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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review highlights areas of clinical research in gastroenterology and hepatology that were published predominantly in the journal Clinical Gastroenterology and Hepatology during the last year and were summarized during the American Gastroenterological Association Presidential Plenary Session in May 2006. The topics included eosinophilic esophagitis in children, detecting high-grade dysplasia or carcinoma in Barrett's esophagus, advances in management of celiac disease with elemental diet or gluten predigestion, the safety of NSAIDs in inflammatory bowel disease, the role of steroids in development of abscesses, prognosis of colorectal cancer associated with inflammatory bowel disease, screening for familial colorectal cancer in apparently sporadic disease, a new syndrome of familial colorectal cancer, new drugs in the treatment of chronic constipation and obesity, hepatoma risk factors and underserved racial/ethnic groups, and the application of new imaging and biology in diagnosis of gastroenterological disorders.
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PMID:Gastroenterology and hepatology clinical research update: 2005-2006. 1694 47

Recently, the incidence of intrahepatic cholangiocarcinoma (ICC) has been increasing in a number of developed (Western) countries. However, risk factors in these low-risk populations are poorly understood. In this nationwide population based case-control study in Denmark, we examined the relationship between selected medical conditions and subsequent ICC risk to provide additional clues to etiopathogenesis. All histologically confirmed ICC cases diagnosed in Denmark between 1978 and 1991 were identified from the Danish cancer registry. Population controls were selected from the central population registry and were matched 4:1 to cases on sex and year of birth. Cases and controls were linked to the Danish hospital discharge registry to obtain information on prior hospital diagnoses. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived using conditional logistic regression. A total of 764 ICC cases and 3,056 population controls were included in the study. Chronic liver diseases were significantly related to ICC: alcoholic liver disease (OR = 19.22, 95% CI = 5.55-66.54), unspecified cirrhosis (OR = 75.9, 95% CI 10.2-565.7). Bile duct diseases were also associated with risk: cholangitis (OR = 6.3, 95% CI = 2.3-17.5), choledocholithiasis (OR = 23.97, 95% CI = 2.9-198.9), cholecystolithiasis (OR = 4.0, 95% CI = 2.0-7.99), though gallbladder removal did not change risk (OR = 1.6, 95% CI = 0.65-3.7). Among other conditions, chronic inflammatory bowel disease (OR = 4.7, 95% CI = 1.65-13.9) was significantly associated with ICC. Diabetes was associated with risk in the year prior to diagnosis of ICC (OR = 3.02, 95% CI = 1.05-8.69). Obesity was unrelated to risk. These results confirm that prior bile duct diseases increase risk of ICC and suggest that alcoholic liver disease and diabetes may also increase risk.
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PMID:Risk factors for intrahepatic cholangiocarcinoma in a low-risk population: a nationwide case-control study. 1710 84

Genetic diversity, most notably through single nucleotide polymorphisms and copy-number variation, together with specific environmental exposures, contributes to both disease susceptibility and drug response variability. It has proved difficult to isolate disease genes that confer susceptibility to complex disorders, and as a consequence, even fewer genetic variants that influence clinical drug responsiveness have been uncovered. As such, the candidate gene approach has largely failed to deliver and, although the family-based linkage approach has certain theoretical advantages in dealing with common/complex disorders, progress has been slower than was hoped. More recently, genome-wide association studies have gained increasing popularity, as they enable scientists to robustly associate specific variants with the predisposition for complex disease, such as age-related macular degeneration, Type 2 diabetes, inflammatory bowel disease, obesity, autism and leukemia. This relatively new methodology has stirred new hope for the mapping of genes that regulate drug response related to these conditions. Collectively, these studies support the notion that modern high-throughput single nucleotide polymorphism genotyping technologies, when applied to large and comprehensively phenotyped patient cohorts, will readily reveal the most clinically relevant disease-modifying and drug response genes. This review addresses both recent advances in the genotyping field and highlights from genome-wide association studies, which have conclusively uncovered variants that underlie disease susceptibility and/or variability in drug response in common disorders.
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PMID:Recent development in pharmacogenomics: from candidate genes to genome-wide association studies. 1762 46

