Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity is non-infectious pandemic. Its association with cardiovascular pathology is especially widely discussed, but an overweight patient is actually polymorbid. An increase of body mass provides a pathogenetic basis for many diseases including those of digestive system This review deals with pathogenesis, clinical features, and treatment of gastroesophageal reflux disease, cholelithiasis and non-alcoholic fatty liver disease in obese patients. This pathology and its aggravation result from such pathophysiological processes as a rise in intra-abdominal pressure, excess adipokine, cholesterol and free fatty acid synthesis, activation of lipid peroxidation. Gastroesophageal reflux disease in obese patients has an atypical clinical course characterized by discrepancy between clinical, endoscopic and morphological features in oesophagus and frequent formation of Barrett's oesophagus. Cholelethiasis in obesity is fraught with further progress of the disease after prescription of low-fat diet. The risk of calculi formation can be reduced by prescription of ursodeoxycholic acid that produces both litholytic and hypolipidemic effects. Treatment of non-alcoholic fatty liver disease requires combined therapy with statins, insulin sensitizers, hepatoprotectors and adequate physical activity. Sustained remission of diseases of digestive organs is impossible without correction of body mass and their pharmacotherapy requires increasing doses of medicines and duration of their administration.
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PMID:[Obesity and diseases of digestive organs]. 2441 71

Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett's esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.
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PMID:Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression. 3316 21