Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008370 (cholestasis)
 9,378 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. Jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.
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PMID:Patterns of hepatic injury induced by methyldopa. 42 37

For several weeks a 58-year-old woman had suffered from intermittent right upper abdominal and flank pain, loss of appetite, weight loss (2 kg in 8 weeks), as well as constipation. She had a mild eosinophilia of 0.48/nl, while the blood picture and differential count were normal. There was no evidence of cholestasis, liver disease or an inflammatory process. Upper abdominal ultrasound examination demonstrated a gall-bladder polyp with cholelithiasis and sludge. Although the intrahepatic biliary tract was normal, the gallbladder was much enlarged and contracted only moderately after a test meal. A parasitological disease was included in the differential diagnosis because the patient had lived in Tomsk, Siberia, until the previous year. Examination of faeces and duodenal secretion discovered eggs of Opisthorchis felineus, a liver fluke especially common in Siberia and the Ukraine. It was successfully treated by a single-day administration of praziquantel, 3 times 25 mg/kg after meals. A week later the patient was symptom-free and no eggs were found in the stool.
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PMID:[Opisthorchis felineus--the cat liver fluke. Differential diagnosis of right-side upper abdominal pain]. 154 52

Acalculous cholangitis and cholecystitis may occur in the course of AIDS. The symptoms are always the same: pain in the right upper quadrant, fever, nausea, vomiting, anorexia and diarrhoea, associated with biochemical signs of cholestasis, often without jaundice. Morphological explorations show thickening of the gallbladder wall and dilatation of the extrahepatic bile ducts, sometimes associated with stenosis of the major duodenal papilla and dilatation of the intrahepatic bile ducts.
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PMID:[Acalculous cholangitis and cholecystitis in two AIDS patients]. 182 15

Over the period of two weeks a 19-year-old man developed gradually increasing painless jaundice with dark urine and light-coloured soft stools (6-7 times daily), as well as loss of appetite, nausea and nagging itch. Biochemical tests indicated marked cholestasis (alkaline phosphatase 800 U/l, gamma-GT 206 U/l). Abdominal ultrasound examination revealed high-grade stenosis of the distal choledochal duct caused by an enlargement of the head of the pancreas and computed tomography confirmed a tumour in this location. Endoscopic retrograde cholangiopancreatography demonstrated filiform stenosis of the major pancreatic duct and prepapillary stenosis of the choledochal duct. Several needle biopsies failed to establish a definitive diagnosis. A Whipple operation was performed: the stomach was preserved but about 40% of pancreatic tissue resected. Histologically there was chronic suppurative pancreatitis of the head of the pancreas. The patient was symptom-free 6 months after the operation. The case illustrates that it is not always possible in a painless pancreatic tumour to distinguish between pancreatitis and malignant tumour.
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PMID:[Chronic purulent, draining, indolent pancreatic head pancreatitis with extrahepatic cholestasis]. 193 34

Cases are reported of two patients in whom acute hepatitis and cholestatic jaundice were induced by a tricyclic antidepressant, amineptine. A 29-year old woman received amineptine for 10 days before the onset of acute hepatitis. Slight jaundice and pruritus were preceded by fever, nausea and anorexia. The case is documented by a rapid return to normality of the liver function tests after amineptine was discontinued. We also report the case of a 55-year old woman to whom amineptine was administered for 4 weeks: she was admitted to our Department due to a 14-day history of pruritus and painless jaundice. Histological examination, in this case showed marked cholestasis without inflammatory infiltration. After suspending the treatment, it took 3 weeks for the liver function tests to return to normal. These observations, and the features of the cases published in the literature, suggest that amineptine can produce a wide spectrum of liver injuries, in different patients, taking the form of hepatocellular necrosis, cholestasis or a combination of both.
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PMID:Hepatic injury associated with amineptine therapy. 213 27

A 67-year-old black male diabetic who had never consumed alcohol presented with anorexia, weakness, weight loss, and jaundice. Ultrasound demonstrated common bile duct obstruction; computed tomography scanning revealed multiple liver masses; endoscopic retrograde cholangiopancreatography showed a filling defect; aortogram confirmed the neovascularity of tumor proliferation; and percutaneous transhepatic cholangiography confirmed high-grade common duct obstruction. Operative intervention demonstrated hepatocellular emboli to the common bile duct causing obstruction. We review the literature on this problem.
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PMID:Obstructive jaundice caused by hepatoma fragments in the common hepatic duct. 215 47

