Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present pathologic findings for 52 livers (51 autopsy specimens and one wedge biopsy specimen) from patients with systemic lupus erythematosus (SLE). Hepatic congestion was the most common disease (40 livers), followed by fatty liver (38), arteritis (11), cholestasis (nine), peliosis hepatis (six), chronic persistent hepatitis (six), nonspecific reactive hepatitis (five), cholangiolitis (four), nodular regenerative hyperplasia of the liver (three), and hemangioma (three). The data obtained here suggest that arteritis of the SLE liver is more common than has been recognized previously. One patient had hepatic infarction complications induced by arteritis. On the basis of the findings in the present study and a review of the literature, we suggest that hepatic infarction resulting from arteritis is rare in SLE. On the other hand, while occurrence of nodular regenerative hyperplasia of the liver in SLE patients has been considered to be rare, our findings suggest that it may be more common than has been recognized previously. Although congestion and cholestasis may be acute terminal illnesses, fatty change is considered to be specific to the SLE liver. Statistical analysis indicates that exposure to a large dosage of glucocorticoids is a significant factor in the etiology of severe fatty liver. In addition, our review of Japanese autopsy registry data for 1,468 patients with SLE indicates that the incidence of chronic liver diseases in SLE autopsy cases is as follows: chronic hepatitis, 2.4%; cirrhosis, 1.1%; and liver fibrosis, 0.8%.
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PMID:The liver in systemic lupus erythematosus: pathologic analysis of 52 cases and review of Japanese Autopsy Registry Data. 139 43

An overview about drug-induced liver injury is presented. The most frequent changes of the hepatocytes are those of the organelles, which are adaptive at the beginning, but in later stages they can develop to degenerative alterations leading to necrosis. Cases of drug-induced hepatitis simulating all types of non-suppurative hepatitis are a major problem of diagnosis. Bile duct lesions can include pure cholestasis, cholangiolitis and destruction of intrahepatic ducts. Drug-induced vascular lesions including tumours can be found as isolated phenomenon or in association with other signs of drug-induced liver damage. Hyperplasia (focal or diffuse) and neoplasia of the liver can develop in the course of a longstanding application of some drugs.
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PMID:[Drug-induced liver damage from the morphologic viewpoint]. 220 23

Fifty-five chemoinfusion devices have been implanted in patients with metastasis of colorectal cancer confined to the liver. There were no episodes of pump malfunction or of catheter clotting. Side effects included gastric ulcers in 13 patients and duodenal ulcers in four patients, including one episode of total gastric obstruction. Chemical hepatitis occurred in 13 patients, sclerosing cholangiolitis in one patient, and duodenal dismotility requiring gastroenterostomy in one patient. The response criterion was taken as reduction by at least 50% of the pretreatment carcinoembryonic antigen level; consequently, the response rate was 88%. Median survival of all patients was 19.2 months from the time of diagnosis of hepatic metastases to death, as determined by the Kaplan-Meier method. Median survival from the time of pump implantation to death was 10.1 months.
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PMID:The use of the implantable chemoinfusion pump in the treatment of hepatic metastases of colorectal cancer. 294 51

