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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although cannabinoids have been recreationally employed for thousands of years, it was not until the discovery of their specific receptors, in the early nineties, that the molecular basis of cannabinoid activity have began to be understood. Growing research in this field has demonstrated not only that the action of cannabinoids in mammals is mainly receptor-mediated, but also that endogenous cannabinoids, such as anandamide, are produced, metabolized, and taken up across the cell membrane through a facilitated uptake process. The exogenous administration of cannabinoids, as well as the manipulation of their endogenous levels have been related to a variety of effects, such as analgesia, impairment of cognition and learning, appetite enhancement and peripheral vasodilation. Hence, the endocannabinoid system, including the CB1 and CB2 receptors, the metabolizing enzyme fatty acid amide hydrolase and the anandamide transporter, is a potential target for the development of novel therapeutic drugs in the treatment of various conditions, such as pain, feeding disorders and vascular disease among others. Although most of the research in the field of cannabinoids has been focused on their effects in the central nervous system, a growing line of evidence indicates that cannabinoids can also play a major role in the control of physiopathological functions in the cardiovascular system. In this context, endocannabinoids have been proposed as novel possible hypotensive agents, and have been involved in the hypotension observed in septic shock, acute myocardial infarction and cirrhosis. In addition, a protective role for endocannabinoids has been described in ischemia.
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PMID:Cannabinoid system as a potential target for drug development in the treatment of cardiovascular disease. 1532 Apr 76

The latest advances in hepatology were presented in oral and poster presentations. In order to cover the varying subspecialties, the sessions were divided into various sections including 'Acute Liver Failure and Artificial Liver Support', 'Biliary Tract and Immunologic Liver Diseases', 'Cellular and Molecular Biology', 'Clinical and Experimental Hepatobiliary Surgery', 'Hepatotoxicity and Cell Death', 'Transport and Biliary Physiology', 'Viral Hepatitis', 'Evaluation and Treatment of Biliary Disease', 'Necrosis/Apoptosis', 'Portal Hypertension', 'Blood Flow and Vascular Disorders of Cirrhosis', 'Liver Transplantation', 'Fibrogenesis', 'Hepatocellular Carcinoma', 'Metabolism and Genetic Disease', and 'Public Policy, Epidemiology and Decision Analysis'. Drug therapy focused on treatments for viral hepatitis, autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis, and recurrent viral disease following liver transplant. High dose interferon therapy or various combinations of interferon/ribavirin (ICN Pharmaceuticals Inc) therapy seem to offer the best current therapy for chronic HCV. PEGylated interferon (F Hoffmann-La Roche Ltd) offers hope for treatment and histologic improvement in patients with chronic HCV. Following liver transplantation, combination interferon/ribavirin therapy may also find success, but caution with new potent immunosuppressant monoclonal antibodies is advised. For HBV, intramuscular H-BIG (NABI) appears to be effective and less costly than iv H-BIG administration following liver transplantation. Percutaneous radiofrequency ablation may hold promise over conventional ethanol injection therapy for small hepatocellular carcinoma. Autoimmune hepatitis may respond to tacrolimus therapy whereas budesonide therapy did not provide any advantage to prednisone therapy. For primary biliary cirrhosis, eicosapentate and ursodeoxycholic acid may provide benefit to some patients while silymarin from milk thistle did not provide any additional benefit. In primary sclerosing cholangitis, high dose ursodeoxycholic acid may provide benefit. Ursodeoxycholic acid may also provide benefit for mothers with intrahepatic cholestasis of pregnancy by decreasing pruritus, lowering laboratory values and allowing deliveries to occur closer to term.
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PMID:Digestive disease week 2000. American Association for the Study of Liver Diseases. 1605 98

Non-alcoholic fatty liver disease (NAFLD) is present in up to one-third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors, including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however, staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as cirrhosis and hepatocellular carcinoma, which occur in a minority of patients. NAFLD is also now recognized to account for a substantial proportion of patients previously diagnosed with 'cryptogenic cirrhosis'. Diabetes, obesity and the necroinflammatory form of NAFLD known as non-alcoholic steatohepatitis, are risk factors for progressive liver disease. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Further research is needed to identify which patients will achieve the most benefit from therapy.
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PMID:Recent concepts in non-alcoholic fatty liver disease. 1610 37

