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)

The jejuno-ileal bypass for weight reduction can hardly be considered a non-specific treatment: 3-4% of the patients develop chronic hepatic damage, 1-2% suffer hepatic failure due to massive fatty liver, rapidly progressing liver cirrhosis or hepatic fibrosis. Fatty liver is an invariable sequel of this operation. Once the above-mentioned symptoms set in or an incipient cirrhosis or fibrosis is diagnosed, immediate restoration of normal passage is required. The intestinal bypass syndrome observed in the patient (fem.) (viz. table 1) does not wholly coincide with the enteral bile acid loss syndrome occurring in extensive ileum resection (56) where usually there is no evidence of fatty liver, icterus, cholestasis or encephalopathy. Animal experiments seem to confirm that the blind loop in the broadest sense of the term is responsible for the sometimes fatal hepatic damage. Possibly we are confronted here with a pattern of hepatic damage due to toxic nutritive effects similar to cirrhosis as a sequel of low-protein and low-calorie intake or to the phenomenon observed in animal experiments. The cholestasis confirmed by biopsy and chemical methods is a manifestation of these hepatic disorders. The clinical aspects resemble the Reye syndrome that we know in pediatrics. Patients have to be carefully selected and informed about possible postoperative damage; a continuous clinical follow-up with biopsy of the hepatic tissue is also indicated.
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PMID:[Liver damage following intestinal by-pass surgery for weight reduction]. 122 12

Aluminum remains a significant contaminant of total parenteral nutrition (TPN) solutions and may be elevated in bone, urine, and plasma of infants receiving TPN. Aluminum accumulation in tissues of uremic patients and adult TPN patients has been associated with low-turnover bone disease. Furthermore, aluminum has also been linked with encephalopathy and anemia in uremic patients and with hepatic cholestasis in experimental animals. Because of the toxic effects of aluminum, the Food and Drug Administration (FDA) recently published a notice of intent to set an upper limit of 25 micrograms/L for aluminum in large-volume parenterals and to require manufacturers of small-volume parenterals, such as calcium and phosphate salts, to measure aluminum content and note this content on the package label. The ASCN/A.S.P.E.N. Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions supports these intentions and further urges the FDA to require that cumulative aluminum intake in terms of safe, unsafe, and toxic quantities of aluminum per kilogram be made known to physicians and pharmacists preparing the TPN solutions, to ensure that manufacturers use appropriate control procedures in aluminum measurements, and to employ a standard unit of aluminum measurement.
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PMID:Parenteral drug products containing aluminum as an ingredient or a contaminant: response to Food and Drug Administration notice of intent and request for information. ASCN/A.S.P.E.N. Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions. 173 29

Part II: The side-effects of Sandimmune that have also been observed clinically include hepatic dysfunction, glucose intolerance, thrombo-embolic complications and nervous system disorders. To determine the cause and significance of such effects, the actions of Sandimmune on the liver, the pancreas, on hematostasis and the nervous system were examined. Comparisons were made between animal and human data obtained in vivo and in vitro, and the clinical setting under which the side-effects occur was analyzed. The actions of Sandimmune on the liver seem to reflect mostly a cholestasis with a small depression in protein synthesis and a mild disturbance in lipid metabolism of uncertain origin. The action of Sandimmune on the pancreas suggests insulin resistance and possibly a secretory disturbance, with no evidence for depressed insulin synthesis, except in animals at high doses. Sandimmune does not seem to promote thromboembolism in man, although fibrinolysis may be depressed and platelet aggregation can be enhanced. The effects of Sandimmune on the nervous system are unclear, for tremor is common but of uncertain origin, whereas seizures and encephalopathy are rare and invariably associated with other risk factors.
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PMID:The pathophysiology of Sandimmune (cyclosporine) in man and animals. 208 72

In view of increasing therapeutic possibilities interest focuses on prognosis of liver cirrhosis. Until nowadays studies on prognosis revealed significant importance only for some parameters: Ascites, encephalopathy and portal hypertension as signs of decompensation, bilirubin, albumin and prothrombin time as laboratory indices of decreasing liver function. The commonly used Child-Pugh-score is based on these parameters and allows a reasonable classification of diseased patients. Cholestasis and inflammation seem to be of minor prognostic importance. Assessment of liver function by quantitative tests is desirable (e.g. aminopyrine breath test, bile acids). The prognostic value, however, has not yet been proven in large studies. Use of these tests should therefore be restricted to studies (prognosis, therapy, indication to liver transplantation).
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PMID:[The prognostic value of liver function tests--clinical aspects, laboratory chemical parameters and quantitative function tests]. 219 10

