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)

Serum enzymes are sensitive tools for demonstration of injury to different organs of the body, including lesions that are side effects of drugs or the application of certain compounds for diagnostic purposes. It has been reported that tuberculosis therapy can cause liver damage of the unpredictable drug-induced liver lesion-type. The liver lesions due to tuberculostatics resemble an unspecific or viral hepatitis. Oral contraceptives can also cause hepatic lesions, some of them being quite serious. They have been known to cause hepatosis with or without cholestasis, drug-induced hepatitis, circulatory disturbances such as hepatic peliosis and Budd-Chiari syndrome, and benign and malignant tumors. Therapy control should be instituted in these cases. Enzymes can be used as indicators. A considerable increase of coeruloplasmin (or serum copper) is a useful marker for monitoring contraceptive medication; the aminotransferases initially show a slight increase while later, they may be decreasing to subnormal values. The appearance of serious morphological findings may necessitate delineation of normal ranges and alarm ranges. Serial enzyme determinations are suggested in: 1) high risk patients who have been suffering from hepatitis or intrahepatic cholestasis due to pregnancy or drugs, and 2) in persons complaining of signs or symptoms suggestive of liver involvement. The kidney is another organ which might be influenced by certain drugs leaving the organism via the urinary tract. The presence of enzymes in urine can serve as sensitive indicators of a proximal tubular lesion. The effects of certain hormones on the kidneys are discussed.
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PMID:A review of enzyme changes in serum and urine due to treatment with drugs (tuberculostatics, contraceptive medication, diagnostics and drugs in real diseases). 626 69

Many hepatic lesions, ranging from subcellular alterations to malignant tumors, have been attributed to the use of anabolic steroids (AS) and contraceptive steroids (CS). These lesions that have been attributed to AS and CS are discussed with focus on the following: biochemical changes; subcellular alterations; intrahepatic cholestasis; vascular complications (sinusoidal dilatation, peliosis hepatitis, Budd-Chiari syndrome); hyperplasia and neoplasia (diffuse hyperplasia, nodular transformation, focal nodular hyperplasia, hepatocellular adenoma, hepatocellular carcinoma, and miscellaneous malignant tumors); and miscellaneous effects (effects of preexisting liver disease, cholelithiasis, and pancreatitis). OCs have a number of physiologic effects on the liver. These include decreased bile flow, diminished secretion of organic anions, and decreased synthesis and secretion of bile acids. Retention of bromosulfophthalein has been noted with AS during late pregnancy and in the puerperium. It is well established that the CS can lead to elevations of serum ceruloplasmin and copper levels. Subcellular alterations have been reported in both humans and rats on AS or women on CS and involve multiple organelles of the several systems of the liver. Both AS and CS have been implicated in intrahepatic cholestasis. Jaundice usually develops after 2-5 months of therapy with AS or after 3 months of OC use. The lesions attributed to CS and AS can involve any of the systems of the liver. At times more than 1 system is affected simultaneously. Most of the steroid related lesions resemble similar ones caused by other etiologies. Some, such as peliosis hepatitis, are rarely related to other etiologies, but others can be termed steroid specific. A number of diseases associated with the CS or AS also occur in pregnancy. Acute fatty metamorphosis of pregnancy and the periportal hemorrhagic necrosis characteristic of eclampsia have not been reported in patients on CS. Spontaneous rupture of the liver during pregnancy has not been attributed to the CS.
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PMID:Hepatic lesions caused by anabolic and contraceptive steroids. 628 45

We describe the clinico-pathological characteristics of hepatic injury associated with the toxic-epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic-epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life. No statistical significance was found in relation to alcohol consumption, treatment with potentially hepatotoxic antibiotics, or adult respiratory distress syndrome. Most (91.6%) patients with hepatic injury were asymptomatic; jaundice or abdominal pain was rarely noted. One patient died of acute liver failure following Budd-Chiari syndrome. Serum gamma-glutamyl transpeptidase activity was raised in all cases, alkaline phosphatase in 94.6%, and less frequently lactate dehydrogenase (80%), SGPT (84.7%), and SGOT (76%). Serum total bilirubin was usually normal (89.2%). The histologic lesion was similar to drug-induced cholestatic hepatitis. Lamellar inclusions, canalicular injury, giant mitochondria, and hyperplasia of the smooth endoplasmic reticulum were seen by electron microscopy. Ultrastructural signs of cholestasis were common (78.9%). The pathogenesis of this lesion is unknown; however, because of similarities with chlorpromazine-induced cholestatic hepatitis, we suggest that a combination of hypersensitivity and intrinsic hepatoxicity is a possible mechanism.
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PMID:Hepatic injury in the toxic epidemic syndrome caused by ingestion of adulterated cooking oil (Spain, 1981). 669 64

