Cases reported "Cholestasis, Intrahepatic"

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1/4. liver diseases in pregnancy.

    Mild abnormalities of liver function tests are frequently seen in pregnancy but return to normal after delivery. A raised serum alkaline phosphatase is common, along with a decline in the serum albumin, but the aminotransferases remain within normal limits. The physician must interpret abnormal liver function tests in pregnancy with these changes in mind, but most liver diseases in pregnancy result in more marked alterations. Viral hepatitis is the most common cause of jaundice in pregnancy, and the maternal prognosis is generally good. Perinatal transmission of hepatitis b virus is likely when the mother is positive for HBsAg. Concurrent administration of hepatitis B vaccine and HBIG to the infant has an efficacy of 90 per cent in preventing transmission to the infant. ICP is the second most common cause of jaundice in pregnancy. The condition is generally benign, although maternal and fetal mortality occasionally result, probably due to premature delivery and the bleeding tendency of cholestatic patients. Vitamin K administration may correct the coagulopathy, and cholestyramine is effective in controlling pruritus. AFLP is rare but carries a high mortality rate for both the mother and the fetus. early diagnosis, correction of the coagulopathy, and prompt delivery may improve the outcome significantly. patients with cirrhosis have reduced fertility, and in those who become pregnant, fetal loss is high. The effect of pregnancy or hepatocellular function is variable, but, when evidence of liver failure is present in the first trimester, termination should be considered. Variceal size and the risk of bleeding may be assessed by endoscopy. Pregnant cirrhotic patients with large esophageal varices and a history of bleeding can undergo shunt surgery. Conservative management may be appropriate for patients with small varices and no history of bleeding.
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2/4. Intrahepatic cholestasis during nicotinic acid therapy.

    BACKGROUND: Nicotinic acid, widely used to lower serum cholesterol levels, may rarely cause cholestatic jaundice. SUMMARY: A 61-year-old white man with hypercholesterolemia complained of marked pruritus and became jaundiced after taking 3.0 g of crystalline nicotinic acid daily for 13 months. His total serum bilirubin level was increased at 144 mumol/L (8.4 mg/dL) and his alkaline phosphatase level was markedly elevated at 35.00 mukat/L (2100 U/L). Endoscopic retrograde cholangiopancreatography failed to demonstrate an obstructive lesion in the extrahepatic biliary system, computed tomography showed no intrahepatic dilatation, and ultrasonographic studies of the liver, gallbladder, and pancreas were normal; these factors all suggest intrahepatic cholestasis. Symptoms improved and liver function test results returned to normal within 51 days after stopping the drug. CONCLUSIONS: Nicotinic acid-induced cholestatic jaundice may not be as rare as previously thought, and physicians should observe their patients for it.
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3/4. Unilobar intrahepatic lithiasis 22 years after cholecystectomy.

    Complaints of right upper quadrant pain, jaundice, and fever in the postcholecystectomy patient provide the physician with a challenging diagnosis. This case concerns a patient with intrahepatic lithiasis and fibrotic atrophy of the right lobe 22 years after open cholecystectomy.
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4/4. Possible cholestatic injury from ranitidine with a review of the literature.

    Although one of the histamine-2 (H2) receptor antagonists, oxmetidine, has been shown to be intrinsically hepatotoxic, overt liver injury attributable to the commonly used analogues such as ranitidine is rare, given the millions of patients who have received this medication. However, isolated cases of hepatitis associated with ranitidine have been reported in the literature since the early 1980s when this drug was first introduced. We report a case of cholestatic hepatitis associated with ranitidine use. Liver biopsy showed diffuse panacinar canalicular cholestasis and cholestatic rosettes in zone 3. The clinical syndrome and the laboratory abnormalities resolved completely after discontinuation of the drug. There have been a few other published reports of ranitidine associated acute cholestatic hepatitis, and in this case ranitidine was temporally related to the onset of symptoms and liver enzyme abnormalities. With recent over-the-counter (OTC) availability of the H2 receptor antagonists and the increasing use of these drugs in the general population, physicians need to be aware of this rare but potentially serious side effect of ranitidine.
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