular risk observed with long-term use of rofecoxib should be compared with other COX-2 selective and non-selective NSAID. In patients at very high risk, co-prescription of coxib with proton pump inhibitors has been recommended. In patients at risk, all these strategies are cost-effective.