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

Cirrhosis is known to be associated with numerous cardiovascular abnormalities. These include increased cardiac output and decreased arterial pressure and total peripheral resistance. Despite this increased baseline cardiac output, patients with cirrhosis show an attenuated systolic and diastolic function in the face of pharmacological, physiological and surgical stresses, as well as cardiac electrical abnormalities such as QT prolongation. These abnormalities have been termed cirrhotic cardiomyopathy. The pathogenic mechanisms that underlie this syndrome include impairment of the beta-adrenergic receptor signalling, cardiomyocyte plasma membrane function, intracellular calcium kinetics, and humoral factors such as endogenous cannabinoids, nitric oxide and carbon monoxide. Cirrhotic cardiomyopathy is believed to contribute to the cardiac dysfunction that can be observed in patients with transjugular intrahepatic portosystemic stent-shunt insertion and liver transplantation. Insufficient cardiac contractile function may also play a role in the pathogenesis of hepatorenal syndrome precipitated by spontaneous bacterial peritonitis. In this review, the clinical features, pathogenic mechanisms, clinical consequences and management options for cirrhotic cardiomyopathy are discussed.
Best Pract Res Clin Gastroenterol 2007
PMID:Cardiac dysfunction in cirrhosis. 1722 1

The development of hepatocellular carcinoma (HCC), the mechanisms of hepatocarcinogenesis, the prevention of HCC, and screening for HCC will be discussed. Cirrhosis has been considered as a pre-neoplastic condition for the development of HCC. The worldwide incidence of HCC differs according to different hepatitis viruses, and information is lacking. Hepatocarcinogenesis is a multistep process involving a number of different genetic alterations and is poorly understood. Interferon should help prevent the development of HCC in patients with chronic hepatitis C. Screening is the only practical approach for improving the management of HCC patients, as early detection increases the application of curative treatments. However, the cost-effectiveness of various screening strategies needs to be analysed.
Best Pract Res Clin Gastroenterol 2007
PMID:Hepatocellular carcinoma development in cirrhosis. 1722 3

Transplantation is the only option for reversing liver insufficiency and its complications in patients with end-stage cirrhosis. Transplantation is generally considered after the first episode of decompensation of cirrhosis, provided no specific intervention can result in a longstanding return to the compensated state. Alcohol abuse and hepatitis C virus infection are the predominant causes leading to transplantation in Western countries. In cases of alcoholic cirrhosis, a 6-month period of abstinence is needed before transplantation. Patients with hepatitis C virus infection are considered independent of viral replication, even if post-transplantation recurrence is almost constant. Conversely, in cases of hepatitis B infection, only patients without viral replication (or with extremely low viral load) are suitable candidates. Hepatocellular carcinoma represents an increasing proportion of the indications and offers excellent long-term survival. However, transplantation should be limited to patients with small tumours. HIV infection no longer represents a definitive contraindication.
Best Pract Res Clin Gastroenterol 2007
PMID:Indications of liver transplantation in patients with complications of cirrhosis. 1722 4

In this study, we analyze the demographic features, clinical and histopathological findings in patients who underwent liver transplantation for progressive familial intrahepatic cholestasis. We also analyze outcome and impact of liver transplantation on growth and bone mineral content. Most of the patients were presented with jaundice mainly beginning within the first six months. At the time of initial admission; eight patients had short stature (height SD score<2), and four patients had weight SD score<2. Liver transplantation were performed at the age of 43.2+/-27 months (range 9 to 96 months), 6.5+/-3.5 months later after the first admission. Infection, surgical complications and osmotic diarrhea associated with severe metabolic acidosis were noted in 41.4%, 16.6% and 33.3%, respectively. One patient developed posttransplant lymphoproliferative disorder. Overall; 1 year graft and patient survival was 69.2% and 75%, respectively. At the end of the 1st year only 2 patients had height SD score<2. Linear regression of height gain against increase in total body BMD measured at the time of transplantation and 1 year after liver transplantation gave a coefficient r=0.588 (p=0.074). No correlation was found between the height gain and age and PELD score at time of transplantation, and no difference was noted between the sexes and donor type. Liver transplantation is effective treatment modality with good outcome and little morbidity, and increases the growth acceleration in patients with PFIC associated with cirrhosis.
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PMID:Liver transplantation for progressive familial intrahepatic cholestasis: clinical and histopathological findings, outcome and impact on growth. 1766 86

Dietary cirrhosis of the liver was produced in 223 rats, and then therapy of the condition attempted. Administration of lipotropic factors (casein, methionine, choline) was followed not only by reduction of fat infiltration and by regeneration of hepatic parenchyma but, by a reduction of the degree of the fibrosis. In one group of rats, comparison of sections obtained by biopsy, before treatment, with findings at necropsy, after completed therapy, indicated apparent reduction of the fibrosis and of the amount of ceroid and considerable restoration of architecture. This improvement, however, was obtained neither with complete regularity nor in a short time. In very severe cirrhosis, as a rule, the effect of a lipotropic diet was disappointing, even after prolonged treatment up to 200 to 240 days. It is assumed that factors determining prevention are beneficial only to a limited extent in treatment. The therapy of very severe cirrhosis may require the interaction of further beneficial factors (nutritional and hormonal). Best therapeutic results were obtained by the combination of an adequate amount of casein with methionine or liver extract, and by the combination of methionine with liver extract. Methionine and thiouracil, both of which, singly, are effective in the prevention of dietary hepatic cirrhosis in rats, have proved to be less effective for the therapy of cirrhosis, when administered together, than methionine given alone for the same purpose. Under identical conditions, female rats have shown greater resistance to the production of dietary hepatic cirrhosis and a more favorable response to therapeutic dietary factors, than male rats.
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PMID:Treatment of experimental dietary cirrhosis of the liver in rats. 1815 40

