Digestive diseases
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Helicobacter pylori induces an inflammatory immune response in the gastric mucosa. The degree of gastric mucosal inflammation and its topographic distribution are key factors in the diversity of H. pylori-related complications. Here we summarize substantial evidence reported in the literature concerning the impact of H. pylori density on gastric inflammation, the development of severe complications, and its relation to H. pylori suppression therapy. ⋯ The influence of H. pylori density reduction on the improvement of gastric mucosal changes was observed in studies using 'clearance' therapies. Mucosal agents provoke a significant, but not persistent, reduction in gastritis activity. Treatments suppressing the density and virulence of H. pylori could become strategies to prevent H. pylori-associated disease in the future.
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In chronic pancreatitis over a course of years to decades, pancreatic parenchyma is gradually lost and pain is gradually decreasing as signs and symptoms of malabsorption appear. Appearance of calcifications is a late sign and in many cases coincides with appearance of steatorrhea. Decreasing output of insulin and glucagon results in diabetes mellitus, which is characterized by a high risk of hypoglycemias ('brittle' diabetes). ⋯ Using such preparations, most patients will reduce their steatorrhea to <15 g fat per day during supplementation of 25,000-40,000 IU of lipase per meal, but in selected cases larger doses may be needed, depending on size of the meal and severity of the disease. Efficacy of enzyme replacement therapy is influenced by denaturation of lipase by gastric acid, improper timing of enzymes, coexisting small-intestinal mucosal disease, rapid intestinal transit and effects of diabetes. This review focuses on pathophysiology, diagnosis and treatment of pancreatic steatorrhea.
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Chemoprevention of colorectal cancer is a promising science that has particular importance due to the limited success of current treatments for most advanced common malignancies. Many chemopreventive agents have been studied including cyclooxygenase (COX) inhibitors. Two isoforms of the COX enzymes are COX-1 and COX-2. ⋯ Personalized medicine in this field is also greatly anticipated. Combination therapy is under extensive research in order to improve efficacy while reducing toxicity profiles. Chemoprevention of colorectal cancer is largely possible, but the ultimate drug and proper patient selection, among other elements of the cancer prevention equation, are still needed.
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Overweight and obesity are the most significant risk factors for the development of hepatic steatosis, non-alcoholic steatohepatitis (NASH) and non-alcoholic fatty liver disease (NAFLD) in children and adults. Both have been increasingly implicated in the genesis of hepatic fibrosis and cirrhosis. However, no consensus exists about whether weight reduction may reverse this process. ⋯ Obesity surgery improves steatosis, necroinflammatory activity and hepatic fibrosis in patients with morbid obesity and NASH. The improvement of all obesity-related comorbidities can be confirmed.
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Growing evidence suggests that gastrointestinal immune activation may affect intestinal function and sensory perception, which contribute to symptom generation in patients with irritable bowel syndrome (IBS). The identification of higher counts of immunocytes (e.g. T cells and mast cells), mucosal and systemic immune activation, and increased mucosal permeability in patients with IBS has stimulated interest in the potential development of therapeutic approaches aimed at targeting the immune system and inflammation. ⋯ Nevertheless, the exact mechanism through which this drug affects immune activation in the intestine of patients with IBS remains unknown. There is a need for further studies to prove the efficacy of mesalazine for IBS. Further studies aimed at assessing the role of aminosalicylates and other approaches with potential anti-inflammatory activity, including probiotics, non-absorbable antibiotics, histamine receptor antagonists and protease inhibitors on IBS symptoms or pathophysiology are now warranted.