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Liver disease chronic hepatitis

Swertia pseudochinensis Dang Yao (whole plant) Swertiamarin, swertisin, methyl-bellidifolin, homoorentin, methyl-swertianin, isovitexin, bellidifolin, decussatin, swertifrancheside.33 Choleretic, improve hepatic function. Treat acute icteric hepatitis, chronic liver disease. [Pg.158]

Chronic obstructive pulmonary disease (COPD) Occupational lung diseases Gastroenteritis Worm infestation Dyspepsia / ulcer Enteric fever Acute viral hepatitis Chronic liver diseases Skin infections Scabies Eczemas... [Pg.390]

Hepatocellular carcinoma (HCC) develops in patients with chronic liver diseases associated with hepatitis B and hepatitis C vims infections with high incidences. Here, an acyclic retinoid has been shown to suppress the posttherapeutic recurrence after interferon-y or glycerrhicin treatment in cirrhotic patients who underwent curative treatment of preceding tumors. The retinoid induced the disappearance of serum lectin-reactive a-fetoprotein (AFP-L3), a tumor marker indicating the presence of unrecognizable tumors in the remnant liver, suggesting a deletion of such minute (pre)malignant clones (clonal deletion). As a molecular mechanism of the clonal deletion, a novel mechanism of... [Pg.1076]

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. [Pg.323]

Patients with viral hepatitis B, C, and D may develop chronic disease leading to ESLD. Treatment is only available for chronic liver disease associated with HBV, HCV, and HDV.20,21... [Pg.350]

Persons who have chronic liver disease (e.g., persons with chronic liver disease caused by hepatitis B or C and... [Pg.287]

All susceptible (anti-hepatitis A virus-negative) patients at increased risk for hepatitis A infection (e.g., illegal drug users, men who have sex with men, hemophiliacs) or patients with chronic liver disease including chronic hepatitis B or C... [Pg.460]

Testa, R., Caglieris, S., Risso, D., Arzani, L., Campo, N., Alvarez, S., Giannini, E., Lantieri, P.B., and Celle, G., Monoethylglycinexylidide formation measurement as a hepatic function test to assess severity of chronic liver disease. Am.. Gastroenterol, 92, 2268-2273, 1997. [Pg.373]

No populations with unusual susceptibility to health effects of 1,2-diphenylhydrazine have been identified. It is possible that people with chronic liver disease or possibly compromised hepatic function (e.g., very young or very old people, alcoholics) might be unusually susceptible to... [Pg.40]

Hepatitis B vaccine schedule consists of three injections given at time 0, 1 month after the first injection and a third injection given 6 months after the first injection. Patients at high risk are given a booster after 5 years to maintain the immunity profile. Patients receiving blood transfusions, haemophilia patients, patients with chronic liver disease, and haemodialysis patients are among the high-risk patients who should be vaccinated. [Pg.335]

Hepatic function impairment Use nateglinide with caution in patients with chronic liver disease. Use with caution in patients with moderate to severe liver disease because such patients have not been studied. [Pg.283]

The severity of hepatic events or their outcome may be worse in patients with active or chronic liver disease. Discontinue treatment with terbinafine if biochemical or clinical evidence of liver injury develops. [Pg.1690]

Hypersensitivity reactions Stop all drugs and evaluate at the first sign of a hypersensitivity reaction. If isoniazid must be reinstituted, give only after symptoms have cleared. Restart the drug in very small and gradually increasing doses and withdraw immediately if there is any indication of recurrent hypersensitivity reaction. Renai/Hepatic function impairmentMon ior patients with active chronic liver disease or severe renal dysfunction. [Pg.1714]

Renai/Hepatic function impairment The safety and pharmacokinetics of rimantadine in renal and hepatic insufficiency only have been evaluated after single dose administration. In a single dose study of patients with anuric renal failure, the apparent clearance was approximately 40% lower and the elimination half-life was 1.6-fold greater than that in healthy controls. In a study of 14 people with chronic liver disease (mostly stabilized cirrhotics), no alterations in the pharmacokinetics were observed after a single dose of rimantadine. However, the apparent clearance of rimantadine following a single dose to 10 patients with severe liver dysfunction was 50% lower than that reported for healthy subjects. Because of the potential for accumulation of rimantadine and its metabolites in plasma, exercise caution when patients with renal or hepatic insufficiency are treated with rimantadine. [Pg.1785]

Hepatitis C virus (HCV) is an RNA virus that is a common cause of parenterally acquired viral hepatitis chronic infection follows acute infection in 80% to 85% of cases. Although liver disease resulting from chronic HCV infection is only slowly progressive, HCV is the most common cause of chronic liver disease in the United States, the most common etiology for hepatocellular carcinoma, and the leading indication for liver transplantation [34-36]. [Pg.181]

