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Disease liver

Livera Liver cancer Liver disease Liver flukes Liverworts Liverwurst Livetins... [Pg.575]

Adrenocortical insufficiency Organ transplants Liver disease Adrenogenital syndrome Nephrotic syndrome Acute spinal cord injury Hyp ere alemia Hematologic disorders Myasthenia gravis Neoplastic disease... [Pg.94]

After po dosing, verapamil s absorption is rapid and almost complete (>90%). There is extensive first-pass hepatic metabolism and only 10—35% of the po dose is bioavahable. About 90% of the dmg is bound to plasma proteins. Peak plasma concentrations are achieved in 1—2 h, although effects on AV nodal conduction may be apparent in 30 min (1—2 min after iv adrninistration). Therapeutic plasma concentrations are 0.125—0.400 p.g/mL. Verapamil is metabolized in the liver and 12 metabolites have been identified. The principal metabolite, norverapamil, has about 20% of the antiarrhythmic activity of verapamil (3). The plasma half-life after iv infusion is 2—5 h whereas after repeated po doses it is 4.5—12 h. In patients with liver disease the elimination half-life may be increased to 13 h. Approximately 50% of a po dose is excreted as metabolites in the urine in 24 h and 70% within five days. About 16% is excreted in the feces and about 3—4% is excreted as unchanged dmg (1,2). [Pg.121]

Therapeutic Function Treatment of liver diseases Chemical Name 5-aminoimidazole-4-carboxamide orotate Common Name AICA orotate Structural Formula a... [Pg.1113]

Metformin Renal or liver disease any predisposition to hypoxia Gastro intestinal upsets risk of lactic acidosis if wrongly prescribed Creatinine, Hb or Vit B12b... [Pg.124]

Thiazolidinediones Cardiac failure liver disease Oedema, anaemia, heart failure, fractures in women LFTb... [Pg.124]

Liver diseases Alcoholic hepatitis (A), hepatitis B and C (A), non-alcoholic steatohepatitis (A), liver transplantation (A), Wilson s disease (A)... [Pg.332]

Apart from these two Vertex compounds, only one other caspase inhibitor, BDN-6556, has been used in clinical trials. This compound belongs to the class of oxamyl dipeptides and was originally developed by Idun Pharmaceuticals (taken over by Pfizer). It is the only pan-caspase inhibitor that has been evaluated in humans. BDN-6556 displays inhibitory activity against all tested human caspases. It is also an irreversible, caspase-specific inhibitor that does not inhibit other major classes of proteases, or other enzymes or receptors. The therapeutic potential of BDN-6556 was first evaluated in several animal models of liver disease because numerous publications suggested that apoptosis contributes substantially to the development of some hepatic diseases, such as alcoholic hepatitis, hepatitis B and C (HBV, HCV), non-alcoholic steato-hepatitis (NASH), and ischemia/reperfusion injury associated with liver transplant. Accordingly, BDN-6556 was tested in a phase I study. The drug was safe and... [Pg.333]

Under certain circumstances, and very rarely, the inhibition of gluconeogenesis by metformin may suppress lactic acid metabolism and precipitate a potentially fatal lactic acidosis. Impairment of renal function, liver disease, alcoholism, conditions that give rise to increased lactate production (e.g. congestive heart failure, infections) are therefore contraindications for the application of metformin. [Pg.425]

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]

Ethanol also inhibits ADH-catalyzed retinol oxidation in vitro, and ethanol treatment of mouse embtyos has been demonstrated to reduce endogenous RA levels. The inhibition of cytosolic RolDH activity and stimulation of microsomal RolDH activity could explain ethanol-mediated vitamin A depletion, separate from ADH isoenzymes. Although the exact mechanism of inhibition of retinoid metabolism by ethanol is unclear, these observations are consistent with the finding that patients with alcoholic liver disease have depletedhepatic vitamin A reserves [review see [2]. [Pg.1078]

