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Cholestasis hepatitis

Herbal remedies that have been reported to be he-patotoxic include chaparral (Larrea tridentata), germander (Teucrium chamaedrys), and life root (Senecio aureus) [18]. Cases reported patients developing jaundice, fatigue, pruritus, markedly elevated serum liver enzyme levels, severe cholestasis, hepatitis, and hepatocellular injury or necrosis documented by serial liver biopsies [19-21]. Signs and symptoms may occur as early as 3 weeks to as late as 7 months following ingestion [20,21]. [Pg.735]

Hepatic Hepatic cholestasis, hepatic toxicity, hepatitis, hyperbilirubinemia, increased liver enzymes, jaundice, liver failure. [Pg.1588]

Hepatocellular damage Cholestasis Hepatic function Mesenchymal activity Immunology ... [Pg.93]

Goid Saits Recent studies suggest that gold salts are ineffective for treating arthritis. They are still prescribed, however. Dermatitis, stomatitis, GI upset, nephrotic syndrome, cholestasis, hepatitis. Oral/IM preparations available. Accumulates in synovium and in phagocytic cells. [Pg.136]

Many types of liver injury are caused by a number of biochemical reactions of toxicants or their active metabolites. Such reactions inclnde covalent binding, lipid peroxidation, inhibition of protein synthesis, pertnrbation of calcium homeostasis, disturbance of biliary prodnction, and a variety of immunologic reactions. The types of liver injury from such biochemical reactions include steatosis (fatty liver), liver necrosis, cirrhosis, cholestasis, hepatitis, and carcinogenesis. The toxicants that cause these injuries are discussed in brief. [Pg.26]

Yellow phosphorus was the first identified liver toxin. It causes accumulation of lipids in the liver. Several liver toxins such as chloroform, carbon tetrachloride, and bromobenzene have since been identified. I he forms of acute liver toxicity are accumulation of lipids in the liver, hepartxiellular necrosis, iii-trahepatic cholestasis, and a disease state that resembles viral hepatitis. The types of chrome hepatotoxicity are cirrhosis and liver cancer. [Pg.298]

TABLE 5.13 Examples of Drugs that Induce Intrahepatic Cholestasis or Liver Damage Resembling That Induced by Viral Hepatitis... [Pg.299]

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... [Pg.247]

Total calories Hepatic steatosis, cholestasis, hypercapnia... [Pg.1504]

The incidence of liver complications associated with PN ranges from approximately 7% to 84%, and end-stage liver disease develops in as many as 15% to 40% of adult patients on long-term PN.35 Patients often develop a mild increase in liver enzymes within 1 to 2 weeks of initiating PN, but this generally resolves when PN is discontinued. Severe liver complications include hepatic steatosis (fat deposition in liver), steatohepatitis (a severe form of liver disease characterized by hepatic inflammation that may progress rapidly to liver fibrosis and cirrhosis), cholestasis, and cholelithiasis.35... [Pg.1506]

Oral testosterone-replacement regimens can cause hepatotoxicity, ranging from mildly elevated hepatic transaminases to serious liver diseases (e.g., peliosis hepatitis, hepatocellular and intrahepatic cholestasis, and benign or malignant tumors). [Pg.955]

Toxicologists classify hepatic toxicants according to the type of injuries they produce. Some cause accumulation of excessive and potentially dangerous amounts of lipids (fats). Others can kill liver cells they cause cell necrosis. Cholestasis, which is decreased secretion of bile leading to jaundice (accumulation of gruesome looking pigments that impart a yellowish color to the skin and eyes) can be... [Pg.118]

Chronic use of neuroleptics can, on occasion, give rise to hepatic damage associated with cholestasis. A very rare, but dramatic, adverse effect is the malignant neuroleptic syndrome (skeletal muscle rigidity, hyperthermia, stupor) that can end fatally in the absence of intensive countermeasures (including treatment with dantrolene, p. 182). [Pg.238]

Visual disturbances If treatment continues beyond 28 days, the effect of voriconazole on visual function is not known. If treatment continues beyond 28 days, monitor visual function including visual acuity, visual field, and color perception. Hepatic toxicity There have been uncommon cases of serious hepatic reactions during treatment with voriconazole (eg, clinical hepatitis, cholestasis, and fulminant hepatic failure, including fatalities). Liver dysfunction usually has been reversible on discontinuation of therapy. [Pg.1676]

