ABSTRACT
BACKGROUND: A non-invasive marker is needed to identify patients with significant gastrointestinal injury due to non-steroidal anti-inflammatory drugs. Gastrointestinal permeability to sucrose has been suggested as such a test. AIMS: To assess the utility of sucrose permeability as a marker of gastroduodenal mucosal injury after single and multiple doses of aspirin, to identify the site of increased sucrose permeability, to explore the relation between sucrose permeability and endoscopic findings, and to evaluate whether Helicobacter pylori infection influenced gastroduodenal sucrose permeability. METHODS: After a fasting urine was obtained, 500 ml of a solution containing 100 g of sucrose was ingested. Urine was collected for five hours and assayed for sucrose by high performance liquid chromatography. Sucrose permeability was also assessed 20 minutes after ingestion of 650 mg of aspirin and eight to 12 hours after a 72 hour course of 650 mg aspirin four times a day. The site of increased permeability was identified after pyloric occlusion with a double balloon tube. RESULTS: Thirty seven healthy volunteers participated. Sucrose permeability (mean (SEM)) increased after both single (195.2 (27) mg and multiple (196.4 (31) mg) doses of aspirin compared with baseline (53.7 (10) mg; p < 0.0005). Balloon pyloric occlusion confirmed that the site of increased sucrose permeability was the stomach. The effect of aspirin on sucrose permeability was similar in those with and without H pylori infection. CONCLUSION: These results confirm the use of sucrose permeability as a marker of aspirin induced gastroduodenal mucosal injury and identify the stomach as the major site of increased permeability. H pylori infection does not seem to change gastric mucosal sucrose permeability either at baseline or after ingestion of aspirin.
Subject(s)
Aspirin/adverse effects , Gastric Mucosa/drug effects , Gastrointestinal Diseases/chemically induced , Helicobacter Infections/complications , Helicobacter pylori/isolation & purification , Sucrose/pharmacology , Adult , Biomarkers , Chromatography, High Pressure Liquid , Female , Gastrointestinal Diseases/complications , Humans , Male , Middle Aged , Pyloric Antrum/drug effects , Sucrose/urineABSTRACT
Alpha 1-antitrypsin deficiency is a genetic disorder commonly associated with pulmonary and hepatic injury. Low serum levels of this glycoprotein result in an imbalance between circulating protease and protease inhibitors, which is thought to play a role in the development of emphysema. In recent studies, a protease-to-protease inhibitor imbalance in patients with alpha 1-antitrypsin deficiency was thought to be a mechanism contributing to the development of chronic pancreatitis. The heterozygous phenotype and low levels of this glycoprotein have been reported to occur more frequently in patients with chronic pancreatitis than in healthy controls. We report a patient with Pi-SS phenotype alpha 1-antitrypsin deficiency and chronic pancreatitis complicated by recurrent pancreatic pseudocysts and chronic abdominal pain. Our case supports the association between chronic pancreatitis and alpha 1-antitrypsin deficiency. Furthermore, this case provides support for the use of pancreatic stent drainage in the management of intractable abdominal pain in patients with chronic pancreatitis and a dominant stricture.
Subject(s)
Pancreatitis/etiology , alpha 1-Antitrypsin Deficiency , Abdominal Pain/etiology , Abdominal Pain/therapy , Adult , Cholangiopancreatography, Endoscopic Retrograde , Chronic Disease , Humans , Liver/pathology , Male , Pancreatic Pseudocyst/etiology , Pancreatic Pseudocyst/therapy , Pancreatitis/therapy , Phenotype , Stents , alpha 1-Antitrypsin/geneticsSubject(s)
Isoniazid/adverse effects , Pancreatitis/chemically induced , Acute Disease , Adult , Humans , Male , Tuberculosis/drug therapyABSTRACT
During the past decade it has become evident that colonic mucosal metabolism is more complex than previously suspected. Luminal short-chain fatty acids (SCFAs) are recognized as an essential fuel source for colonocytes, particularly in the distal colon. Their absence may explain the development of diversion colitis; however, this has not been confirmed by clinical trials. The histologic, endoscopic, and metabolic similarities between diversion colitis and ulcerative colitis suggest that a nutritional SCFA deficiency state may play a role in the pathogenesis of these disorders. Diversion colitis and continent urinary diversion, utilizing distal and proximal colon reservoirs, provide in vivo models to study normal colonic mucosa in circumstances of reduced intraluminal SCFA concentrations and altered luminal effluent. Further studies utilizing these models would enhance our understanding of the regional differences in mucosal cell metabolism and adaptability and, hopefully, provide therapeutic alternatives for the management of colonic disorders. The welfare of colonic mucosa, as it relates to SCFA metabolism, awaits another exciting decade of investigation.
