Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The identification of the Hepatitis C virus using molecular cloning techniques, besides making the term Non-A Non-B Hepatitis obsolete, enables the development of specific assays for the detection of antibodies in HCV-infected individuals, thus making it possible to obtain sero-epidemiological data of the disease. The carriage of Hepatitis C antibody varies worldwide. The disease is most prevalent in intravenous drug abusers or haemophiliacs. Parenteral transmission is the most important route of transmission. Sexual, intra-familial and perinatal transmissions are uncommon. About 40% could be community-acquired (sporadic). Diagnostic tests include enzyme-linked immunosorbant (ELISA) anti-HCV assay, recombinant immunoblot assay, HCV-RNA by polymerase chain reaction and HCV-Ag. More than 50% of acute cases becomes chronic and runs a benign and indolent course. About 20% progress to cirrhosis and some of these develop hepatocellular carcinoma. Several published trials have consistently shown that treatment with interferon in some patients is useful. There is however a relapse rate of 50%. Further trials with interferon and other anti-viral agents like ribavirin are awaited for more effective treatment.
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PMID:Hepatitis C: an update. 128 40

Parenteral S-adenosylmethionine proved to be effective in reversing intrahepatic cholestasis in pregnant women. Based on these findings, a prospective multicenter, double-blind, placebo-controlled trial was planned to assess whether oral S-adenosylmethionine is effective in cholestatic patients with chronic liver disease. Accordingly, 220 inpatients (26% chronic active hepatitis, 68% cirrhosis, 6% primary biliary cirrhosis) with stable (1 month or more) at least twofold increases in serum total and conjugated bilirubin and alkaline phosphatase volunteered for the trial. Serum markers of cholestasis significantly (P less than 0.01) decreased after oral S-adenosylmethionine administration (1600 mg/day), and their values were significantly (P less than 0.01) lower than the corresponding values in the placebo group. S-adenosylmethionine significantly (P less than 0.01) improved subjective symptoms such as pruritus, fatigue, and feeling of being unwell, whereas placebo was ineffective. Two patients in the S-adenosylmethionine group and 9 controls (P less than 0.05) withdrew from the trial for reduced compliance because of inefficacy of treatment. Oral S-adenosylmethionine was tolerated to the same extent as placebo. In conclusion, short-term administration of oral S-adenosylmethionine is more effective than placebo in improving clinical and laboratory measures of intrahepatic cholestasis and offers a new therapeutic modality for the symptomatic management of this syndrome.
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PMID:Oral S-adenosylmethionine in the symptomatic treatment of intrahepatic cholestasis. A double-blind, placebo-controlled study. 218 71

We studied a consecutive series of 204 patients who were admitted to a hospital for addictive diseases during 40 months and who had a liver biopsy. Parenteral drug abusers (n = 34) were significantly younger than alcohol abusers (n = 23) or abusers of both (n = 147) and had lower levels of serum alkaline phosphatase, total bilirubin, and aspartate aminotransferase than the other two groups. Chronic active hepatitis and chronic persistent hepatitis were more frequent (p less than 0.001) in abusers of parenteral drugs alone, whereas cirrhosis was found most often (p less than 0.001) in abusers of both alcohol and parenteral drugs. Cirrhosis was present in 10 of 39 (26%) simultaneous abusers of alcohol and parenteral drugs compared with 58 of 96 (60%) alcohol-abusing former parenteral drug abusers (p less than 0.001). Methadone maintenance treatment was not associated with cirrhosis. Thus, methadone-maintained patients who abuse alcohol and develop cirrhosis should remain in methadone maintenance treatment and receive concomitant alcoholism treatment. Also, these data further support the hypothesis that abusers of both alcohol and parenteral drugs have an increased risk of developing cirrhosis.
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PMID:Chronic liver disease in abusers of alcohol and parenteral drugs: a report of 204 consecutive biopsy-proven cases. 354 73

