Cholestasis jaundice

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

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). 

Alkaline phosphatase (ALP) is present in high concentrations in the cells lining the biliary tract and an ALP level exceeding 300 IU/L, together with a raised bilirubin as in the case of Mrs MW, is indicative of cholestasis. Jaundice becomes progressively more severe in unrelieved cholestasis. 

In various forms of genetically determined cholestasis, jaundice can be the most obvious primary clinical symptom leading to the clinical classification of functional hyperbilirubinaemia. However, in most cases, pronounced cholestasis is the principal feature of the clinical picture in the diseases explained below. Many primary storage diseases, especially childhood cholestasis, can only be identified through careful differential diagnosis. Genetically determined intrahepatic cholestasis... 

Intrahepatic obstmctive and non-obstmctive cholestasis/ jaundice (s. tabs. 13.3, 13.4)... 

Toxicity Bone marrow suppression is dose-limiting, but hepatic dysfunction (cholestasis, jaundice, necrosis) also occurs. 

Abdominal pain, dyspepsia, nausea, vomiting, diarrhea, constipation, cholestasis, jaundice, cholelithiasis, pancreatitis, headache, dizzihess, drowsihess, blurred vision, mental depression, impotence, decreased libido, myopathy, myositis, rhabdomyolysis, ahemia, leukopehia, eosihophilia, pruritus, and rash... 

Hepatocellular damage, cholestasis, jaundice, rises in LDH and transaminases... 

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]. 

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... 

Hepatic Hepatic cholestasis, hepatic toxicity, hepatitis, hyperbilirubinemia, increased liver enzymes, jaundice, liver failure. 

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... 

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... 

Bilirubin. An increase in the bilirubin level and an accompanying increase in aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities most often result from obstmctive jaundice developed as a consequence of pancreas head edema and pressure exerted on the papilla of Vater (cholestasis). 

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... 

When a neuroleptic drug causes jaundice it generally occurs within 2-4 weeks and has many characteristics of an allergic reaction, being accompanied by fever, rashes, and eosinophilia, although a direct toxic mechanism has also been implicated. Symptoms generally subside rapidly after withdrawal, but cholestasis may be prolonged. 

Cholestasis occurred in a woman with alpha-1 antitrypsin deficiency (phenotype PiZZ) who had taken prochlorperazine 5-10 mg qds for 27 months (3). She developed jaundice and ascites. Liver biopsy confirmed diffuse advanced chronic cholestasis, moderate portal and periportal inflammation, and bridging necrosis. Her liver function tests normalized within days of withdrawal of prochlorperazine. 

A 25-year-old woman developed abdominal pain, jaundice, and vomiting 5 days after consuming ecstasy. She had hepatocellular failure with a prothrombin ratio of 6.5, cytolysis, cholestasis, renal insufficiency, and encephalopathy. She had a liver transplant 2 days later and recovered fully. 

This is an autosomal dominant hereditary disorder characterised by a progressive loss of the bile ducts within the liver and narrowing of the bile ducts outside the liver. It is also associated with congenital heart disease, and in particnlar pulmonary stenosis. Symptoms are related to chronic cholestasis and include jaundice, pruritus, pale loose stools and poor growth within the first three months of life. The majority of children have a benign course and many cases go undetected however, there is an overall mortality of 20-30% due to progressive liver disease with the development of cirrhosis, cardiac disease or intercnrrent infection. 

Hepatic adverse effects secondary to antiemetic therapy are usually asymptomatic. Metoclopramide has been reported as causing cholestasis and the formation of arteriovenous shunts in the liver [12]. The 5HTj-receptor antagonists have all been documented as occasionally causing mild increases in liver fimction tests. Cholestatic jaundice has been reported with cyclizine, prochlorperazine and promethazine, and hepatitis has been reported with cyclizine. 

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