In liver disease, for example, the ability to metabolize or detoxify a specific type of drug may be impaired. If the average or normal dose of the drug is given, the liver may be unable to metabolize the drug at a normal rate Consequently, the drug may be excreted from the body at a much slower rate than normal. The primary health care provider may then decide to prescribe a lower dose and lengthen the time between doses because liver function is abnormal. [Pg.12]

These dru are contraindicated in patients with a hypersensitivity to the macrolides and patients with pre-existing liver disease... [Pg.86]

The gold compounds are used cautiously in patients with a history of hypersensitivity to other drugs, previous kidney or liver disease, diabetes, or hypertension. [Pg.186]

When administering tacrine, the nurse must monitor the patient for liver damage. This is best accomplished by monitoring alanine aminotransferase (AIT) levels. ALT is an enzyme found predominately in the liver. Disease or injury to the liver causes a release of tiiis enzyme into the bloodstream, resulting in elevated ALT levels, hi patients taking tacrine, ALT levels should be obtained weekly from at least week 4 to week 16 after die initiation of tiierapy. After week 16, transaminase levels are monitored every 3 months. [Pg.308]

A diuretic is a drug that increases die secretion of urine (ie, water, electrolytes, and waste products) by die kidneys. Many conditions or diseases, such as heart failure, endocrine disturbances, and kidney and liver diseases can cause retention of excess fluid (edema). When die patient shows signs of excess fluid retention, die primary healdi care provider may order a diuretic. There are various types of diuretic drugs, and the primary healdi care provider selects the one that best suits die patient s needs and effectively reduces the amount of excess fluid in body tissues. [Pg.443]

Loop diuretics are used cautiously in patients with renal dysfunction. The loop diuretics are Pregnancy Category B (ethacrynic acid and torsemide) and C drugp (furosemide and bumetanide) and must be used cautiously during pregnancy and lactation. Furosemide is used in children but should be used cautiously. The loop diuretics are used cautiously in patients with liver disease, diabetes, lupus erythematosus (may exacerbate or activate the disease), or diarrhea. Patients with... [Pg.448]

These drug are contraindicated in patients with known hypersensitivity to tire drug. Clomiphene is contraindicated in patients with liver disease, abnormal bleeding of undetermined origin, or ovarian cysts, and during... [Pg.511]

Amino acids promote the production of proteins, enhance tissue repair and wound healing, and reduce the rate of protein breakdown. Amino acids are used in certain disease states, such as severe kidney and liver disease, as well as in TPN solutions. (See the last section of this chapter for a more detailed discussion of TPN.) TPN may be used in patients with conditions such as impairment of gastrointestinal absorption of protein, in patients with an increased requirement for protein, as seen in those with extensive bums or infections, and in patients with no available oral route for nutritional intake ... [Pg.634]

Glycogenosis type VIII (phosphorylase b kinase deficiency) gives rise to myopathy and liver disease, either singly or in combination. Phosphorylase b kinase (PBK) converts the inactive b form of both muscle and liver phosphorylases to the active a forms of the enzymes. The ischemic lactate test sometimes shows a flat result as in McArdle s disease, but is more likely to be normal. Histochemical demonstration of myophosphorylase activity in tissue sections shows a near-normal reaction due to the presence of phosphorylase a. Accumulation of glycogen is modest and found mainly in type 2 (fast-twitch glycolytic) muscle fibers. [Pg.302]


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Adverse drug reactions liver disease