Parenteral administration of parathyroid hormone causes dilatation of the main hepatic artery adn the intrahepatic branches, as demonstrable on coeliacography. This applies to healthy persons as well as to patients suffering from cirrhosis of the liver. When hormone is given intraarterially, i.e. into the coeliac trunk, the effect on the hepatic arteries is stronger than after intravenous administration. No effect can be be shown on the splenic, upper mesenteric or gastroduodenal arteries. The reaction of the hepatic arteries to parathyroid hormone seems to be a good parameter of the degree of dilatory capacity of these vessels in cirrhosis. Relevant conclusions can probably be drawn as to the prognosis of porto-systemic shunt operations and their indication. This haemodynamic hormone effect, the cause of which is still unknown enabled better visualisation of primary liver tumours on coeliacography.
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PMID:[Angiographic investigation with parathyroid hormone administration as functional gauge of liver blood flow (author's transl)]. 626 67

The pathophysiology, etiology, and metabolic alterations of severe hepatic failure and nutritional support of patients with this condition are reviewed. Hepatic failure encompasses a broad range of acute and chronic processes; complications may be fatal or quite minimal. Cirrhosis refers to all types of chronic diffuse liver disease. While hepatocytes regenerate in cirrhotic patients, eventually the parenchymal and vascular architecture of the liver is disrupted, leading to a syndrome of hepatic insufficiency. Normal metabolic processes deteriorate, and serum amino acid imbalances and fat intolerance may develop. Aromatic amino acids, which are normally catabolized by the liver, accumulate in the serum, and branched-chain amino acid deficiencies develop as these amino acids are broken down for energy by peripheral muscle. Hepatic encephalopathy often develops in these patients. Successful nutritional support of the patient with severe hepatic failure depends on correction of the specific metabolic abnormalities occurring. Parenteral nutrition with Hepatamine (American McGaw), a product with more branched-chain amino acids and less aromatic amino acids than other amino acid solutions, is useful in patients with altered serum amino acid profiles who develop hepatic encephalopathy. Patients in whom factors other than altered amino acids are primary causes of encephalopathy may not respond to Hepatamine. Enteral nutritional products with amino acid compositions similar to Hepatamine [Hepatic-Aid II (McGaw), Travasorb-Hepatic (Travenol Laboratories)] may be used in patients with encephalopathy, but they must be supplemented to provide complete nutrition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nutritional support of patients with severe hepatic failure. 642 97

1. The role of the liver in synthesis and metabolism of proteins, in the metabolism of certain aminoacids, and in urea synthesis is described. 2. In the liver disease protein synthesis may be reduced. The activity of lysosomal proteases is enhanced during acute hepatitis and in cirrhosis. Diseases of the liver may be associated with various derangements in the metabolic pathways of particular aminoacids. Synthesis of urea is decreased in chronic liver disease. 3. Nutrition for patients with chronic liver disease needs to include sufficient calories and has to be well balanced. Parenteral nutrition and diet in patients with edema and ascites deserves special attention. Dietary treatment of patients with cirrhosis of the liver and impending or already existing hepatic encephalopathy is outlined.
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PMID:[Therapy of aminoacid and protein metabolism disturbances in liver disease (author's transl)]. 678 46

Formerly the diagnosis of acute and chronic non-A, non-B hepatitis was made by the exclusion of other causes. However, in 1989 cloning of an antigenic component of the hepatitis C virus (HCV) was reported. This led to first- and second-generation tests for antibody to HCV (anti-HCV) in serum. HCV has been associated with acute and chronic posttransfusion and sporadic non-A, non-B hepatitis, and with hepatocellular carcinoma. Viral HCV RNA can be estimated with the polymerase chain reaction test, but this technically difficult test is not generally available. The entire viral genome has been sequenced. The envelope region shows considerable variation, and mutant HCV infections are being described already. There are geographic variations in the prevalence of anti-HCV, but usually about 0.5% to 1% of healthy blood donors test positive. Parenteral exposure to blood, especially by transfusion or drug abuse, remains a certain means of acquiring HCV infection. The method by which millions without parenteral risk factors acquire HCV remains uncertain. Vertical transmission and sexual and family spread occur only rarely. Body secretions are free of the virus. The mode of transmission may become clarified when tests for viral HCV as opposed to anti-HCV become generally available. Acute HCV infection usually is mild, and the chronic disease is also indolent. Carriers of hepatitis B virus or alcoholics who also test positive for HCV have more serious disease. Chronic HCV infection must be distinguished from autoimmune chronic active hepatitis. The most important difference is the response to corticosteroid therapy, which is good in autoimmune hepatitis and poor in HCV-related disease. Hepatocellular carcinoma can complicate HCV-related cirrhosis, usually about 20 years after infection with HCV. Recombinant interferon-alpha is used to treat chronic HCV disease, but selection of patients, dose, and duration of therapy are uncertain. In general, 50% of patients respond to the treatment, but 50% of these will have a relapse, with an overall response rate of 25%. Liver transplantation in patients with end-stage HCV disease usually is followed by infection of the graft.
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PMID:Chronic hepatitis C. 751 76