Non-narcotic analgesics can produce a variety of hepatic lesions but clinically significant liver damage is uncommon with normal therapeutic use. The pattern of hepatotoxicity caused by the salicylates, non-steroidal anti-inflammatory drugs (NSAIDs), paracetamol (acetaminophen) and the pyrazolones differs but many of these drugs can cause generalised reactions which involve the liver. Depending on the drugs in question, the risks of liver injury may be conditioned by factors such as age, sex, dose and duration of treatment. Hepatotoxicity associated with the use of salicylates and most NSAIDs has been reported most often in females with collagen diseases but this may simply reflect the greater use of these drugs in such patients. Paracetamol-induced liver damage occurs almost exclusively as a result of overdosage. Except for the microvesicular fatty changes in hepatocytes in patients with Reye's syndrome attributed to salicylate, the acute centrilobular necrosis caused by paracetamol in overdosage and the marked cholestasis produced by benoxaprofen, the pathological changes in hepatic reactions to non-narcotic analgesics are rather variable and nonspecific. About 50% of patients given salicylate in full anti-inflammatory dosage develop minor abnormalities of liver function. There is usually a mild to moderate increase in plasma aminotransferase activity with patchy necrosis and degeneration of hepatocytes. These changes are related to plasma salicylate concentration and are usually rapidly reversible. In a small minority of patients, particularly the young, liver damage is more severe and may be associated with liver failure, acidosis, hypoglycaemia and encephalopathy. This picture closely resembles Reye's syndrome. In overdosage, paracetamol can cause acute hepatic necrosis. Without specific treatment, some 8% of adults suffer severe liver damage with plasma aminotransferase activity greater than 1000 U/L and about 1% die with hepatic failure and encephalopathy. The administration of sulfhydryl compounds such as N-acetylcysteine within 8 to 10 hours effectively prevents liver damage and death. Liver damage has been attributed to the therapeutic use of paracetamol. However, in most reports the dose was excessive and many patients were chronic alcoholics (who seem to be at increased risk). In these cases the features were typical of acute overdosage. A consistent and characteristic pattern of hepatotoxicity is evident with relatively few non-steroidal anti-inflammatory and pyrazolone analgesics. A rank order of relative risk cannot be established and the incidence in relation to use is not known.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Liver damage with non-narcotic analgesics. 354 1

In a prospective study carried out on a group of 1210 patients with liver cirrhosis (LC), the diagnosis was based on clinical, biological and histological criteria, as well as on the prognostic significance of 20 clinical, biochemical and histological parameters. The group, including 830 males (68.59%) and 380 females (31.41%), with an average age of 49.27 +/- 13.18 years, was studied during periods of 6 to 16 months, the initial investigations being periodically repeated. The statistical significance of the prognosis factors was studied by uni- and multivariative methods, according to the model of Cox, with the help of an IMB computer. The survival rate for the group studied ranged from 6 to 204 months, with an average period of survival of 38.29 months. The multivariative analysis demonstrated that the prognosis factor with a best correlation with the death power is ascites, which has additional predictive significance in association with encephalopathy and/or jaundice. The multivariative analysis selects as clinical factors of unfavourable prognosis the cholestasis, the hepatocytolytic syndrome, the syndrome of liver deficiency and the age over 50. The limits of the biochemical parameters with unfavourable significance were: bilirubinemia level greater than 3 mg%, ASAT/ALAT = 50.24/70.33 u.i., prothrombinemic index less than 50% and albuminemia greater than 3 g%. The multivariative method proved also superior in appreciating the interrelations of the prognostic factors, emphasizing the significance of the clinical parameters (ascites, encephalopathy, jaundice), while the multivariative analysis differentiated the biochemical prognosis factors (bilirubinemia, ASAT/ALAT, prothrombinemic index, albuminemia) and their level of significance.
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PMID:Study of the prognosis factors in liver cirrhosis. 365 5

The diagnosis and treatment of a case of lead poisoning in a cynomolgus monkey (Macaca fascicularis) are described. The clinical signs were jaundice and amaurosis. Clinicopathological findings suggested cholestasis. A tentative diagnosis of lead poisoning was made when basophilic stippling of erythrocytes was observed in a peripheral blood smear. The diagnosis was confirmed by finding a lead concentration of 2280 micrograms/litre in a venous blood sample. Cage bars painted with red lead appeared to be the source of the poison. The lead was chelated by the intramuscular administration of 2,3 dimercapto-1-propanol (BAL) and calcium disodium edetate for seven days, followed by oral D-penicillamine for five weeks. The encephalopathy was treated with dexamethasone sodium phosphate. Recovery from the blindness was noted after 10 days and marked improvement of the general well being of the animal was observed after one month.
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PMID:Icterus and amaurosis caused by lead poisoning in a cynomolgus monkey (Macaca fascicularis). 395 44