Albumin levels liver disease

Alcohol chronic liver disease

Alcohol liver disease

Alcohol-induced liver disease

Alcoholic liver disease

Alcoholic liver disease cirrhosis

Alcoholic liver disease ibuprofen

Alcoholic liver disease renal impairment

Alcoholic liver disease stages

Alcoholism liver disease

Baccharis crispa in treatment of liver disease

Baccharis genistelloides use in liver diseases

Biliary atresia chronic liver disease

Blood chronic liver diseases

Causes of liver disease and dysfunction

Children chronic liver disease

Children liver disease

Cholestasis liver disease

Cholestatic liver disease

Cholestatic liver disease bile acid synthesis

Cholestatic liver disease blood

Cholestatic liver disease metabolism

Cholestatic liver disease transport

Chronic alcoholic liver disease

Cirrhosis chronic liver disease

Coumarin anticoagulants liver disease

Cytochrome liver disease

Effects of Liver Disease on Patient Response

Enzymes Released from Diseased Liver Tissue

Fatty liver disease

Fatty liver disease, diagnosis

Focal liver disease

Food-drug interactions liver disease

HbsAg-positive chronic liver disease

Hepatic disease liver fibrosis

Hepatitis chronic liver disease

Hypoalbuminemia in liver disease

Hypoalbuminemia liver disease

Induced Liver Disease

Jaundice, liver disease

Lipoproteins liver disease

Lithocholic acid liver disease

Liver Disease Starvation

Liver Disease and Cirrhosis

Liver chronic disease, plasma protein

Liver cirrhotic disease

Liver disease acute

Liver disease acute hepatitis

Liver disease altered drug metabolism

Liver disease and

Liver disease assessment

Liver disease autoimmune hepatitis

Liver disease bile acids

Liver disease bile handling

Liver disease biliary excretion

Liver disease biliary tract disorders

Liver disease cancer

Liver disease causes

Liver disease chronic

Liver disease cirrhosis

Liver disease classification

Liver disease clinical manifestations

Liver disease compensated

Liver disease congenital malformation

Liver disease contraceptives

Liver disease decompensated

Liver disease diabetes mellitus

Liver disease diagnosis

Liver disease differential diagnosis

Liver disease drug metabolism

Liver disease drug treatment

Liver disease drug-induced

Liver disease drug-related

Liver disease drugs

Liver disease during pregnancy

Liver disease end-stage

Liver disease follow

Liver disease hemochromatosis

Liver disease hepatic blood flow

Liver disease hepatitis

Liver disease hepatorenal syndrome

Liver disease immune

Liver disease infections

Liver disease infertility

Liver disease inherited disorders

Liver disease ischemic hepatitis

Liver disease management

Liver disease metabolic disorders

Liver disease nonalcoholic steatohepatitis

Liver disease obstructive

Liver disease overview

Liver disease patient response

Liver disease pharmacokinetic effects

Liver disease portal hypertension

Liver disease pregnancy

Liver disease protein synthesis alterations

Liver disease prothrombin time

Liver disease risk factors

Liver disease severity

Liver disease signs/symptoms

Liver disease subacute

Liver disease toxic hepatitis

Liver disease toxin-induced

Liver disease treatment choices

Liver disease vascular abnormalities

Liver disease viral infection

Liver disease vitamin

Liver disease with parenteral nutrition

Liver disease, drug contraindications

Liver disease, nitric oxide

Liver disease, pharmacokinetic

Liver disease, viii

Liver diseases, enzyme activity

Liver diseases, lipid hydroperoxides

Liver diseases/disorders

Liver drug-induced disease/damage

Liver glycogen storage diseases

Liver hepatic disease

Liver in Wilson’s disease

Liver infectious diseases

Liver malignant disease

Liver neoplastic disease

Liver polycystic disease

Liver radiation-induced disease

Liver vascular disease

Liver, copper disease

Lung and Liver Diseases

Model for end-stage liver disease

Nitric oxide in liver disease

Non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease NAFLD)

Nonalcohol Fatty Liver Disease

Nonalcoholic fatty liver disease

Pantothenic Liver disease

Parenteral nutrition liver disease

Parenteral nutrition-associated liver disease

Pharmacokinetics Liver disease

Pharmacokinetics liver disease effects

Pharmacokinetics of drugs in liver disease

Plasma Alpha-Class GST Measurements in Liver Disease

Portal hypertension chronic liver disease

Relative Synthesis Rates in Liver Disease

Severe liver disease

Skin stigmata in liver disease

Steroid Liver disease

Thyroid Liver disease

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