Alcoholics with abnormal liver function tests are generally assumed to have one of the recognised patterns of alcoholic liver injury. This report described a group of nine patients who were initially thought to have alcoholic liver disease but were found on liver biopsy to have a variety of liver disorders unrelated to alcohol. Liver biopsy showed granulomatous hepatitis in three, primary biliary cirrhosis in two, and cholestasis of unknown cause, large duct biliary obstruction, haemochromatosis with secondary carcinoma and Budd-Chiari syndrome in one each. The histological changes observed in liver biopsy samples are believed to represent a chance occurrence of liver disease due to some agent other than alcohol and illustrates that forms of hepatic disease that affect the population at large can and do occur in heavy alcohol consumers.
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PMID:Alcohol unrelated hepato-biliary disorders in the alcoholic: the role of liver biopsy in determining the aetiology of liver disease. 695 38

A case is described wherein a 29 year old woman was admitted to the hospital because of the possibility of a hepatic tumor; symptoms included abdominal pain, diffuse hepatic enlargement and absence of uptake in an area of the right hepatic lobe. After a normal pregnancy and delivery 11 years earlier the patient used oral contraceptives (OCs) composed of norethindrone with mestranol until 8 years before entry; 5 years before admission she resumed use of an OC containing norethindrone and ethinyl estradiol. She smoked 1.5 packages of cigarettes and drank 1 glass of wine daily, and there was no history of nausea, vomiting, melena, jaundice, dark urine, light stools, hepatitis, or blood transfusions. Benign lesions which are known to be caused by OCs fall into 2 groups: designated focal nodular hyperplasia and liver-cell adenoma. The evidence linking the latter with OCs is more convincing since in case-controlled studies the risk of development of adenomas has been shown to increase with the estrogen strength of the OCs and duration of use; in women who have been taking OCs over 7 years the relative risk is 500 times that for matched control nonusers. The vascular complications of OC therapy include Budd-Chiari syndrome, peliosis hepatis, and periportal sinusoidal dilatation. The patient in this case was diagnosed to have periportal and midzonal hepatic sinusoidal dilatation association with OC medication. She underwent an operation on her liver which proved to be successful combined with cessation of OC use. The mechanism by which OCs cause these lesions is not known. In 5 of 13 cases similar to the one described here clinical and biochemical abnormalities resolved and 1 patient had a follow-up liver biopsy that revealed normal findings 10 months after cessation of OC therapy; there is no evidence to suggest that sinusoidal dilatation is irreversible.
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PMID:Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 40-1982. Tender hepatomegaly in a 29-year-old woman. 711 Feb 74

Drug injury of the liver presents as I. functional disorder without jaundice; 2. predominant cholostatic disease; 3. predominant hepatitic disease; 4. a combination of 2 und 3.--A predictable dose related direct toxic injury can be differentiated from an unpredictable dose independent indirect injury mostly of the hypersensitivity type. Special varieties are severe fatty liver, peliosis, Budd-Chiari-Syndrome, liver tumors and granulomas. The diagnosis can be proven by reexposition or better--by the in vitro lymphocyte stimulation test. --There is no specific treatment apart from stopping the responsible drug. Prognosis is good but in some cases a chronic course develops presenting as chronic aggressive hepatitis or cirrhosis.
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PMID:[Liver damage caused by drugs]. 716 50

