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Hepatocellular disease

Acute or chronic hepatocellular disease with abnormal liver function, cirrhosis, hepatic adenomas, or hepatic carcinomas... [Pg.344]

Transaminases The transaminases catalyze the reversible transformation of a-ketoacids into amino acids. Most frequently, the 2 transaminases GPT (= glutamic pyruvic transaminase) (or ALT = alamine transaminase) and GOT (= glutamic oxaloacetic transaminase) (or AST = aspartate transaminase) are used for enzyme diagnostics (F. DeRitis et at., 1955 F. Wroblewski et al., 1955). (s. tab. 5.4) While GOT is distributed evenly, the GPT concentration continuously decreases from periportal to pericentral in the acinus. These are considered to be the basic parameters in the diagnosis and follow-up of hepatocellular disease. If the cause of elevated transaminases remains unclear, the indication for liver biopsy is given. (28, 30, 31, 34)... [Pg.95]

Leong, A.S., Alp, M.H. Hepatocellular disease in the giant cell arteri-itis/polymyalgia rheumatica syndrome. Ann. Rheum. Dis. 1981 40 ... [Pg.823]

An infant developed hepatic veno-occlusive disease after having been fed a herbal tea known as gordolobo yerba, commonly used as a folk remedy among Mexican-Americans there was acute hepatocellular disease and portal hypertension, which progressed over 2 months to extensive hepatic fibrosis (36). [Pg.364]

In severe hepatocellular disease the prothrombin concentration can be further depressed by high doses of vitamin K (6,7). [Pg.3681]

Hepatic Disease. The liver retains the ability to synthesize even increased amounts of albumin until parenchymal damage or loss is severe, with the loss of 50% to 95% of function. Thus other mechanisms are responsible for the decreased levels seen in most cases of hepatocellular disease." These include, among others, increased immunoglobulin levels, third space loss (extravasation into the extravascular space), and direct inhibition of synthesis... [Pg.547]

Acute phase response corticosteroid or androgen effect Hemolysis hepatocellular disease (with increased red blood cell turnover) Hemolysis plus acute, phase response, corticosteroid therapy, or both Estrogen effect hepatocellular disease... [Pg.560]

Decreased Plasma Levels. Decreased levels of Hp are seen with genetic deficiency, hemolytic disease, ineffective erythropoiesis, estrogens, and hepatocellular disease and in neonates. [Pg.560]

Hepatocellutar Disease. Most forms of acute or chronic hepatocellular disease, including acute viral hepatitis and cirrhosis with jaundice, are associated with decreased levels of Hp, possibly caused in part by altered estrogen metabolism. Increased red cell breakdown secondary to erythrocyte membrane lipid alterations may also play a role, although this has never been documented with turnover studies. In contrast, biliary obstruction is also associated with significant lipid alterations but with increased Hp levels, in the absence of severe hepatocellular disease. [Pg.561]

Disturbances of Bile Acid Metabolism in Hepatocellular Disease. Fasting plasma bile acid concentrations are elevated in hepatocellular diseases, such as hepatitis and cirrhosis. The mechanisms responsible are regurgitation of bile acids from cholestatic hepatocytes and portosystemic shunting. These defects allow the plasma concentrations to rise proportionately much higher than normal following meals, suggestmg that the postprandial rise in plasma bile acids may be a sensitive test for the detection of liver disease. [Pg.1787]

The liver synthesizes fibrinogen factors V, VIII, XI, and XII, and the vitamin K-dependent factors II, VII, IX, and X. Furthermore the liver plays an important role in platelet growth and function. The vitamin K-dependent proteins contain y-carboxy-glutamic acid. Vitamin K is necessary for the carboxylation of these proteins, which facilitate the conversion of prothrombin to thrombin. Patients with severe hepatocellular disease have decreased synthesis of the vitamin K-dependent clotting factors, especially factor VII. Furthermore, patients with cholestatic disease have decreased bile salt secretion, which is necessary for the absorption of vitamin K, leading to failure of activation of factors II, VII, IX, and X. In these patients, unlike those with hepatocellular disease, the prothrombin time can be corrected with an injection of vitamin K. [Pg.1796]

