Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phlegmonous enteritis is a rare inflammatory bowel disease. A 52-yr-old man with a history of alcoholic abuse was admitted to the hospital for an acute abdomen and died of septicemia and its complications. Autopsy revealed phlegmonous inflammation of the ileum and severe fatty liver. Numerous Gram-negative rod bacilli were demonstrated in the ileal mucosa. Shortened villi and decreased lysozyme activity of Paneth cells in the small intestine might be results of chronic alcohol ingestion. The relationship between phlegmonous enteritis and alcoholic abuse was strongly suggested in this case.
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PMID:Phlegmonous enteritis in alcoholic fatty liver. 192 52

Clinically significant liver and biliary disorders occur in approximately 5 percent of persons with inflammatory bowel disease. The most common hepatobiliary disorders encountered in patients with inflammatory bowel disease are fatty liver, sclerosing cholangitis and gallstones. In addition, chronic hepatitis, cirrhosis, biliary cancer and amyloidosis sometimes occur. Family physicians should be alert for these gastrointestinal problems in patients with inflammatory bowel disease.
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PMID:Hepatobiliary complications of inflammatory bowel disease. 757 66

Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.
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PMID:Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease. 786 97

Gastrointestinal diseases in pregnancy can be divided into diseases specific to pregnancy, for example, hyperemesis gravidarum, obstetric cholestasis, HELLP syndrome and acute fatty liver of pregnancy, and diseases incidental to pregnancy, for example, inflammatory bowel disease, dyspepsia, peptic ulcer disease and viral hepatitis. Disorders in the second category may present for the first time in pregnancy. This chapter considers the drug management of each of these conditions, with the exception of HELLP syndrome and acute fatty liver. The preferred drug treatment and the known complications associated with their use in pregnancy are also described. Where possible, studies relating to the safety of different therapeutic options are discussed.
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PMID:Drugs in pregnancy. Gastrointestinal disease. 1180 May 34

Liver steatosis is a common human disease, most often caused by long-term alcohol consumption. Non-alcoholic steatohepatitis (NASH) is characterized by similar histopathological features to those observed in alcoholic liver disease, but occurs in the absence of significant alcohol consumption. Several aetiological factors contribute to NASH: obesity, type 2 diabetes mellitus, hyperlipidaemia, pregnancy, different chemical intoxications, parenteral nutrition, jejeuno-ileal bypass, chronic inflammatory bowel disease, nutritional protein deficiency and congenital metabolic disorders. Biochemically, oxidative stress and lipid peroxidation and their ensuing damage are implicated in the pathogenesis of NASH and alcoholic steatohepatitis (probably resulting from free fatty acids in the mitochondria, and induction of the cytochrome P450 isoform CYP2E1 in hepatocytes and Kupffer's cells). This paper deals with the pathomechanisms, clinical findings and currently available therapies for NASH. The potential use of metadoxine in the treatment of NASH is also discussed.
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PMID:A new approach to drug therapy in non-alcoholic steatohepatitis (NASH). 1470 19

This review highlights areas of clinical research in gastroenterology and hepatology that were published during the last year and were summarized during the most recent American Gastroenterological Association Plenary Session. The topics include a comparison of the risk of recurrent bleeding in patients taking clopidogrel versus aspirin plus a proton pump inhibitor, the introduction of rifaximin for the treatment of traveler's diarrhea, and the results of an oral vaccine for cholera tested in a high endemic area where there is also a high prevalence of human immunodeficiency virus infection. In inflammatory bowel disease, the impact of a biomarker of inflammation, C-reactive protein, to the response to a new biologic therapy is identified as potentially important because it might facilitate the selection of patients for these treatments. Results of device, endoscopic, and surgical treatment of obesity are reviewed, including the evidence of significant impact of surgery-induced weight loss on comorbid diseases. In the field of cancer, colonoscopic screening results in more polyps detected, down-staging of cancers identified, and improved cancer survival. A new familial syndrome associated with a serrated adenoma/carcinoma phenotype and variability in microsatellite instability is described. A controlled study demonstrates that a urine-derived substance, ulinastatin, reduces the risk of post-endoscopic retrograde cholangiopancreatography pancreatitis. Hepatic stellate cells are involved in the fibrogenesis associated with nonalcoholic fatty liver disease. These areas of clinical research demonstrate the breadth of significant advances that will impact on the clinical practice of gastroenterology and hepatology.
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PMID:GIH clinical research update: 2004-2005. 1636 Oct 39

The pregnane X receptor (PXR; NR1I2), a member of the nuclear receptor superfamily, regulates the expression of drug-metabolic enzymes and transporters involved in the responses of mammals to their chemical environment. The same enzyme and transporter systems are also involved in the homeostasis of numerous endogenous chemicals. The regulatory function of PXR is implicated in normal physiology and diseases, such as drug-drug interactions, hepatic steatosis, vitamin D homeostasis, bile acids homeostasis, steroid hormones homeostasis and inflammatory bowel diseases. As such, any genetic variations of this receptor could potentially have widespread effects on the disposition of xenobiotics and endobiotics. Knowledge concerning the genetic polymorphisms of PXR may help to understand the variations in human drug response and ensure safe drug use. The correlation of PXR genetic polymorphisms with several disease conditions also suggests that this receptor may represent a valid therapeutic for hepato-intestinal disorders such as inflammatory bowel disease and primary sclerosing cholangitis.
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PMID:PXR: a xenobiotic receptor of diverse function implicated in pharmacogenetics. 1901 24