We reviewed 37 living related liver transplantations (LRLT) performed by our department during the last 27 months on children with end-stage liver disease. The patients were 15 boys and 22 girls aged 7 months to 15 years with biliary atresia (27), cryptogenic cirrhosis (3), Budd-Chiari syndrome (2), progressive intrahepatic cholestasis (2), protoporphyria (1), Wilson's disease (1), and fulminant hepatitis (1). The donors were 14 fathers and 23 mothers. Grafts were made from the left lateral segment (19), left lateral segment with partial S4 (11), left lobe (6), and right lobe (1). After graft harvesting all donors resumed normal liver function and normal life. The recipient underwent total hepatectomy with preservation of the inferior vena cava. FK506 and low-dose steroids were used for immunosuppression. The survival rate was 90% (27/30) in elective cases and 57% (4/7) in emergency cases. Six recipients had functioning grafts but died of extrahepatic complications. Hepatic vein stenosis occurred in 3 cases at 3 months after LRLT and was successfully treated by balloon dilatation. Portal vein stenosis occurred in 1 case at 8 months after LRLT and was also safely dilated. We incurred no hepatic artery thrombosis after introducing microsurgery techniques. Among 12 viral, 5 bacterial, and 3 fungal postoperative infections, 1 Candida pneumonia and 1 EBV-associated lymphoma were lethal. Three patients with ABO-blood group compatible grafts and one with an incompatible graft developed acute rejection, which was controlled in evey case by steroid bolus and/or increasing the dose of FK506. There were no definite episodes of rejection in ABO-identical cases. Children with moderate growth retardation (> or = -1.5 SD of normal growth) caught up in growth soon after LRLT, but those with severe retardation (<-1.5 SD) were slow to attain age-normal height. Appropriate timing, meticulous surgical procedures, and comprehensive management of complications are crucial for successful outcome with LRLT. LRLT is a promising option for alleviating the shortage of livers for pediatric transplantation and may be regarded as an independent modality to supplement cadaver donation.
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PMID:Living related liver transplantation in children. 751 49

From more than 900 articles in the medical literature, published between August 1, 1991 and July 31, 1992, 46 were selected for review. During the year of review, major international symposiums were held on a new drug, FK506, and intestinal transplantation. In addition, at least one new attempt at a unifying hypothesis regarding graft adaptation was proposed. Other studies included living related donor transplantation, results with transplantation for alcoholics, and the controversy regarding the role of liver transplantation for the treatment of Budd-Chiari syndrome. Concerns regarding the recurrence of both hepatitis and primary hepatic malignancy following liver transplantation were also addressed. Two innovative approaches to the treatment of acute liver failure offer exciting promise for the future. Other subjects include histologic evaluation of renal dysfunction in patients with liver disease, quality of life after transplantation, and the proper distribution of precious donor livers.
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PMID:Liver transplantation. 758 80

During the last 31 months, 50 children between 3 months and 15 years of age have undergone living related liver transplantation (LRLT) for end-stage liver diseases (39 biliary atresia, 2 Budd-Chiari syndrome, 2 progressive intrahepatic cholestasis, 3 liver cirrhosis, 1 Wilson disease, 1 protoporphyria, 1 tyrosinemia, and 1 fulminant hepatitis). Combined FK-506 and low-dose steroids were routinely used for immunosuppression. There were seven deaths, two of which were related to infection (Candida pneumonia and Epstein-Barr virus [EBV]-associated lymphoproliferative syndrome [LPS]). Five patients had a bacterial infection, all of which were associated with surgical complications. Three patients had Candida infection, all of which were malnourished, had biliary atresia, and had been managed with prolonged antibiotics against obstinate ascending cholangitis. There were 14 symptomatic viral infections (1 herpes simplex virus, 1 herpes zoster virus, 5 cytomegalovirus [CMV], 6 EBV, and 1 EBV-associated LPS). Three of the five CMV infections appeared in patients whose graft was ABO-incompatible, who were managed with prophylactic OKT-3. Most of the viral infections (except 1 EBV-associated LPS) were minor and were treated successfully. The low incidence and successful treatment of CMV infection are related to the high compatibility and low incidence of allograft rejection in LRLT. Bacterial and fungal infections can be decreased by greater refinement of surgical technique and more aggressive preoperative management. Treatment of EBV infection is still an unsolved problem.
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PMID:Infectious complications in living related liver transplantation. 801 5

Patients with systemic lupus erythematosus (SLE) have a 25-50% chance of developing abnormal liver tests in their lifetime. This percentage does not include unconjugated hyperbilirubinaemia due to haemolysis associated with SLE, or elevated aspartate-aminotransferase caused by SLE-associated myositis. The most common cause is drug-induced hepatitis, while mild, predominantly lobular-but sometimes also portal and periportal-hepatitis reflecting SLE activity is another possibility. Other liver disease in SLE can be related to thrombotic events, whether or not associated with the lupus anticoagulant, including Budd-Chiari syndrome and veno-occlusive disease. Other liver abnormalities have been more or less frequently associated with SLE, such as nodular regenerative hyperplasia, perihepatitis, and hepatic or splenic rupture. Also viral hepatitis, obstructive jaundice, autoimmune hepatitis, primary biliary cirrhosis, granulomatous hepatitis, cryptococcus infection of the liver, chronic hepatitis with IgA or IgD deficiency, porphyria or idiopathic portal hypertension co-existing with SLE have been described.
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PMID:The spectrum of liver disease in systemic lupus erythematosus. 871 47


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