Most drugs used in anaesthesia are metabolised in the liver by phase I reactions, mediated by cytochrome P-450 enzymes. These are susceptible to destruction by cirrhosis, so that the biotransformation of drugs, such as opioids (except morphine), benzodiazepines, barbiturates, and inhalational agents, may be markedly altered in severe liver disease. These enzymes are found in the centrilobular areas, which are more prone to hypoxia. In contrast, the enzymes responsible for phase II reactions, found predominantly in the peripheral areas, often function normally even in advanced disease. The disposition of benzodiazepines that are eliminated primarily by glucuronidation, e.g. lorazepam and oxazepam, are unaffected by chronic liver disease. For drugs with low hepatic extraction, advanced hepatocytic dysfunction decreases phase I and II biotransformation with a reduced clearance and prolongation of the elimination half-life. This is often partially offset by an increased free fraction due to decreased protein binding. [Pg.286]

Individuals with chronic liver disease may have disorders of fluid and electrolyte balance, including ascites, edema, and effusions. Alterations of whole body potassium induced by vomiting and diarrhea, as well as severe secondary aldosteronism, may contribute to muscle weakness and can be worsened by diuretic therapy. The metabolic derangements caused by metabolism of large amounts of ethanol can result in hypoglycemia, as a result of impaired hepatic gluconeogenesis, and in ketosis, caused by excessive lipolytic factors, especially increased cortisol and growth hormone. [Pg.498]

Symptomatic adverse effects of darunavir include diarrhea, nausea, headache, and rash. Laboratory abnormalities include dyslipidemia (though possibly less frequent than with other boosted PI regimens) and increases in amylase and hepatic transaminase levels. Liver toxicity, including severe hepatitis, has been reported in some patients taking darunavir the risk of hepatotoxicity may be higher for persons with HBV, HCV, or other chronic liver disease. [Pg.1081]

Portal hypertension most commonly occurs as a consequence of chronic liver disease. Portal hypertension Is caused by Increased blood flow within the portal venous system and increased resistance to portal flow within the liver. Splanchnic blood flow is increased in patients with cirrhosis due to low arteriolar resistance that is mediated by increased circulating vasodilators and decreased vascular sensitivity to vasoconstrictors. Intrahepatic vascular resistance is increased in cirrhosis due to fixed fibrosis within the spaces of Disse and hepatic veins as well as reversible vasoconstriction of hepatic sinusoids and venules. Among the consequences of portal hypertension are ascites, hepatic encephalopathy, and the development of portosystemic collaterals—especially gastric or esophageal varices. Varices can rupture, leading to massive upper gastrointestinal bleeding. [Pg.1330]

A 70-year-old woman with a 2-year history of primary biliary cirrhosis confirmed by histological and immunological criteria took colestyramine sachets twice daily for 2 months and developed lethargy, confusion, and drowsiness (3). She had signs of chronic liver disease, portal hypertension, and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis, and a urinary pH of 4.85 together with tests of renal acidification excluded renal tubular acidosis. No other cause was found and she responded to 600 mmol of sodium bicarbonate intravenously over 36 hours. [Pg.556]

Milk thistle has been used to treat acute and chronic viral hepatitis, alcoholic liver disease, and toxin-induced liver injury in human patients. Milk thistle has most often been studied in the treatment of alcoholic hepatitis and cirrhosis. In both of these disorders, outcomes have been mixed and reports include significant reductions in markers of liver dysfunction and in mortality, as well as no effect. In acute viral hepatitis, studies have generally involved small sample sizes and have shown mixed outcomes of improved liver function (eg, aminotransferase values, bilirubin, prothrombin time) or no effect. Studies in chronic viral hepatitis and toxin-induced injury have also been of small size but have reported mostly favorable results. Parenteral silybin is marketed and used in Europe as an antidote in Amanitaphalloides mushroom poisoning, based on favorable outcomes reported in case-control studies. [Pg.1543]

Adverse effects Adverse effects are a minor problem with rifampin, but can include nausea and vomiting, rash, and fever. The drug should be used judiciously in patients with hepatic failure because of the jaundice that occurs in patients with chronic liver disease, alcoholics, or in the elderly. [Pg.345]


See other pages where Liver disease chronic hepatitis is mentioned: [Pg.61]    [Pg.574]    [Pg.1243]    [Pg.597]    [Pg.536]    [Pg.221]    [Pg.46]    [Pg.95]    [Pg.1712]    [Pg.1360]    [Pg.165]    [Pg.34]    [Pg.99]    [Pg.27]    [Pg.213]    [Pg.194]    [Pg.195]    [Pg.201]    [Pg.204]    [Pg.274]    [Pg.250]    [Pg.302]    [Pg.525]    [Pg.604]   
See also in sourсe #XX -- [ Pg.53 ]




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