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Compensated cirrhosis

Fattovich G, Giustina G, Christensen E, Pantalena M, Zagni I, Realdi G, Schalm SW (2000) Influence of hepatitis delta virus infection on morbidity and mortahty in compensated cirrhosis type B. Gut 46 420 26... [Pg.233]

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... [Pg.247]

Chronic HCV- In combination with peginterferon alfa-2a for the treatment of adults with chronic HCV infection who have compensated liver disease and have not been previously treated with interferon alpha. Patients in whom efficacy was demonstrated included patients with compensated liver disease and histological evidence of cirrhosis (Child-Pugh class A). [Pg.1772]

However, in a double-blind study in 100 patients with compensated non-alcoholic liver cirrhosis and type 2 diabetes, acarbose for 28 weeks did not alter liver function (64). The number of hypoglycemic episodes was reduced. [Pg.363]

In compensated cirrhosis, sodium retention can occur in the absence of vasodilatation and effective hypovolaemia. Sinusoidal portal hypertension can reduce renal blood flow even in the absence of haemodynamic changes in the systemic circulation, suggesting the existence of a hepatorenal reflex. Portal hypertension increases the hydrostatic pressure within the hepatic sinusoids and favours transudation of fluid into the peritoneal cavity. [Pg.351]

Sansoe G, Ferrari A, Castellana CN, Bonardi L, Villa E, Manenti F. Cimetidine administration and tubular creatinine secretion in patients with compensated cirrhosis. Clin Sci (Lond) 2002 102(l) 91-8. [Pg.166]

Transaminases Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Liver, heart, skeletal muscle 0 0 lU/L 0 0 lU/L Raised levels indicate hepatocyte damage/necrosis ALT is more liver specific but has a longer half-life, so less sensitive May be normal in compensated liver cirrhosis... [Pg.82]

A single-dose pharmacokinetic study was performed using tenoxicam 20 mg in six patients with compensated cirrhosis. Compared to healthy subjects, no differences in pharmacokinetics were seen [43]. [Pg.187]

Overall, clinical trials have shown that the metabolism of single doses of morphine is significantly impaired in patients with decompensated cirrhosis, bnt possibly not in those with compensated cirrhosis. [Pg.196]

The half-life has been shown to be prolonged in some single-dose studies, but no accumulation or hepatotoxicity has been shown after repeated dosing, therefore normal doses and frequency can be used. Further advice as for Patient 3 with compensated cirrhosis. [Pg.204]

Compensated cirrhosis - category 3 risks outweigh the advantages. [Pg.285]

La Villa, G., Salmeron, J.M., Arroyo, V., Bosch, X, Gines, R, Garda-Pagan, XC., Gines, A., Asbert, M., Jimenez, W., Rivera, F., Rodes, J. Mineralocorticoid escape in patients with compensated cirrhosis and portal hypertension. Gastroenterology 1992 102 2114-2119... [Pg.317]

Latent and compensated forms of consumptive coagulopathy frequently occur in the course of severe acute or chronic liver disease. In 80-85% of cirrhosis patients, the values of at least one basic test (thrombocytes. Quick s value, fibrinogen, AT III, bleeding time) are pathological. In 15-30% of cases, clinically relevant haemorrhagic diathesis evolves. [Pg.345]

Depending on the time period involved in the course of the disease, acute liver failure without pre-existing liver disease can initially be differentiated by massive liver cell disintegration due to a variety of causes. In contrast, chronic liver insufficiency with pre-existing liver disease is mostly found in advanced liver cirrhosis with a progressive loss of function. A sudden necrotising episode is also able to precipitate the change from chronic and still compensated liver insufficiency into acute liver failure ( acute on chronic ) in the same way that acute liver failure which has been overcome can develop into chronic liver insufficiency. [Pg.376]

V., Carrasco, D., San-Juan, F., Bnrgneno, M.D.J., Mir, J., Berenguer, J. Natural history of clinically compensated hepatitis C virus-related graft cirrhosis after liver transplantation. Hepatology 2000 32 852-858... [Pg.710]

Apart from histological activity (= progressive) or inactivity (= stationary), biochemical activity must also be defined. The latter is determined by (i.) enzymatic activity, (2.) mesenchymal activity, and (3.) immunological activity, (s. p. 121) Compensated cirrhosis may be either active or inactive. Even decompensated cirrhosis can sometimes be kept in an inactive (stationary) stage for a limited period of time. Jaundice (>3 mg/dl) is a typical sign of decompensation. [Pg.722]

Complications Generally, complications can occur during the stages of compensation and decompensation. Some complications predominantly arise from a decompensated situation, whereas others do not necessarily occur at all in the natural course of cirrhosis. However, in view of the cirrhosis-induced lability of the metabolic functions, they may easily be provoked by the patient s inappropriate behaviour or by iatrogenic measures. Viruses, such as CMV or influenza A (50), may cause deterioration of the liver function or decompensation. (59, 157) (s. tab. 35.3)... [Pg.723]


See other pages where Compensated cirrhosis is mentioned: [Pg.150]    [Pg.161]    [Pg.163]    [Pg.167]    [Pg.306]    [Pg.882]    [Pg.150]    [Pg.161]    [Pg.163]    [Pg.167]    [Pg.306]    [Pg.882]    [Pg.233]    [Pg.292]    [Pg.344]    [Pg.190]    [Pg.190]    [Pg.250]    [Pg.36]    [Pg.53]    [Pg.89]    [Pg.158]    [Pg.164]    [Pg.200]    [Pg.202]    [Pg.220]    [Pg.250]    [Pg.271]    [Pg.287]    [Pg.290]    [Pg.299]    [Pg.300]    [Pg.279]    [Pg.331]    [Pg.78]    [Pg.108]    [Pg.364]    [Pg.537]    [Pg.709]   


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