Hereditary Haemorrhagic Telangiectasia (HHT), also known as Rendu-Osler-Weber disease, is an autosomal-dominant vascular disease characterised by mucocutaneous or visceral angiodysplastic lesions (telangiectases and arteriovenous malformations), which may be widely distributed throughout the cardiovascular system. Its diagnosis is based on clinical criteria. Liver, lungs and brain, in order of prevalence, are the most frequently involved visceral districts of the body other than skin and nasal mucosa. Liver involvement is frequent and characterised by the presence of intrahepatic shunts, disseminated intraparenchymal telangiectases and other vascular lesions. Although it is usually asymptomatic, congestive cardiac failure, portal hypertension, portosystemic encephalopathy, cholangitis or atypical cirrhosis are possible complications. Pulmonary arteriovenous malformations involve more than one third of HHT patients and can consist of diffuse telangiectases or high-flow low-pressure shunts between pulmonary arteries and veins. Pulmonary involvement can cause serious complications: hypoxaemia, pulmonary or pleural hemorrhage, paradoxical embolism into cerebral circulation. Various types of cerebrovascular malformations can affect HHT patients and the most common are arteriovenous malformations, consisting of one or more feeding arteries connected to one or more draining veins. Diagnostic imaging has a fundamental role in detecting the alterations involving these various districts in the body. The possibility to perform fast and complete studies and to provide high quality multiplanar and angiographic reconstructions, gives multi-detector row helical computed tomography and magnetic resonance the ability to detect and characterise the complex anatomo-pathological alterations typical of HHT. Ultrasonography seems to be the best screening modality for hepatic and pulmonary involvement.
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PMID:Hereditary haemorrhagic teleangiectasia: diagnostic imaging of visceral involvement. 1661 Nov 5

Nonalcoholic fatty liver disease (NAFLD) is present in up to one third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn, exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as due to cirrhosis and hepatocellular carcinoma, which occurs in a minority of patients. NAFLD is also now recognized to account for a substantial proportion of patients previously diagnosed with 'cryptogenic cirrhosis'. Diabetes, obesity and the necroinflammatory form of NAFLD known as non-alcoholic steatohepatitis, are risk factors for progressive liver disease. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Further research is needed to identify which patients will achieve the most benefit from therapy.
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PMID:Nonalcoholic fatty liver disease. 1747 59

Human and other biological tissues face a continual threat of damage by alpha-oxoaldehydes formed endogenously. Glyoxal, methylglyoxal and 3-deoxyglucosone are formed by the degradation of glycolytic intermediates, glycated proteins and lipid peroxidation. They are potent glycating agents of protein and nucleotides leading to the formation of advanced glycation endproducts (AGEs). With proteins, they are arginine residue-directed glycating agents forming mainly hydroimidazolones, found at 0.1-1% of total arginine residues in tissues (2-20% of proteins modified). With nucleotides, imidazopurinone- and N2-carboxyalkyl- derivatives of deoxyguanosine are formed, found at 0.1-0.8 per 10(6) nucleotides in DNA. Glycation occurs in all tissues and body fluids. Cellular proteolysis of AGE-modified proteins and DNA releases glycated amino acids and nucleosides. Glycated amino acids and nucleosides are released into plasma, undergo glomerular filtration and are excreted in urine. The damage to tissue protein and nucleotides by alpha-oxoaldehydes is suppressed by the metabolism of alpha-oxoaldehyde glycating agents by the glutathione-dependent enzyme, glyoxalase I, and aldo-keto reductases. These enzymatic activities are part of the enzymatic defence against glycation. Tissue damage by alpha-oxoaldehyde glycation is implicated in diabetic and non-diabetic vascular disease, renal failure, cirrhosis, Alzheimer's disease, arthritis and ageing.
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PMID:Endogenous alpha-oxoaldehydes and formation of protein and nucleotide advanced glycation endproducts in tissue damage. 1759 Sep 98