Cholangiocarcinoma occurs with a varying frequency in different areas of the world. Some of the variations in incidence rates can be explained by the distribution of risk factors in different geographic regions and ethnic groups. Several accepted risk factors for cholangiocarcinoma include infestation with liver flukes, primary sclerosing cholangitis, hepatolithiasis, choledochal cysts, cirrhosis, and infusion of certain chemical agents. Approximately, 90% of patients diagnosed with cholangiocarcinoma do not have a recognized risk factor for the malignancy. The study by Ahrens et al. [16] finds that obesity and gallstones are risk factors for developing extrahepatic cholangiocarcinoma in men patients. Obesity was found to have a 'dose-effect' relationship with the strength of statistical association. No significant association was reported for tobacco or alcohol use, hepatitis, cirrhosis, diabetes, or inflammatory bowel disease. Although the author's definition of extrahepatic cholangiocarcinoma was unusual, the association of obesity with the risk of developing cholangiocarcinoma persisted for all anatomic subsites.
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PMID:Risk factors for cholangiocarcinoma. 1762 30

Circulating levels of adiponectin decrease with increasing visceral obesity and are lower in patients with type 2 diabetes, the metabolic syndrome, and cardiovascular disease compared with controls matched by body mass index. Several reports demonstrated anti-inflammatory effects of adiponectin. Because increased adipose tissue is associated with low-grade chronic inflammation and proinflammatory factors inhibit adiponectin production, the current hypothesis states that chronic inflammation associated with visceral obesity inhibits production of adiponectin, perpetuating inflammation. The negative correlation between adiponectin and markers of inflammation in the aforementioned conditions supports this hypothesis. In contrast with disorders typically associated with excess adiposity and positive energy balance, adiponectin levels are elevated--rather than decreased--in classic chronic inflammatory/autoimmune diseases that are unrelated to increased adipose tissue, such as rheumatoid arthritis, SLE, inflammatory bowel disease, type 1 diabetes, and cystic fibrosis. In these patients, adiponectin levels positively--rather than negatively--correlate with inflammatory markers. Furthermore, proinflammatory effects of adiponectin have been reported in tissues such as joint synovium and colonic epithelium. Thus, adiponectin is regulated in the opposite direction and may exert differential functions in classic versus obesity-associated inflammatory conditions. This article discusses this apparent paradox and presents possible alternative and/or complementary explanations.
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PMID:Adiponectin and inflammation: consensus and controversy. 1877 64

Based on the painful effects of exposure to capsaicin, TRPV1 (transient receptor potential vanilloid subfamily member 1) localization is most readily associated with peripheral sensory neurons, however, TRPV1 is now known to be expressed, albeit at lower levels, in the spinal cord, brain and a wide-range of non-neuronal cells. The latter includes epithelial cells (e.g. keratinocytes, urothelium, gastric epithelial cells, enterocytes, and pneumocytes) through vascular endothelium and cells of the immune system (e.g. T-cells and mast cells) to smooth muscle, fibroblasts and hepatocytes. Despite extensive research, the physiological function of TRPV1 in the brain and in non-neuronal tissues remains elusive. The preliminary results are exciting, but many are unconfirmed and/or contradictory. As yet, studies with TRPV1 knock-out mice have proven unhelpful in clarifying such biological roles. Now that a range of potent and selective TRPV1 antagonists are available in this rapidly expanding research field, further understanding of the biological roles of TRPV1 throughout the body is within reach. In this article, we will summarize the known roles of peripheral TRPV1 receptors in physiology and disease and review the current perspectives for the therapeutic potential of TRPV1 agonists and antagonists in the treatment of a wide range of conditions such as pain, cancer, migraine, chronic cough, asthma, rectal hypersensitivity, inflammatory bowel disease, obesity, overactive bladder and diabetes. New applications of targeting central TRPV1 receptors are reviewed in the accompanying article by Starowicz et al. (in this issue).
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PMID:Peripheral TRPV1 receptors as targets for drug development: new molecules and mechanisms. 1822 Aug 16