We measured glutathione and cysteine concentrations in erythrocytes of chronic alcohol misusers with (20 subjects) and without liver cirrhosis (20 subjects). Glutathione levels were decreased, whereas those of cysteine were increased in all patients. Parenteral treatment with S-adenosylmethionine (SAME); (2 g daily in 250 ml 0.15 M NaCl for 15 days) corrected the erythrocyte thiol alterations. We conclude that parenteral treatment with SAME affects the metabolism of SH compounds in erythrocytes of alcoholic patients.
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PMID:Effect of S-adenosyl-L-methionine administration on red blood cell cysteine and glutathione levels in alcoholic patients with and without liver disease. 781 44

Parenteral nutrition associated cholestasis in preterm infants and newborn children is a frequent and serious disease with an incidence of 23% depended on duration of parenteral nutrition and birthweight. The incidence of liver cirrhosis is 40% when parenteral nutrition is given 74-242 days. The pathogenesis remains unclear. Several predisposing factors are discussed like immaturity, lack of hormonal stimulation by oral feeding, bacterial infection, liver toxicity of aminoacids and their products of photooxidation, lack of taurine, lack of antioxidation substances, hypermanganesaemia and pollution of infusion solutions. Furthermore sepsis during parenteral nutrition seems to multiply the risk of cholestasis. For prevention controlled studies recommend: 1. Early enteral nutrition. 2. The reduction of parenteral amino acids to less than 3 g/kg/d. 3. Light protection for parenteral solutions. 4. Cyclic infusion of parenteral nutrition. 5. The application of antibiotics (metronidazole, gentamicin) during parenteral nutrition. The most important therapeutic intervention is the beginning of oral feeding. Most of the time this leads to a decrease of icterus within two weeks. An icterus persisting longer than 3 weeks should be treated because of the risk of liver cirrhosis. Further therapeutic interventions are: 1. Cholecystokinin, good results in case studies which still has to be verified by a controlled study. 2. Ursodeoxycholic acid, its choleretic effectiveness is verified in several liver diseases by controlled studies, but it is not proven in parenteral nutrition associated cholestasis. 3. Laparoscopic biliary irrigation, successful in several case studies.
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PMID:[Parenteral nutrition associated cholestasis in the newborn]. 987 92

Evaluation of nutritional status is a major problem in patients with liver cirrhosis this is due to water retention and the effect of liver function on protein synthesis. Despite problems evaluating the patient, malnutrition has been found to be a common complication in liver cirrhosis and is associated with poorer outcome. Nutritional restrictions, like protein restriction, are no longer recommended in most patients with liver cirrhosis but are considered harmful. An intake of 1 to 1.5 g/kg protein and 25 to 40 kcal/kg body weight a day is recommended (depending on the situation of the patient). If adequate intake cannot be achieved by oral nutrition, stepwise nutritional support with the introduction of an additional late evening meal, sip feeding or tube feeding is recommended. Parenteral nutrition should be used as a second line treatment for acutely ill patients. Data indicate that improvement of nutritional status prior to liver transplantation might reduce complications.
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PMID:Liver cirrhosis: rationale and modalities for nutritional support--the European Society of Parenteral and Enteral Nutrition consensus and beyond. 1045 18


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