Liver disease cirrhosis

Cholestatic liver disease/cirrhosis (e.g., primary biliary cirrhosis)... 

Liver disease is now recognised as a major complication of type 2 diabetes. Diabetes mellitus can lead to metabolic changes that alter normal hepatic and biliary function and structure. Type 2 diabetes is associated with an increased risk of a range of hepatobiliary diseases, including non-alcoholic fatty liver disease, cirrhosis, acute liver failure, hepatocellular carcinoma and cholelithiasis [22]. 

Hepatic cirrhosis is typically the end stage of liver disease. Cirrhosis describes an irreversible change (Treinen-Moslen, 2001) characterized by accumulation of excessive collagen deposition in the form of bridging fibrosis which disrupts the hepatic architecture. Cirrhosis may be micronodular or macronodular depending on the amount of fibrosis and tissue regeneration. Liver transplantation is the only solution to restore adequate liver fimction in human medicine. 

In liver disease (cirrhosis and cholestasis), the plasma clearance of vecuronium is reduced, its half-life is increased, and its duration of action is prolonged (SEDA-10, 112) (38,39). Rapid uptake in the liver appears to be an important factor in its plasma clearance and in determining its relatively short duration of action it is estimated that about 40% of the injected drug is excreted via the bile (40). Prolongation of the action of large single doses and accumulation after repeated doses are therefore to be expected in liver disease. 

A. Friedman SL. Alcohohc liver disease, cirrhosis, and its major sequelae. In Goldman L, Bennett JC eds. Cecil textbook of medicine. 2T ed. Philadelphia W B Saunders, 2000 804 12. 

Kidney dysfunction can lead to edema formation as a result of decreased formation of urine and the subsequent imbalance of water and electrolyte (e.g., sodium ion) homeostasis. Retention of salt and water results in an expansion of the extracellular fluid volume and, thus, edema formation. Thus, when salt intake exceeds salt excretion, edema can form. Edema formation also is associated with deceased protein levels in blood, as seen in nephrotic syndrome and liver disease. Cirrhosis of the liver leads to increased lymph in the space of Disse. Eventually, the increased lymph volume results in movement of fluid into the peritoneal cavity and ascites develops. 

Persons aged 2 to 64 years who are at increased risk for pneumococcal disease or its complications if they become infected should be vaccinated. Persons at increased risk for severe disease include those with chronic illness such as chronic cardiovascular disease (e.g., congestive heart failure [CHF] or cardiomyopathies), chronic pulmonary disease (e.g., chronic obstructive pulmonary disease [COPD] or emphysema, and asthma that occurs with chronic bronchitis, emphysema, or long-term use of systemic corticosteroids), diabetes melli-tus, alcoholism, chronic liver disease (cirrhosis) (36-39), or cerebrospinal fluid leaks. 

Hepatic cirrhosis is typically the end stage of liver disease. Cirrhosis describes an irreversible change (Treinen-Moslen, 2001) characterized by accumulation of excessive... 

Heart attack or liver disease (cirrhosis, hepatitis) Lactate dehydrogenase (LDH) Aspartate transaminase (AST)... 

Worldwide, 15 million HBsAg carriers are also infected with hepatitis D/delta virus (HDV) (Gaeta et al. 2000). This situation represents a major therapentic challenge, as most of these patients have advanced liver disease, inclnding cirrhosis in 60-70% of cases, and hepatocellular carcinoma (Fattovich et al. 2000 Saracco et al. 1987). No specific HDV inhibitors have been developed, and IFN-a-based treatment is more difficnlt in HBV-HDV infection than in HBV monoinfection. HDV RNA levels in sernm can be nsed to monitor treatment efficacy. The endpoint of therapy is HDV RNA clearance and ALT normalization, and this is sometimes achieved after the end of treatment. A snstained response can lead to HBsAg clearance from serum. 

There is very little evidence relating to the role of ROMs in cholestatic liver disease. Serum selenium and glutathione peroxidase activity are decreased in humans with intrahepatic cholestasis of pregnancy (Kauppila et al., 1987). Low levels of vitamin E have been reported in patients with primary biliary cirrhosis, and in children with Alagille s syndrome or biliary atresia (Knight et al., 1986 Jeffrey etal., 1987 Lemonnier etal., 1987 Babin etal., 1988 Kaplan et al., 1988 Sokol etal., 1989). Serum levels of Mn-SOD are increased in patients with all stages of primary biliary cirrhosis compared with patients with other forms of chronic liver disease, although whether this causes or results from the disease process is unclear (Ono etal., 1991). 