We retrospectively evaluated the utility of hepatobiliary scintigraphy and various clinical factors in differentiating intrahepatic cholestasis from biliary atresia in 28 consecutive infants with neonatal cholestasis. One millicurie of technetium-labeled diisopropyliminodiacetic acid (DISIDA) was administered intravenously, and images were obtained for up to 24 hours or until gastrointestinal excretion was noted. Nine separate studies in seven infants with biliary atresia were correctly interpreted as showing no gastrointestinal excretion of radionuclide. Of the 21 patients with intrahepatic cholestasis, only nine had gastrointestinal excretion on the first study; in eight without excretion, a second study was done, and five of these showed gut excretion. All infants with either neonatal hepatitis (six) or inspissated bile syndrome (three) had demonstrable gastrointestinal excretion either on the first or second DISIDA study. However, five of six infants with paucity of intrahepatic bile ducts, two of six infants with cholestasis secondary to total parenteral nutrition, and one infant with cholangiolitis did not show evidence of gastrointestinal excretion. The mean birth weight, mean gestational age, and mean weight at study were significantly greater (P less than 0.005) for infants with biliary atresia without excretion than for infants with intrahepatic cholestasis without excretion. The mean direct bilirubin concentration was 6.0 mg/dL for both infants with biliary atresia and infants with intrahepatic cholestasis without excretion; however, infants with excretion had a significantly lower (P less than 0.02) mean direct bilirubin value of 3.4 mg/dL. Excretion was noted in four infants with total bilirubin values greater than 10.0 mg/dL. The absence of gut excretion on the first DISIDA study was 100% sensitive but only 43% specific for biliary atresia. In infants without gut excretion of DISIDA, birth weight greater than 2200 g was 100% sensitive and 92% specific for biliary atresia. We conclude that DISIDA scanning, together with clinical data, is useful in differentiating extrahepatic from intrahepatic cholestasis. The absence of gut excretion on the first DISIDA study does not necessarily indicate extrahepatic obstruction; the study should be repeated if the diagnosis is not clear.
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PMID:Diagnostic utility of hepatobiliary scintigraphy with 99mTc-DISIDA in neonatal cholestasis. 358

Morphologically identical liver damage may be caused by dihydralazine (Depressan, Nepresol) and propranolol (Obsidan, Dociton). Among 24 patients with clinical manifestations of drug-induced hepatitis associated with Depressan or Obsidan treatment, liver biopsies in 15 showed drug hepatitic changes with confluent necrosis. In five of these cases this finding was combined with cholangiolitis, in four there was a drug-induced hepatopathy resembling the picture of viral hepatitis. In 20 cases of Ketazon-induced liver damage the biopsy demonstrated toxic hepatosis with or without cholestasis, reactive hepatitis or cholangiolitis. A drug-related hepatitis with central lobular necrosis was observed in one patient with Ketazon-induced liver damage. In 28 patients a lymphocyte proliferation test was undertaken to confirm a causal relationship between the use of either Depressan, Obsidan or Ketazon and the morphologically demonstrated liver damage. The test was positive in 25 cases (18 with Depressan, 2 with Obsidan and 5 with Ketazon). In several uncertain cases, for example, exposure to both Depressan and Obsidan or to Ketazon and Rewodina, the morphologic picture could be attributed to a specific medication by the use of the lymphocyte proliferation test. The results of the lymphocyte proliferation test and the morphologic findings emphasize the role of cell-mediated immune reactions in the pathogenesis of liver damage from dihydralazine, propranolol, and ketophenylbutazone.
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PMID:[Morphology and pathogenesis of liver injury produced by dihydralazine , propranolol and ketophenylbutazone]. 384 42

The antihypertensive drugs dihydralazine and propranolol can produce identical liver injuries which must be distinguished clinically and morphologically from acute viral hepatitis. In 19 cases selected from our biopsy file during the last two years, clinical and morphological findings suggested that the liver injury diagnosed by light microscopy had been caused by an adverse reaction to dihydralazine and/or propranolol. In order to establish a causal relation the lymphocyte proliferation test (LPT) was performed with dihydralazine in 11 cases. Positive results were observed in 9 cases, demonstrating an etiologic role for dihydralazine in liver injury in these cases. The dihydralazine and/or propranolol induced liver injury consisted mainly of drug-induced hepatitis with confluent (bridging) necrosis. Different findings were observed in three cases: In two of these drug-induced hepatitis with confluent necrosis was observed together with eosinophilic cholangio-cholangiolitis. In one other case the histologic changes corresponded to drug hepatitis resembling viral hepatitis. Each of the three cases showed conspicuous centrolobular cholestasis, a feature which is unusual in drug-induced hepatitis with confluent necrosis irrespective of serum bilirubin levels. In one third of our cases we found morphological features of hypersensitivity reactions in the liver biopsies. Considered together with the results of LPT these features emphasize the role of cell mediated immune reaction in the mechanism of liver injury caused by dihydralazine and/or propranolol.
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PMID:[Liver lesions induced by dihydralazine and propranolol]. 398 41