Effectiveness of surgically induced acute hepatic failure in pig and most suitable time to apply artificial support in hepatic coma are evaluated in this work. Five male pigs weighing about 30-35 kg are employed. Latero-lateral porto-caval shunt was performed; the vascular disconnection of liver was obtained by ligature of blood vessels. Ligature was also placed on main biliary way after cholecistectomy. Blood samples were obtained (at 0, 1, 2, 6, 12, 18, 24 hours) to essay serum bilirubin, alkaline phosphatase and GOT-GPT levels as index of cholestasis and necrosis. Porto-caval encephalopathy was evaluated by means of serum ammonium levels, aminoacid pattern and E.E.G. Serum aminoacid pattern was carefully determined; its changes were found similar in man during coma. All pigs died 24-36 hours after surgery with liver ischemic and necrosis. Clinical and laboratory data obtained in experimental conditions were found similar to picture of acute hepatic failure in man, confirming validity of our model.
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PMID:[Acute experimental hepatic insufficiency in pigs. Validity of a model with biohumoral and electroencephalographic monitoring]. 667 5

In order to assess the prevalence of venocclusive disease in autopsied recipients of bone marrow transplantation, we reviewed coded liver histology from 204 consecutive autopsied recipients transplanted for leukemia (142), other malignancies (5), or aplastic anemia (57). Twenty-seven patients with leukemia, 2 with carcinoma, and 3 with aplasia had venocclusive disease and survived 2-86 days post-transplant. Early lesions showed subintimal edema and hemorrhage within small central venules and centrilobular congestion with hepatocyte degeneration. Later lesions showed subtotal to complete fibrous obliteration of the central venule lumina and centrilobular sinusoidal fibrosis. Thirteen patients had a subclinical course, and 19 were symptomatic. Venocclusive disease was life-threatening or lethal in 13. Typical symptoms developed 1-3 wk post-transplant and consisted of sudden weight gain, hepatic enlargement, ascites, high bilirubin, and encephalopathy. Statistical analyses showed a significantly higher prevalence of venocclusive disease associated with transplantation for leukemia (P = 0.014), pretransplant conditioning with more rigorous chemoradiotherapy regimens (P < 0.001) and three- to fourfold increase of venocclusive disease in patients whose conditioning included dimethyl busulfan (P < 0.005). Abnormal liver tests before transplant were also more prevalent among patients with venocclusive disease. No factors predicted the clinical outcome of established venocclusive disease. Venocclusive disease showed no association with hepatic graft-versus-host disease even among prolonged cases with severe periportal hepatitis and cholestasis. Other centrilobular lesions (hepatocyte degeneration, sinusoidal fibrosis, and phlebosclerosis) were identified in 23 patients. These non-specific changes may occur with viral hepatitis, graft-versus-host disease or chemoradiotherapy effects.
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PMID:An analysis of hepatic venocclusive disease and centrilobular hepatic degeneration following bone marrow transplantation. 700 4

Endogenous digitalis-like factor (EDLF), an inhibitor of membrane Na+/K(+)-ATPase, is discussed to be involved in the pathogenesis of cirrhogenic portal hypertension, ascites formation and development of functional hepatorenal failure. Therefore, we investigated the serum content of this mediator in patients with liver cirrhosis Child-Pugh stage A, B, and C (n = 27) by means of enzyme immunoassay with a specific digoxin antibody. Furthermore, a correlation analysis was performed in order to find out correlations between signs of cell injury, cholestasis, synthetic cell function, ascites formation, and hepatorenal failure. Our results demonstrate that EDLF is significantly elevated in Child C cirrhosis (0.61 +/- 0.15 ng/ml) in comparison to Child A cirrhosis (0.013 +/- 0.2 ng/ml) and is also higher than in Child B cirrhosis (0.23 +/- 0.25 ng/ml). In patients without ascites EDLF (0.056 +/- 0.19 ng/ml) differs significantly from that of patients with non-complicated ascites (0.156 +/- 0.176 ng/ml) and from that of patients with therapy refractory ascites (0.66 +/- 0.17 ng/ml) or hepatorenal failure (1.56 ng/ml). There are no correlations between EDLF and renal function. Significant correlations were demonstrated for cholestasis (serum bilirubin), synthesis function (serum protein, Quick's value, cholinesterase, fibrinogen, albumin), and the degree of portasystemic encephalopathy (number connection test). We conclude that EDLF may act as a mediator in the process of progressive portal hypertension and its complications due to cirrhosis. This process of progression is caused by the inhibition of Na+/K(+)-ATPase, vasoconstriction, and endothelin secretion.
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PMID:[Endogenous digitalis-like factor in liver cirrhosis and cholestasis]. 748 6


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