Variceal bleeding is one of the most severe complications of portal hypertension related to liver cirrhosis. Primary prophylaxis is considered mandatory in patients with cirrhosis and high-risk oesophageal varices, and once varices have bled, every effort should be made to arrest the haemorrhage and prevent further bleeding episodes. In acute variceal bleeding, vasoactive drugs that lower portal pressure should be started even before endoscopy, and should be maintained for up to 5 days. The choice of vasoactive drug should be made according to local resources. Terlipressin, somatostatin and octreotide can be used; vasopressin plus transdermal nitroglycerin may be used if no other drug is available. In variceal bleeding, antibiotic therapy is also mandatory. In primary and secondary prophylaxis, beta-blockers are the mainstay of therapy. In secondary prophylaxis (but not in primary prophylaxis) these drugs can be combined with organic nitrates.
Best Pract Res Clin Gastroenterol 2008
PMID:Acute variceal bleeding: pharmacological treatment and primary/secondary prophylaxis. 1834 84

Classification of vascular abnormalities of the gastrointestinal tract on the basis of anatomy and pathophysiology has recently been suggested. Angiodysplasia, an example of an arteriovenous lesion, may cause either acute or chronic bleeding. Diagnosis may be difficult. High-quality standard endoscopy, capsule endoscopy, and double-balloon enteroscopy are most efficacious. Therapy using argon plasma coagulation is currently preferred. Pharmacological therapy has been employed, but a final conclusion about its efficacy cannot yet be drawn. Dieulafoy lesion, an arterial type of vascular abnormality, is rare but serious. It can be responsible for severe haemorrhage. Mechanical endoscopic methods are the most efficacious. Gastric antral vascular ectasia (GAVE), a capillary lesion, can be safely biopsied; it coincides with several diseases (including liver cirrhosis), may cause chronic iron-deficiency anaemia, and is best treated by argon plasma coagulation. Haemangiomas, benign neoplastic lesions, usually occur as part of other specific syndromes; they are difficult to manage due to the multiplicity and size of the lesions.
Best Pract Res Clin Gastroenterol 2008
PMID:Vascular lesions of the gastrointestinal tract. 1834 86

This article will focus on the impact caused by chronic viral hepatitis B and C globally and will discuss public health measures that have to be implemented in order to prevent and control these diseases. Chronic viral hepatitis is a major global public health problem, an important cause of morbidity and mortality from sequelae which include chronic hepatitis, cirrhosis and primary liver cancer. Being a 'silent' disease, the contribution of chronic hepatitis to global morbidity and mortality is generally underestimated. Hepatitis B and C prevention and control should seek to reduce both the incidence of new infections and the risk of chronic liver disease. A comprehensive public health prevention programme should include the prevention and detection of HBV and HCV infections, the diagnosis and control of viral hepatitis related chronic liver disease, conducting surveillance and monitoring the effectiveness of prevention activities, and setting up a research agenda.
Best Pract Res Clin Gastroenterol 2008
PMID:Chronic viral hepatitis as a public health issue in the world. 1918 63

Chronic hepatitis B and hepatitis C virus infections are the major causes of liver disease, hepatocellular carcinoma (HCC) and liver-related mortality worldwide. Among factors known to influence the natural history of viral hepatitis are age at the time of infection, duration of infection, serum alanine aminotransferase (ALT) levels, male sex, alcohol consumption, and coinfections. In hepatitis B, serum HBV DNA concentration emerges as the key factor for predicting the development of liver disease. Even patients with low viraemia seem at increased risk for liver cirrhosis and HCC. Coinfections with hepatitis C, hepatitis D and/or HIV are common and are associated with a more severe liver disease. The course of chronic hepatitis C is variable, but usually fibrosis advances slowly. In addition to the better-known factors- including coinfections with HBV and HIV- progression of liver disease is adversely affected by smoking, hepatic steatosis and insulin resistance.
Best Pract Res Clin Gastroenterol 2008
PMID:Natural history: the importance of viral load, liver damage and HCC. 1918 67

Studies in the past decades have shown that active hepatitis B virus (HBV) replication is the key driver of liver injury and disease progression, and thus sustained viral suppression is of paramount importance in the management of chronic HBV infection. The nucleos(t)ide analogues lamivudine, adefovir, entecavir, telbivudine and tenofovir are potent inhibitors of HBV polymerase/reverse transcriptase activity and are highly effective in the suppression of HBV replication, but rarely eliminate the virus. Long-term therapy is usually required to achieve sustained hepatitis B e antigen seroconversion, HBV DNA suppression, ALT normalization and fibrosis reversal. Maintained long-term therapy has been demonstrated to significantly lower the rate of hepatic decompensation and development of cirrhosis or hepatocellular carcinoma. However, drug resistance is a serious risk on prolonged nucleos(t)ide analogue therapy, and this poses a critical challenge. Prevention and proper management of drug resistance are crucial to ensure long-term success.
Best Pract Res Clin Gastroenterol 2008
PMID:Nucleos(t)ide analogues for hepatitis B virus: strategies for long-term success. 1918 68


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