Cimetidine-induced liver injury has only very rarely been reported. Three patients are described who developed signs of hepatic damage after the institution of cimetidine therapy. Transient signs of acute liver failure were noticed in one patient. Histologically, a cytotoxic type of injury with centrilobular confluent and bridging portal-central necrosis, accompanied by a mixed mono- and polymorphonuclear infiltrate with signs of cholangiolitis in the portal tracts was observed in two patients, whereas a hepatocanalicular type of cholestatic hepatitis was noticed in another patient. It is proposed that the mechanism of cimetidine-induced liver injury may vary in different patients: it may be due either to a 'metabolic idiosyncrasy' because of the production of hitherto unknown toxic metabolites or to a hypersensitivity reaction.
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PMID:Cimetidine-induced liver injury. Report of three cases. 405 48

Cholestasis is a combination of defined clinical, paraclinical and morphological findings of which icterus is the direct symptom. It is the consequence of the delay or detention of the bile flow. By means of light microscopy different changes can be observed in hepatic tissue: formation of biliary thrombi, intracellular deposition of biliary components, ductal cholestasis with dilatation of the bile-duct lumina and applanation of the bile-duct epithelium, ductular proliferates and furthermore inflammatory mesenchymal reactions with cholangiolitis and cholangitis. These changes strengthen in dependence on the intensity and duration of the existing cholestasis. Bile lakes, bile extravasates, and biliary infarctions may occur in the process. The differentiation between intrahepatic non-mechanically and (extra-)hepatic mechanically conditioned cholestasis is of clinical importance. In the former the production and secretion of bile is disturbed (hepatosis, hepatitis and others), in the latter the extrahepatic bile ducts are above all affected: the bile flow is disturbed by stenosis, compression and obturation. The differentiation between the two kinds of cholestasis is impossible in the first three weeks because both of them develop identical lesion patterns. Distinguishable changes occur only after that. Consequently, findings from liver biopsy can only be a statement of probability. Reliable differentiation between the two kinds of cholestasis is however possible by means of modern technical methods for diagnostic purposes.
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PMID:[Histological changes in liver tissue in cholestasis]. 748 20

We report a case of ductopenia associated with cholestatic hepatitis in a 59-year-old woman treated for 41 years for temporal epilepsy. The patient developed jaundice, without any clinical or biochemical features of hypersensitivity, 10 months after the beginning of treatment with sulpiride. Liver biopsy showed ballooning and acidophilic degeneration of the hepatocytes, macrophages packed with lipofuscin, biliary pigment in Kupffer cells, some biliary plugs, confluent necrosis and absence of biliary ducts in all the portal tracts. These features and the presence of foci of cholangiolitis suggest a destructive cholangitis as the pathogenetic mechanism causing ductopenia. Other causes of ductopenia were excluded. Sulpiride is known to produce severe cholestatic jaundice, which we believe is due to ductopenia. The absence of hypersensitivity and the 10-month latency suggest that sulpiride may cause liver damage through a toxic mechanism in genetically susceptible subjects.
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PMID:Bile ductopenia following therapy with sulpiride. 758 54

Eleven cases of hepatic injury attributed to the intake of flucloxacillin were reported to the Netherlands Center for Monitoring of Adverse Reactions to Drugs between 1982 and 1992. They concerned four men and seven women, with a mean age of 57 years, treated for 2-28 days with an oral dose varying from 1500-4000 mg per day. Symptoms mostly appeared 10 to 30 days after starting treatment with flucloxacillin. Biochemically, the pattern was compatible with cholestatic hepatitis in seven cases, with a mixed cholestatic-hepatocellular type of injury in one case, a hepatocellular pattern in two cases, and mild liver enzyme elevations in one patient. Two patients died, one due to fatal bleeding from the liver after biopsy, and the second patient to a combination of hepatic and cardiac failure. The other patients recovered, on average 72 days after peaking of serum aminotransferase values. Histology in seven cases showed cholestatic hepatitis in five, with cholangitis or cholangiolitis in four of these patients. In the other two patients, there was centrilobular cholestasis with extensive bridging fibrosis and portal-central bridging necrosis, respectively.
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PMID:Flucloxacillin-associated hepatic injury. 799 79


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