Cell death occurs by necrosis or apoptosis or both. The target cell determines the pattern of injury, with hepatocyte injury leading to hepatocellular disease and bihary cell injury leading to cholestasis. AH cellular injury induces fibrosis as an adaptive or healing response, with the duration of injury and genetic factors determining whether cirrhosis and ultimately carcinoma occur (Figure 47-13). [Pg.1798]

Sensitive test of hepatocellular disease AST > ALT in alcoholic disease v... [Pg.1825]

Sensitive and more specific test of hepatocellular disease... [Pg.1825]

In practice, the plasma aminotransferases and ALP are the most useful tests as they allow differentiation of hepatocellular disease from cholestatic disease. The importance of this distinction cannot be overstated failure to recognize cholestatic disease caused by extrahepatic biliary obstruction will result in liver failure if the obstruction is not quickly corrected. It is also important to recognize that there may be a gray zone of mixed hepatocellular and cholestatic disease where the tests do not distinguish one disease from the other. In this case, it is wise to assume that the problem is cholestatic and rule out biliary obstruction. [Pg.1826]

Serial PT measurements also can be used to differentiate between cholestasis and severe hepatocellular disease. In practice, PT should be measured again after vitamin K injection, because cholestasis wiD. cause a decrease in PT because of malabsorption of vitamin K. The patient has cholestasis if the PT corrects after vitamin K replacement (10 mg sub-cutaneously or intramuscularly, followed by PT measurement 4 hours later). With time, if the PT does not return to normal, the patient has severe hepatocellular disease. [Pg.1827]

In liver disorders, serum levels of bile acids are elevated, and their measurement is a sensitive indicator of liver disease. Bile acids are not normally found in urine owing to efficient uptake by the liver and excretion into the intestines. In hepatocellular disease and obstructive jaundice, however, their urinary excretion increases. [Pg.426]

Impaired intrahepatic excretion Hepatocellular disease Intrahepatic cholestasis Congenital... [Pg.697]

Factor V is synthesized by hepatic cells, but is not dependent on vitamin K. Therefore it may be useful in distinguishing vitamin K deficiency from liver disease. Deficiency of antithrombin occurs with severe hepatocellular disease and may contribute to the development of DIG. In acute hepatic failure, the level of plasminogen may be low, reflecting decreased synthesis or increased catabolism associated with DIG. The level of factor VIII is usually normal or elevated in fiver disease, whereas it is decreased in DIG. [Pg.1852]

Severe hepatocellular disease (high bilirubin levels) will cause a shift in the excretion pattern, with the highest radiation absorbed dose delivered to the urinary bladder (Brown et al. 1982). The effective (whole body) dose equivalent is 0.024 mSv/MBq (International Commission on Radiological Protection 1987). The effective dose in adults (70 kg) resulting from 185 MBq (5 mCi) of intravenously injected Tc-IDA complex is... [Pg.321]

In the absence of significant hepatocellular disease, the prothrombin activity of the blood rapidly returns to normal. If oral administration is not feasible, a parenteral preparation of vitamin K should be used the usual dose is 10 mg/day. [Pg.965]

Eairly predictable changes occur in the various metabolic pathways of lipid metabolism in patients with moderately advanced hepatocellular disease. Which one of the following changes would you expect to see under these conditions ... [Pg.861]

Use is cautioned in persons with severe or acute hepatocellular disease, septic cholecystitis, unconjugated hyperbilirubinemia, intestinal spasms or ileus, or liver cancer (Chan 1993 Mills and Bone 2005). [Pg.130]

Type B HE associated with portal-systemic bypass with no intrinsic hepatocellular disease (in practice this type is rare)... [Pg.149]

Negative acute-phase reactant Hepatocellular disease Nephrotic syndrome Hyperthyroidism Inherited deficiency of vitamin A... [Pg.5283]

Estrogens/pregnancy Acute-phase reactant Hepatocellular disease... [Pg.5284]


See other pages where Hepatocellular disease is mentioned: [Pg.90]    [Pg.165]    [Pg.267]    [Pg.282]    [Pg.282]    [Pg.43]    [Pg.50]    [Pg.198]    [Pg.807]    [Pg.1200]    [Pg.1788]    [Pg.1826]    [Pg.1922]    [Pg.1923]    [Pg.716]    [Pg.1852]    [Pg.217]    [Pg.290]    [Pg.728]    [Pg.3941]   


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