Jeffrey, G.P., Muller, D.P.R., Burroughs, A.K., Matthews, S., Kemp, C., Epstein, O., Metcalfe, T.A., Southam, E., Tazir-Melbourcy, M., Thomas, P.K. and McIntyre, N. (1987). Vitamin E deficiency and its clinical significance in adults with primary biliary cirrhosis and other forms of chronic liver disease. J. Hepatol. 4, 307-317. 

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. 

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... 

Cirrhosis is the result of long-term insult to the liver, so damage is typically not evident clinically until the fourth decade of life. Chronic liver disease and cirrhosis combined were the 12th leading cause of death in the United States in 2002. In patients between the ages of 25 and 64, damage from excessive alcohol use accounted for over one-half of the deaths.2 Alcoholic liver disease and viral hepatitis are the most common causes of cirrhosis in the United States and worldwide. 

Ascites is the accumulation of fluid in the peritoneal space and is often one of the first signs of decompensated liver disease. Ascites is the most common complication of cirrhosis and portends a dire prognosis.14... 

Progression of alcoholic liver disease moves through several distinct phases from development of fatty liver to the development of alcoholic hepatitis and cirrhosis. Fatty liver and alcoholic hepatitis may be reversible with cessation of alcohol intake, but cirrhosis itself is irreversible. Although the scarring of cirrhosis is permanent, maintaining abstinence from alcohol can still decrease complications and slow development to end-stage liver disease.22 Continuing to imbibe speeds the advancement of liver dysfunction and its complications. 

Non-alcoholic fatty liver disease begins with asymptomatic fatty liver but may progress to cirrhosis. This is a disease of exclusion elimination of any possible viral, genetic, or environmental causes must be made prior to making this diagnosis. Non-alcoholic fatty liver disease is related to numerous metabolic abnormalities. Risk factors include diabetes mellitus, dyslipidemia, obesity, and other conditions associated with increased hepatic fat.26... 

Lifestyle modifications can limit disease complications and slow further liver damage. Avoidance of additional hepatic insult is critical for successful cirrhosis treatment. The only proven treatment for alcoholic liver disease is the immediate cessation of alcohol consumption. Patients who have cirrhosis from etiologies other than alcoholic liver disease should also abstain from alcohol consumption to prevent further liver damage. 

Runyon BA. American Association for the Study of Liver Diseases (AASLD) Practice Guideline Management of adult patients with ascites due to cirrhosis. Hepatology 2004 39 841-856. 

O Prevention and treatment of viral hepatitis may prevent progression to chronic hepatitis, cirrhosis, and end-stage liver disease. 

Chronic hepatitis (disease lasting longer than 6 months) is usually associated with hepatitis B, C, and D. Chronic viral hepatitis may lead to the development of cirrhosis, which may induce end-stage liver disease (ESLD). Complications of ESLD include ascites, edema, jaundice, hepatic encephalopathy, infections, and bleeding esophageal varices. Therefore, prevention and treatment of viral hepatitis may prevent ESLD. 

The incidence of liver complications associated with PN ranges from approximately 7% to 84%, and end-stage liver disease develops in as many as 15% to 40% of adult patients on long-term PN.35 Patients often develop a mild increase in liver enzymes within 1 to 2 weeks of initiating PN, but this generally resolves when PN is discontinued. Severe liver complications include hepatic steatosis (fat deposition in liver), steatohepatitis (a severe form of liver disease characterized by hepatic inflammation that may progress rapidly to liver fibrosis and cirrhosis), cholestasis, and cholelithiasis.35... 

Steatohepatitis A severe form of liver disease caused by fat deposition in the liver, characterized by hepatic inflammation that may rapidly progress to liver fibrosis and cirrhosis. 

Generally, a CA 15-3 cutoff of 25 U/ml is used to detect stage I breast cancer. In higher stages, the sensitivity is reported to be much better, which makes it a good test of tumor burden. CA 15-3 is reported to be elevated in other disease conditions such as liver disease (particularly chronic hepatitis, cirrhosis, and carcinoma), some inflammatory conditions (sarcoidosis, tuberculosis, systemic erythematosus), and other carcinoma (lung and ovary). For this reason, positive CA 15-3 results should be interpreted with caution (20,21). 

Cirrhosis A liver disease commonly associated with chronic alcohol misuse and characterised by the replacement of once-healthy hepatocytes with abnormal connective tissue. 

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