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Enzyme induction renal disease

Other- Liver disease with impaired hemostasis severe renal disease. Hyperlipidemia Heparin may increase free fatty acid serum levels by induction of lipoprotein lipase. The catabolism of serum lipoproteins by this enzyme produces lipid fragments that are rapidly processed by the liver. Patients with dysbetalipoproteinemia (type III) are unable to catabolize the lipid fragments, resulting in hyperlipidemia. [Pg.132]

Absorption of the synthetic steroids given orally is rapid. The tY in plasma of most is 1-3 h but the maximum biological effect occurs after 2-8 h. Administration is usually 2 or 3 times a day. They are metabolised principally in the liver (some undergoing hepatic first-pass metabolism, see above) and some are excreted unchanged by the kidney. The t/ is prolonged in hepatic and renal disease and is shortened by enzyme induction to an extent that can be clinically important. [Pg.667]

Except for the less lipid-soluble aprobarbital and phenobarbital, nearly complete metabolism and/or conjugation of barbiturates in the liver precedes their renal excretion. The metabolic elimination of barbiturates is more rapid in young people than in the elderly and infants, and half-lives are increased during pregnancy partly because of the expanded volume of distribution. Chronic liver disease, especially cirrhosis, often increases the tj of the biotransformable barbiturates. Repeated administration, especially of phenobarbital, shortens the tj of barbiturates that are metabolized as a result of the induction of microsomal enzymes (see above). [Pg.273]


See other pages where Enzyme induction renal disease is mentioned: [Pg.248]    [Pg.356]    [Pg.514]    [Pg.672]    [Pg.672]    [Pg.191]    [Pg.267]    [Pg.78]    [Pg.223]   
See also in sourсe #XX -- [ Pg.123 ]




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