Hepatotoxicity Severe hepatic reactions, including acute liver failure, jaundice, hepatitis, and cholestasis, have been reported rarely in postmarketing data in patients receiving infliximab. Autoimmune hepatitis has been diagnosed in some of... [Pg.2017]

Sokol, RJ. et al. (2006) Let there be bile —understanding hepatic injury in cholestasis. Journal of Pediatric Gastroenterology and Nutrition, 43 (Suppl 1). S4-S9. [Pg.381]

Dose-related myelosuppression is the major adverse effect produced by 6-thioguanine. Patients deficient in thiopurine methyltransferase (TPMT), a cytosolic enzyme required for metabolism of 6-thioguanine, are at heightened risk. Other adverse effects include gastrointestinal complaints and elevations of liver transaminases. There have been rare reports of more serious he-patotoxicity, including acute hepatitis, acute cholestasis, and hepatic venoocclusive disease. [Pg.494]

Intrahepatic cholestasis and hepatitis similar to that seen in chronic active hepatitis can rarely occur fatalities have been reported. Nitrofurantoin can interfere with immature red blood cell enzyme systems found in babies less than 1 month of age and in nursing infants. This leads to cellular damage and anemia. Nitro-... [Pg.522]

Cholestatic. Pertaining to or characterized by suppression or stopping of the flow of bile (cholestasis), having intrahepatic or extra-hepatic causes. [Pg.565]

Peptic ulcer, G1 bleeding, gastritis, and severe hepatic reaction, including cholestasis, jaundice occur rarely. [Pg.367]

Rare reactions with long-term use include peptic ulcer disease, GI bleeding, gastritis, a severe hepatic reaction (cholestasis, jaundice), nephrotoxicity (dysuria, hematuria, proteinuria, nephrotic syndrome), and a severe hypersensitivity reaction (particularly in patients with systemic lupus erythematosus or other collagen diseases). [Pg.609]

Carbamazepine therapy is occasionally associated with hepatic toxicity, usually a hypersensitivity hepatitis that appears after a latency period of several weeks and involves increases in ALT, AST, and lactate dehydrogenase levels. Cholestasis is also possible, with increases in bilirubin and alkaline phosphatase concentrations. Mild, transient increases in transaminase levels generally do not necessitate discontinuation of carbamazepine. If ALT or AST levels increase more than three times the upper limit of normal, carbamazepine should be discontinued. [Pg.154]

Adverse effects include nausea, vomiting, diarrhoea, cholestasis, bone marrow depression, pancreatitis, oral and intestinal ulcers. Rarely hepatic necrosis. [Pg.374]

Cunningham and Matthews (1991) treated male Fischer 344 rats with 0.5, 1 or 2 mmol/kg bw 2-nitropropane daily for 10 days by gavage. At the higher dose levels, but not at 0.5 mmol/kg bw, increased hepatic DNA synthesis was found, together with moderate signs of cholestasis and hepatotoxicity. [Pg.1083]

Jaundice as a result of oral contraceptive treatment has been repeatedly described. Whereas in the Swedish population figures between 1 100 and 1 4000 were published when the early high-dose formulations were still in use (213), the overall incidence was estimated in 1979 at about 1 10 000 (9), and the current incidence is certainly further reduced. When such hepatic symptoms occur, they usually do so within the first month of medication (214), and jaundice may be accompanied by anorexia, malaise, and pruritus. Very few cases arise after the third month of medication and those reported are regarded by some as unlikely to be due to oral contraceptives. Microscopic examination of the liver shows intrahepatic cholestasis. When medication is stopped, symptoms usually disappear rapidly and the reaction does not seem to leave any sequelae (215). Genetic components seem to be important for the development of the reaction women who have experienced jaundice or severe pruritus in late pregnancy seem to be especially susceptible to jaundice or gallbladder disease when using... [Pg.230]


See other pages where Cholestasis hepatitis is mentioned: [Pg.183]    [Pg.73]    [Pg.183]    [Pg.73]    [Pg.6]    [Pg.957]    [Pg.198]    [Pg.327]    [Pg.109]    [Pg.111]    [Pg.365]    [Pg.206]    [Pg.91]    [Pg.745]    [Pg.523]    [Pg.524]    [Pg.920]    [Pg.1053]    [Pg.629]    [Pg.230]   
See also in sourсe #XX -- [ Pg.56 ]




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