Halothane hepatitis is now a well-recognized distinct entity in adults, but there prevails an often-taught "axiom" that halothane hepatitis "does not occur" in children. We describe 2 children who developed cholestatic hepatitis following halothane anesthesia. The first patient had no antecedent liver disease, and presented with anorexia, abdominal pain and delayed onset of jaundice after multiple halothane exposures. Halothane-specific antibodies were positive, and liver tests resolved completely. The second patient had antecedent liver disease and presented with delayed onset of unexplained high fevers for 10 days following a single halothane exposure. Gradually increasing cholestasis ensued in the absence of other causes of liver disease. Halothane antibodies were negative. These cases illustrate different clinical presentations of halothane hepatitis, such as delayed onset of jaundice or fever following halothane exposure. The difficulties in making a definitive diagnosis and the need to exclude other causes of liver disease are detailed. Risk factors and other presentations are discussed. While halothane hepatitis appears to be an uncommon entity in children, it does occur, and may present with manifestations less than fulminant hepatic failure. A high index of suspicion and a detailed history of the time sequence of events are necessary as the diagnosis is primarily clinical. Halothane-specific antibodies are helpful if positive. In any child developing unexplained jaundice or high fevers following halothane anesthesia, further exposures should be avoided and halothane-specific antibodies obtained.
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PMID:Halothane hepatitis in children. 178 63

Alterations in serum lipid and lipoprotein concentrations in ponies with experimentally induced liver disease were investigated. Hepatocellular damage was induced, using a nonlethal dose of carbon tetrachloride. In a separate group of ponies, obstructive jaundice was induced by surgical ligation of the common bile duct. Over a 6-day period, blood samples were obtained from ponies after treatment with carbon tetrachloride and for 12 days in ponies subjected to surgery. Serum cholesterol and triglyceride concentrations were unaffected in both groups of ponies, except for significantly (P less than 0.01) high triglyceride concentration in ponies of the ligated group during the second postsurgical week. This increase was most likely attributable to anorexia observed during that period. Hyperbilirubinemia was observed early in ponies of the ligated group; most of the bilirubin was of the conjugated type. Using electrophoretic and ultracentrifugal methods, serum lipoprotein alterations were detected only in ponies of the ligated group. Increases of very low-density and low-density lipoprotein cholesterol concentrations and decrease in high-density lipoprotein cholesterol concentration were found. Although no changes were seen in total serum cholesterol concentration, a redistribution of lipoprotein cholesterol was observed in ponies of the ligated group. Similar alterations in lipoprotein distribution have been found in dogs, rats, and human beings with obstructive jaundice and cholestasis. The association between serum lecithin:cholesterol acyl transferase activities and these lipoprotein alterations remains to be elucidated.
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PMID:Serum lipid and lipoprotein changes in ponies with experimentally induced liver disease. 239 85

Differential diagnosis of viral hepatitis begins with a check for darkened urine and bile in the urine. These hallmarks of conjugated hyperbilirubinemia immediately rule out prehepatic liver disease. Next, studies are done for the elevated transaminase levels that are characteristic of hepatitis infection, and a thorough history is taken to rule out drug- and toxin-induced hepatitis that may mimic acute viral hepatitis. Elevated alkaline phosphatase is a good marker of cholestasis. Ultrasonography can clarify this diagnosis. The classic presenting symptoms of viral hepatitis are jaundice, nausea, vomiting, malaise, anorexia, and dull right upper quadrant pain. However, serologic studies are needed to detect the presence of specific viral agents.
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PMID:Viral hepatitis. The alphabet game. 305 Sep 28

A computer system for probabilistic diagnosis of jaundice was tested on a patient sample from a geographical area different from that for which it was first constructed. 144 consecutive patients with jaundice seen in two Stockholm hospitals were interviewed and examined to record a total of 82 indicants from history, demographic details, physical findings and laboratory tests. Data were compared with those of 319 jaundiced patients previously interviewed and examined at different London hospitals. It was found that disease incidences were different in the two patient samples. There were more patients with acute viral hepatitis, chronic active hepatitis and primary biliary cirrhosis in the London data base whereas the Stockholm data base included significantly more patients with Gilbert's syndrome and alcoholic cirrhosis. Indicant frequencies, standardised for disease incidence, differed with respect to age (Stockholm patients were on average six years older), time from onset of first symptom to hospital admission (Stockholm patients had on average a two-week shorter history of disease) and a number of symptoms such as nausea, vomiting, anorexia, weight loss, itching, pale stools and dark urine which were more frequent among the London patients. Differences in hospital admission policy was regarded as an important reason for the differences in indicant frequency. The results of probabilistic diagnosis were poor. Only 49% of the cases were correctly classified into twelve diagnostic groups. In particular the computer model was poor at separating different causes of malignant bile duct obstruction and at differentiating between malignant and benign bile duct obstruction. However, all cases of acute viral hepatitis were correctly classified and the computer model was 87% accurate in differentiating between medical and surgical jaundice. Reclassification of the 144 patients on their own data showed the computer system to be well calibrated and 97% of the cases were correctly classified according to this procedure. In conclusion, the computer system could not be directly transferred for use in a Swedish hospital but the results of reclassification were sufficiently encouraging to warrant prospective studies.
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PMID:Computer aided diagnosis of jaundice. A comparison of two data bases. 330 98


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