Diseases involving the hepatopancreatobiliary (HPB) system are frequently encountered in patients with inflammatory bowel disease (IBD). Hepatobiliary manifestations constitute some of the most common extraintestinal manifestations of IBD. They appear to occur with similar frequency in patients with Crohn's disease or ulcerative colitis. HPB manifestations may occur in following settings: 1) disease possibly associated with a shared pathogenetic mechanism with IBD including primary sclerosing cholangitis (PSC), small-duct PSC/pericholangitis and PSC/autoimmune hepatitis overlap, acute and chronic pancreatitis related to IBD; 2) diseases which parallel structural and physiological changes seen with IBD, including cholelithiasis, portal vein thrombosis, and hepatic abscess; and 3) diseases related to adverse effects associated with treatment of IBD, including drug-induced hepatitis, pancreatitis (purine-based agents), or liver cirrhosis (methotrexate), and reactivation of hepatitis B, and biologic agent-associated hepatosplenic lymphoma. Less common HPB manifestations that have been described in association with IBD include autoimmune pancreatitis (AIP), IgG4-associated cholangitis (IAC), primary biliary cirrhosis (PBC), fatty liver, granulomatous hepatitis, and amyloidosis. PSC is the most significant hepatobiliary manifestation associated with IBD and poses substantial challenges in management requiring a multidisciplinary approach. The natural disease course of PSC may progress to cirrhosis and ultimately require liver transplantation in spite of total proctocolectomy with ileal-pouch anal anastomosis. The association between AIP, IAC, and elevated serum IgG4 in patients with PSC is intriguing. The recently reported association between IAC and IBD may open the door to investigate these complex disorders. Further studies are warranted to help understand the pathogenesis of HPB manifestations associated with IBD, which would help clinicians better manage these patients. An interdisciplinary approach, involving gastroenterologists, hepatologists, and, in advanced cases, general, colorectal, and transplant surgeons is advocated.
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PMID:Hepatopancreatobiliary manifestations and complications associated with inflammatory bowel disease. 2019 12

Using a combination of N-ethyl-N-nitrosourea-mediated mutagenesis and metabolomics-guided screening, we identified mice with elevated blood levels of short-chain C4-acylcarnitine and increased urine isobutyryl-glycine. Genome-wide homozygosity screening, followed by fine mapping, located the disease gene to 15-25 Mb of mouse chromosome 9 where a candidate gene, Acad8, encoding mitochondrial isobutyryl-CoA dehydrogenase was located. Genomic DNA sequencing revealed a single-nucleotide mutation at -17 of the first intron of Acad8 in affected mice. cDNA sequencing revealed an intronic 28-bp insertion at the site of the mutation, which caused a frame shift with a premature stop codon. In vitro splicing assay confirmed that the mutation was sufficient to activate an upstream, aberrant 3' splice site. There was a reduction in the expression of Acad8 at both the mRNA and protein levels. The mutant mice grew normally but demonstrated cold intolerance at young age with a progressive hepatic steatosis. Homozygous mutant mice hepatocytes had abnormal mitochondria with crystalline inclusions, suggestive of mitochondriopathy. This mouse model of isobutyryl-CoA dehydrogenase deficiency could provide us a better understanding of the possible role of IBD deficiency in mitochondriopathy and fatty liver.
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PMID:Alternative splicing in Acad8 resulting a mitochondrial defect and progressive hepatic steatosis in mice. 2165 59

This review evaluates the current understanding of the benefits and risks of physical activity and exercise on the gastrointestinal system. A significant portion of endurance athletes are affected by gastrointestinal symptoms, but most symptoms are transient and do not have long-term consequences. Conversely, physical activity may have a protective effect on the gastrointestinal system. There is convincing evidence that physical activity reduces the risk of colon cancer. The evidence is less convincing for gastric and pancreatic cancers, gastroesophageal reflux disease, peptic ulcer disease, nonalcoholic fatty liver disease, cholelithiasis, diverticular disease, irritable bowel syndrome, and constipation. Physical activity may reduce the risk of gastrointestinal bleeding and inflammatory bowel disease, although this has not been proven unequivocally. This article provides a critical review of the evidence-based literature concerning exercise and physical activity effects on the gastrointestinal system and provides physicians with a better understanding of the evidence behind exercise prescriptions for patients with gastrointestinal disorders. Well-designed prospective randomized trials evaluating the risks and benefits of exercise and physical activity on gastrointestinal disorders are recommended for future research.
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PMID:Physical activity benefits and risks on the gastrointestinal system. 2208 64


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