Helicobacter pylori infection might be associated with vascular diseases, such as primary Raynaud phenomenon and coronary heart diseases. The possible mechanism might be due to H. pylori antigens causing intermittent vasospasm of arterioles, which also played roles in the development of liver cirrhosis. Migraine, a functional vascular disease, was observed in many patients with cirrhosis in the clinic. This study aimed to assess the effects of H. pylori eradication on migraine symptoms in patients with hepatitis-B-virus-related cirrhosis. The results clearly showed that the intensity, duration, and frequency of attacks of migraine were significantly reduced in all the patients in whom H. pylori has been eradicated. Thus, the study pushed further insight into the mechanisms of migraine pathogenesis.
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PMID:Reversal of migraine symptoms by Helicobacter pylori eradication therapy in patients with hepatitis-B-related liver cirrhosis. 1766 2

A complex balance exists between endogenous procoagulants and the anticoagulant system in liver disease patients. Hypercoagulable events occur in cirrhosis patients despite the well-known bleeding diathesis of liver disease. These events may be clinically evident, such as in portal vein thrombosis or pulmonary embolism, but these conditions may also be a silent contributor to certain disease states, such as portopulmonary hypertension or parenchymal extinction with liver atrophy as well as thrombosis of extracorporeal circuits in dialysis or liver assist devices. Moreover, liver disease-related hypercoagulability may contribute to vascular disease in the increasingly common condition of non-alcoholic fatty liver disease. Despite the incidence of these problems, there are few widely accessible and practical laboratory tests to evaluate the risk of a hypercoagulable event in cirrhosis patients. Furthermore, there is little research on the use of commonly accepted anticoagulants in patients with liver disease. This article is a result of an international symposium on coagulation disorders in liver disease and addresses several areas of specific interest in hypercoagulation in liver disease. Critical areas lacking clinical information are highlighted and future areas of research interest are defined with an aim to foster clinical research in this field.
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PMID:Hypercoagulation and thrombophilia in liver disease. 1789 32

Patients with chronic liver disease (CLD) often develops glucose intolerance. We explored the prevalence of diabetes mellitus in viral CLD, and analyzed factors profoundly affecting the diabetic angiopathies. 229 CLD patients (124 chronic hepatitis and 105 liver cirrhosis) entered the study. The diagnosis of diabetes was made with the criteria by World Health Organization. Laboratory investigation included serum asparate aminotransferase, alanine aminotransferase, albumin, fasting blood sugar, hemoglobin A1c (HbA1c), fasting immunoreactive insulin, and HOMA-R (FBS*IRI/405). The incidence of macro- and microangiopathy were also examined. Forty (17.5%) CLD patients were diagnosed diabetes, giving a significantly higher incidence than that of general cohort (5.3%) (p<0.001). Among them, 12 (30%) had the triopathy, significantly lower than that in a matched group of diabetic patients without CLD (65%) (p<0.001). Significantly increased levels of HbA1c and HOMA-R were observed in diabetic CLD with angiopathy compared with diabetic CLD without. Incidence of diabetes was increased in viral CLD patients. The rate of diabetic angiopathies in CLD, however, was relatively low, this could be explained by low coagulability in these patients. Poor control of hyperglycemia, partly due to insulin resistance, might explain the onset of angiopathy in diabetic CLD.
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PMID:Prevalence of diabetes and incidence of angiopathy in patients with chronic viral liver disease. 1818 13

This paper summarizes several important studies published during the previous year that have an impact on the practice of inpatient internal medicine, because they either modify or reinforce current practices. The selected domains include the treatment of thrombo-embolic disease, the role of implantable defibrillators in left cardiac failure, the management of cerebro-vascular disease, of community-acquired pneumonia, and of type 2 diabetes, as well as the prevention of spontaneous bacterial peritonitis in cirrhosis and of osteoporosis fractures. Some data stimulating our reflection on the integration of medical education in health care centres and on the validity of some scientific publications are also presented.
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PMID:[Update in hospital internal medicine (2007): a selection]. 1838 36


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