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Enzymes hepatic

The best-known effect of APOE is the regulation of lipid metabolism (see Fig. 10.13). APOE is a constituent of TG-rich chylomicrons, VLDL particles and their remnants, and a subclass of HDL. In addition to its role in the transport of cholesterol and the metabolism of lipoprotein particles, APOE can be involved in many other physiological and pathological processes, including immunoregu-lation, nerve regeneration, activation of lipolytic enzymes (hepatic lipase, lipoprotein lipase, lecithin cholesterol acyltransferase), ligand for several cell receptors, neuronal homeostasis, and tissue repair (488,490). APOE is essential... [Pg.295]

The most frequently reported side effects are Gl-related complaints i.e. nausea, dyspepsia, abdominal pain and diarrhoea. Other side effects include headache, skin rash and transient elevation of liver enzymes, hepatic dysfunction with or without jaundice and psychosis. [Pg.333]

From either a Cp or In Cp versus time plot, one feature is immediately clear the drug concentration drops over time. This process is called elimination and is determined by clearance (CL). Clearance is the process of removal of drug from the bloodstream. As was discussed in Chapter 3, clearance occurs primarily either through filtration of a drug by the kidneys (renal clearance, CLR) or metabolism of a drug in the liver by the action of enzymes (hepatic clearance, CLH). Other clearance processes are possible, but CLR and CLh normally comprise the large majority of total clearance (CLy or simply CL) (Equation 7.6). [Pg.155]

Idiosyncratic toxicity Metabolic abnormality No No Weeks-months Any Increased liver enzymes, hepatitis, jaundice Diclofenac Ketoconazole... [Pg.62]

Oral acyclovir is a remarkably safe drug. Common side effects include nausea, vomiting, diarrhea, and abdominal pains. Additional side effects include skin rash, photosensitivity, headaches, dizziness, hallucinations, lethargy, confusion, seizures, and coma. Side effects are most frequent in patients with renal impairment. Rarer complications include anemia, leukopenia, thrombocytopenia, increases in blood urea and creatinine, acute renal failure, reversible increases in bilimbin and liver enzymes, hepatitis, and jaimdice. Cautious dosing and monitoring are recommended in elderly and immunocompromised patients and in patients with renal or liver disease. [Pg.201]

The lactic acidosis seen with these drugs has ranged from mild and chronic to acute, severe, and fatal [95-106]. The acidosis generally develops after several months of therapy. Patients with NRTl-associated lactic acidosis present with symptoms of nausea, vomiting and abdominal pain. Other features often include elevated liver enzymes, hepatic steatosis, pancreatitis and elevated creatinine kinase with evidence of a myopathy, and liver failure. The lactic acidosis may persist for many weeks despite discontinuation of the NRTl [95-106]. NRTl-related mitochondrial toxicity may also present with rhabdomyolysis and acute kidney failure [110]. Mortality related to NRTl-induced acute lactic acidosis is high, in the range of 50% to 100%, despite drug discontinuation. [Pg.389]

Liver Elevation of hepatic enzymes, hepatitis, cholestatic jaundice... [Pg.96]

Rifampin Inhibits DNA-dependent RNA polymerase (nucleic acid synthesis inhibitor) Resistance via change in enzyme Hepatitis Induction of P450 Red-orange metabolites... [Pg.193]

The choice of steady-state plasma concentrations (Cmax, Cave, and Ctrough) or the concentration in hepatic circulation (Chept inlet,max) of the inhibitor as an estimate of the concentration at the active site of the enzyme (hepatic intracellular concentration). The Chept inlet,max is estimated using Cmax and the rate of absorption after oral administration [Eq. (4.10)]. The DDI may be under- or overpredicted if the drugs are substrates of hepatic transporters (efflux or uptake), show poor membrane permeability, and/or are prone to rapid metabolism. [Pg.109]


See other pages where Enzymes hepatic is mentioned: [Pg.268]    [Pg.129]    [Pg.93]    [Pg.385]    [Pg.174]    [Pg.638]    [Pg.138]    [Pg.856]    [Pg.537]    [Pg.91]    [Pg.471]   
See also in sourсe #XX -- [ Pg.319 , Pg.320 , Pg.321 , Pg.322 , Pg.323 , Pg.324 , Pg.325 , Pg.326 , Pg.327 , Pg.328 , Pg.329 , Pg.330 , Pg.331 , Pg.332 ]

See also in sourсe #XX -- [ Pg.604 , Pg.605 , Pg.606 , Pg.607 , Pg.608 , Pg.609 , Pg.610 , Pg.611 , Pg.612 , Pg.613 , Pg.614 , Pg.615 ]




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Drug-metabolizing enzyme system hepatic microsomal, effects

Enzymes hepatic drug metabolism, metabolite

Hepatic P-450 enzyme

Hepatic clearance/enzymes

Hepatic cytochrome P450 enzymes

Hepatic drug-metabolizing enzyme system

Hepatic enzyme induction

Hepatic enzyme induction anticonvulsants

Hepatic enzyme induction rifampicin

Hepatic enzyme systems

Hepatic enzymes alkaline phosphatase

Hepatic enzymes aminotransferases

Hepatic enzymes cholinesterase

Hepatic enzymes gamma-glutamyl transferase

Hepatic enzymes glutamate dehydrogenase

Hepatic enzymes mutagenicity

Hepatic glucose metabolizing enzymes, inhibition

Hepatic microsomal enzyme

Hepatic microsomal enzymes stimulation

Induction of hepatic drug metabolizing enzyme

Mammalian hepatic enzyme preparations

Nuclear Receptor Regulation of Hepatic Cytochrome P450 Enzymes

P450 enzymes, hepatic

Polycyclic hydrocarbons, hepatic microsomal enzymes inducers

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