Acutely ill medical patients are at moderate to high risk of venous thromboembolism: ~10 to 30% of general medical patients may develop deep vein thrombosis or pulmonary embolism, and the latter is a leading contributor to deaths in hospital. Medical conditions associated with a high risk of venous thromboembolism include cardiac disease, cancer, respiratory disease, inflammatory bowel disease, and infectious diseases. Predisposing risk factors in medical patients include a history of venous thromboembolism, history of malignancy, complicating infections, increasing age, thrombophilia, prolonged immobility, and obesity. Heparins, including unfractionated and low molecular weight, as well as fondaparinux have been shown to be effective agents in prevention of VTE in this setting. However, it has not yet been possible to demonstrate a significant effect on mortality rates in this population. In medical patients, unfractionated heparin has a higher rate of bleeding complications than low molecular weight heparin. There is no evidence for the use of aspirin, warfarin, or mechanical methods. We recommend either low molecular weight heparin or fondaparinux as safe and effective agents in the thromboprophylaxis of medical patients.
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PMID:Venous thromboembolism prophylaxis for the medical patient: where do we stand? 1830 89

It is well known that the steroid hormone glucocorticoid and its nuclear receptor regulate the inflammatory process, a crucial component in the pathophysiological process related to human diseases that include atherosclerosis, obesity and type II diabetes, inflammatory bowel disease, Alzheimer's disease, multiple sclerosis, and liver tumors. Growing evidence demonstrates that orphan and adopted orphan nuclear receptors, such as peroxisome proliferator-activated receptors, liver x receptors, the farnesoid x receptor, NR4As, retinoid x receptors, and the pregnane x receptor, regulate the inflammatory and metabolic profiles in a ligand-dependent or -independent manner in human and animal models. This review summarizes the regulatory roles of these nuclear receptors in the inflammatory process and the underlying mechanisms.
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PMID:Nuclear receptors and inflammatory diseases. 1837 23

The human intestine provides an expansive interface for interactions with the microflora. Increasing data support the hypothesis that host-microflora relationships are markedly dynamic, contributing to host health and disease pathogenesis. Despite outnumbering human cells 10-fold, the microflora most often assist the host through symbiotic relationships. The microflora are involved in maximizing host utilization of nutrients, induction of host immune responses, and promotion of intestinal cell and mucosal development. However, evolving data suggest that disturbances in this symbiotic relationship can lead the microflora to be pathogenic in diverse conditions such as inflammatory bowel disease, irritable bowel disease, obesity, graft-versus-host disease, HIV immunopathogenesis, and possibly cancer. Defining those microflora attributes that result in health and those that trigger disease is key to harnessing the microflora to promote human health.
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PMID:New horizons for the infectious diseases specialist: how gut microflora promote health and disease. 1846 81

In their intestine, humans possess an "extended genome" of millions of microbial genes-the microbiome. Because this complex symbiosis influences host metabolism, physiology, and gene expression, it has been proposed that humans are complex biologic "superorganisms." Advances in microbiologic analysis and systems biology are now beginning to implicate the gut microbiome in the etiology of localized intestinal diseases such as the irritable bowel syndrome, inflammatory bowel disease, and colon cancer. These approaches also suggest possible links between the gut and previously unassociated systemic conditions such as type 2 diabetes and obesity. The elucidation of the intestinal microbiome is therefore likely to underpin future disease prevention strategies, personalized health care regimens, and the development of novel therapeutic interventions. This review summarizes the research that is defining our understanding of the intestinal microbiome and highlights future areas of research in gastroenterology and human health in which the intestinal microbiome will play a significant role.
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PMID:The human gut microbiome: implications for future health care. 1862 53


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