Cases reported "Hyperbilirubinemia"

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1/5. Acute cholestatic hepatitis associated with celecoxib.

    OBJECTIVE: To report a case of acute cholestatic hepatitis associated with the selective cyclooxygenase-2 inhibitor celecoxib. CASE SUMMARY: A 41-year-old white man was hospitalized for jaundice after 2 doses of celecoxib 200 mg for pain associated with right-knee trauma. Laboratory workup showed hyperbilirubinemia, mildly elevated serum transaminase concentrations, and cholestasis. Abdominal imaging showed no dilation of the biliary tree. histology showed cholestasis, with bile plugs in dilated bile canaliculi and a mild portal infiltrate that are highly suggestive of drug-induced cholestasis. DISCUSSION: This is the fourth report in the English-language literature describing cholestatic hepatitis temporally related to celecoxib use, the second supported by histologic findings typical of drug-induced cholestasis, and the first in a patient who denied use of alcoholic beverages and was taking no other drugs or herbal products at the time of the reaction. The Naranjo probability scale indicated that celecoxib was a probable cause of acute cholestatic hepatitis in this patient. CONCLUSIONS: Cholestatic hepatitis is a well-recognized adverse effect of several drugs. Although celecoxib is considered to have a very low potential for hepatic toxicity, well-documented reports of adverse reactions can contribute significantly to the definition of more accurate safety profiles for new drugs introduced into clinical practice.
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2/5. pyloric stenosis and direct hyperbilirubinemia with alpha-1-antitrypsin deficiency.

    The occurrence of unconjugated hyperbilirubinemia in infants with pyloric stenosis is common. We report an infant who presented with projectile vomiting secondary to pyloric stenosis. In addition, he had conjugated hyperbilirubinemia which proved to be due to alpha-1-antitrypsin deficiency of PiZZ phenotype. This is the first case report of such an association. Infants with pyloric stenosis and conjugated hyperbilirubinemia should be investigated for underlying infectious, metabolic causes or anatomical defects of the biliary tree.
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3/5. Hepatocellular injury in streptococcus pneumoniae-associated hemolytic uremic syndrome in children.

    streptococcus pneumoniae is an uncommon etiological organism in hemolytic uremic syndrome (HUS). Production of neuraminidase by S. pneumoniae results in exposure of red blood cell T-antigen, resulting in hemolysis, thrombocytopenia, and acute renal failure. Hepatic involvement in this form of HUS has not been described in the literature. We report in three children with S. pneumoniae-associated HUS the presence of severely elevated transaminases and conjugated hyperbilirubinemia. Increases in asparagine transaminase ranged from 11 to 46 times normal values and an increase in alanine transaminase ranged from 1.6 to 8 times normal. In all patients the rise in total bilirubin was 7-15 times normal. Biliary tree obstruction and viral causes for liver dysfunction were absent. Hepatocellular injury in S. pneumoniae-associated HUS likely results from mechanisms involved in sepsis and pneumonia-induced jaundice, combined with severely increased bilirubin production following massive hemolysis. The hepatic injury in all three patients resolved within 9, 5, and 10 days. Our experience suggests that an extensive evaluation including liver biopsy is not indicated.
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4/5. Prolonged cholestatic jaundice after endoscopic retrograde cholangiography.

    The main complications of endoscopic retrograde cholangiography and sphincterotomy are bleeding, pancreatitis, perforation and sepsis. Two cases of unexplained prolonged cholestatic jaundice in patients who underwent endoscopic retrograde cholangiography (ERC) for biliary obstruction due to choledocholithiasis are reported. The patients were admitted because of right upper quadrant pain, vomiting and jaundice. Laboratory tests showed increased levels of total and conjugated serum bilirubin and increased alkaline phosphatase. Ultrasound examination showed cholelithiasis and choledocholithiasis with bile duct dilatation. ERC with sphincterotomy was performed and gallstones obstructing the common bile duct were removed endoscopically. Following ERC and despite complete patency of the biliary tree, a progressive increase of total and conjugated bilirubin and of alkaline phosphatase was noted, associated with itching and total stool discoloration. The insertion of nasobiliary drain did not improve the jaundice. prednisolone treatment for 12 days was associated with progressive restoration of serum bilirubin alkaline phosphatase to normal levels. It was postulated that the radiocontrast material used may have acted toxically on the liver with disruption of the canalicular plasma membrane. It is proposed that intrahepatic cholestasis should be added in the list of complications of endoscopic retrograde cholangiography.
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5/5. hyperbilirubinemia associated with a cystic abdominal mass in a 6-week-old girl: case report.

    Abdominal cysts in girls are frequently observed by abdominal ultrasound (US) and are usually ovarian. In this case a cystic structure located in the right abdomen was seen in a female newborn without symptoms and was initially described as a possible ovarian cyst. Frequent US examinations showed an increase in volume and diameter, and temporary, recurring episodes of hyperbilirubinemia were observed. The US scans showed no relationship to the biliary tree. During a diagnostic laparoscopy, a cystic structure attached to the pyloric region was seen. A laparotomy revealed a cystic duplication of the stomach, which could be resected completely. The finding is discussed emphasizing the importance of clinical findings and diagnostic methods in the diagnosis and management of abdominal cystic masses in females.
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