Jaundice drug-induced

Parenteral Anticoagulant-induced prothrombin deficiency hypoprothrombinemia secondary to conditions limiting absorption or synthesis of vitamin K (eg, obstructive jaundice, biliary fistula, sprue, ulcerative colitis, celiac disease, intestinal resection, cystic fibrosis of the pancreas, regional enteritis) drug-induced hypoprothrombinemias due to interference with vitamin K metabolism (eg, antibiotics, salicylates) prophylaxis and therapy of hemorrhagic disease of the newborn. 

Hepatotoxicity Prolonged use of high doses of androgens has been associated with the development of potentially life-threatening peliosis hepatis, hepatic neoplasms, and hepatocellular carcinoma. Cholestatic hepatitis and jaundice occur with fluoxymesterone and methyltestosterone at relatively low doses. Drug-induced jaundice is reversible when the medication is discontinued. 

Monitor carefully in first 3 mo of therapy for signs of intolerance/drug-induced hepatitis (rash, fever, jaundice, hepatomegaly)... 

The incidence of drug-induced liver injury with rosiglitazone has been calculated at 0.02% for alanine transaminase activity 10 times the upper end of the reference range and 0.001% for jaundice (120). The above case report is unusual because, although liver damage is rare, hepatic necrosis occurs more commonly than cholestatic hepatitis. 

Dose-independent, drug-induced liver dysfunction (cholestatic jaundice) is not an unusual adverse reaction. Caused by a number of different, commonly used drugs, cholestasis is a hypersensitivity reaction that primarily affects the biliary canaliculi, causing an intrahepatic obstructive jaundice. An alteration in... 

Interference with bilirubin metabolism and excretion. Jaundice is induced selectively with minimal or no disturbance of other liver function tests recovery ordinarily occurs on stopping the drug. Examples are ... 

In addition, biliary obstructive jaundice can also be caused by drug-induced toxicity, e.g. with Ciy-substi-tuted steroids, erythromycin estolate, chlorpromazine, chlorpropamide, ajmaline, halothane, methylthiouracil. 

Liver damage caused by drug-induced toxicity, more specifically the intrahepatic obstructive type of jaundice resulting from the intake of arsphenamine, was first described by EM. Hanger et al. in 1940. (42)... 

A 77-year-old man took amlodipine for 1 month and developed jaundice and raised aspartate transaminase, alanine transaminase, and bilirubin (9). A liver biopsy suggested a drug-induced hepatitis and the amlodipine was withdrawn. His symptoms and laboratory values normalized. Other drugs (metformin, fluindione, and omeprazole) were not withdrawn. 

A 76-year-old woman with previous exposure to isoflurane 3 years earlier underwent an above-knee amputation for a liposarcoma using isoflurane anesthesia. On day 3 postoperatively she became febrile and confused. Bacterial cultures later showed Staphylococcus aureus in the sputum and Escherichia coli in the urine. Associated hypotension for 2 hours resolved with inotropic support and here renal function remained normal. On day 6 she became jaundiced and developed further hypotension. Despite intensive care treatment she died on day 7. An autopsy showed centrilobular necrosis consistent with drug-induced hepatitis. All liver serology was negative. 

Glucose-6-phosphate dehydrogenase deficiency This is an X-linked disorder associated with neonatal jaundice on the 2nd or 3rd day of life and drug-induced haemolytic crises (p. 149)... 

Drug-induced hepatotoxicity was reported in a 33-year-old woman who had been taking 15 tablets (dose unspecified) of chaparral daily for 3 to 4 months. The patient had presented with jaundice, ascites, abdominal pain, fatigue. 

Urinary excretion of bile salts by healthy subjects is apparently very limited. The urine contained 2 % of the radioactivity administered orally as i C-cholic acid to a healthy subject in whom 100% of the radioactivity was recovered (80) and 0.12% of radioactivity administered to four normal subjects when i C-cholate was given intravenously (25). Conventional methods do not detect bile salts in the urine of healthy subjects (81,82). In jaundice patients, however, bile salts are excreted in the urine regularly (83). The highest 24-hr excretion rates reported by Gregg occurred in patients with common bile duct obstruction (58 mg/24 hr) and drug-induced cholestasis (40 mg/24 hr). The cholate/chenodeoxycholate ratio was greater than 0.59... 

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