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)

Jaundice developing in critically ill or injuried patients should probably be thought of as a manifestation of severe sepsis until proven otherwise. Septic jaundice occurs in about 50 to 60 per cent of patients with generalized peritonitis. Biochemically, jaundice associated with bilirubin (particularly the direct fraction) and liver enzymes (particularly the alkaline phosphatase) and a decrease in the serum albumin. Histologically there is intrahepatic cholestasis. The etiology of these changes in unknown, but they appear to be due to an end organ response to sepsis. Optimal treatment involves control of the sepsis and maintenance of a glood flow of well-oxygenated blood to the liver.
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PMID:Hepatobiliary complications of sepsis. 104 57

In the serum of many patients with sarcoidosis, alkaline phosphatase activity is increased due to sarcoid liver involvement. A study was carried out of various tests expressing intrahepatic cholestasis in 26 patients with sarcoidosis, 18 of them with a positive liver biopsy and 8 with a negative liver biopsy. SAP was elevated in 23% of the patients and its thermoresistance pointed to an hepatic origin. The predictive value of a positive test (PV-positive, the percentage of times that a positive test is in agreement with an involved liver) and the predictive value of a negative test (PV-negative, the percentage of times that a negative test will detect a nondiseased liver) were calculated. LP-X test is more reliable than SAP, which in turn is better than CB, BSP retention, and gamma-glutamyl-transpeptidase, in that order. LP-X seems to be more specific and more sensitive than alkaline phosphatase for predicting liver involvement in sarcoidosis.
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PMID:LP-X test in sarcoidosis patients with liver involvement: comparison with other liver function tests. 106 29

Eleven adults with refractory leukemia treated with a combination of 6-mercaptopurine and Adriamycin developed hepatic dysfunction manifested by elevations of serum total bilirubin, alkaline phosphatase, and glutamic oxaloacetic transaminase. Liver tissue obtained at necropsy showed intrahepatic cholestasis (eight cases), hepatocellular necrosis (ten cases), leukemic infiltration (two cases), and fatty change (nine cases). Neither this frequency nor severity of hepatocellular destruction has hitherto been associated with 6-mercaptopurine at the dose levels used in this study, nor has Adriamycin previously been found to be hepatotoxic. It is postulated that Adriamycin potentiated the hepatotoxicity of 6-mercaptopurine in these patients.
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PMID:Clinico-pathologic correlation of liver damage in patients treated with 6-mercaptopurine and Adriamycin. 106 39

Fifteen patients with cholestatic disorders were treated for 1 to 5 months with phenobarbital. Primary biliary cirrhosis was diagnosed in seven, sclerosing cholangitis in two, intrahepatic biliary hypoplasia in three, and cholestatic hepatitis in three. Except for the patients with cholestatic hepatitis, in whom marked cholestasis was virtually the only abnormality in liver biopsy specimens, serum bilirubin and bile acid concentrations were diminished during therapy, the hepatic clearance of sulfobromophthalein and 131-I-rose bengal was variably enhanced, and there was relief from pruritus. Serum cholesterol concentrations and other measures of hepatic function were not significantly changed during therapy except for serum alkaline phosphatase activity, which rose in twelve patients. Parallel changes occurred in 5'-nucleotidase, suggesting a hepatic origin for the alkaline phosphatase activity. These studies indicate that phenobarbital therapy is associated with improvement in organic anion clearance in some patients with cholestatic disorders and may be beneficial to such patients.
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PMID:Phenobarbital effects in cholestatic liver diseases. 111 64

Investigations on the high molecular weight isozyme of alkaline phosphatase (R type of AP), which is typically found in the serum of patients with cholestasis, have revealed that AP of the R type corresponds to the conventional liver AP which is attached to vesicular material. The isolation of these vesicles by Sepharose gel filtration is described. Several features were found to be characteristic for these vesicles: 1. The presence of the following enzymes known to be membrane bound: alkaline phosphatase (AP), 5FEET-NUCLEOTIDASE, L-leucyl-beta-naphthylamidase (LAP), and gamma-glutamyl transpeptidase (gamma-GT). 2. The absence of the following enzymes known not to be present on cell membranes: glutamic pyruvic transaminase (SGPT), glutamic oxalacetic transaminase (SGOT), lactate dehydrogenase (LDH), and acid phosphatase. 3. The typical ultrastructural appearance and the cytochemical visualization of alkaline phosphatase and 5feet-nucleotidase. It is concluded that the vesicles correspond to fragments of the liver cell membranes that appear and continue to circulate in the blood of patients with cholestasis.
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PMID:The separation and characterization of liver plasma membrane fragments circulating in the blood of patients with cholestasis. 112 24

7 cases of pruritus in pregnancy are reported and their laboratory findings compared with a group of normal pregnant women; then pruritus is reviewed with respect to diagnosis, pathogenesis, therapy, and prognosis. The 7 women developed pruritus in 28-38 weeks of typically the 2nd pregnancy, although during oral contraception in 1 woman. The frequency was about 2/1000 pregnancies. Lab findings suggestive of cholestasis included normal prothrombin, elevated transaminaes, alkaline phosphatase, total bilirubin, total cholesterol, and slowed BSP clearance. None of these women had any history of hepatitis, medication, or positive Australia antigen. It is important in diagnosis to rule out infections, toxic or iatrogenic hepatitis, and especially herpes gestationis, which is teratogenic. Pruritus of pregnancy is identical to that seen during oral contraception, i.e., it is a less severe form of cholestatsis than jaundice. It can be treated with cholestyramine, or will regress spontaneously after delivery, but may cause prematurity.
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PMID:[Significance of pruritus during pregnancy. Relations with the hepatic disorders of gestation]. 113 31

In 36 children with cystic fibrosis (CF) the isoenzymes of alkaline phosphatase (AP) were determined microelectrophoretically in polyacrylamide- and starch-gel. The study was done to evaluate the clinical significance of these additional data for the diagnosis of liver involvement in DF. The results led to the following conclusions: 1. Serum activity of total AP is comparatively unsensitive "masking" alterations in the isoenzyme pattern contributing to the AP serum activity. 2. In 17 children resp. 47% bile-duct phosphatase was increased indicating a secretostasis while other marker enzymes of cholestasis were normal in part. 3. The activity of bone phosphatase in the serum showed a significant correlation to the degree of growth retardation in these patients. 4. Intestinal phosphatase was present in the serum of only one child with cirrhosis of the liver being an indicator for liver insufficiency. 5. Determination of AP isoenzymes in the serum may provide additional information about the organs involved for the physician in handling CF patients.
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PMID:Isoenzymes of alkaline phosphatase in the serum of patients with cystic fibrosis. 113 40

The development of the syndrome of chronic intrahepatic cholestasis in five young, black men who had systemic granulomatous disease and clinical features consistent with those of sarcoidosis is described. Clinical and biochemical aspects, similar to those of primary biliary cirrhosis, included pruritus, jaundice, hepatomegaly and striking elevations of serum levels of alkaline phosphatase and cholesterol. (One patient had skin xanthomas.) Mitochondrial antibodies were not found; and survival of the patients (7 to 18 years) exceeded the usual survival of patients with primary biliary cirrhosis. The histologic abnormalities included noncaseating granulomas, chronic intrahepatic cholestasis, increased copper in hepatocytes, progressive diminution in number of interiobular bile ducts, periportal fibrosis and the eventual development of a micronodular "biliary" cirrhosis. The histologic evolution of the disease suggests a slow, progressive destruction of the bile ducts by granulomas. Although the end stage of this syndrome resembles primary biliary cirrhosis, the characteristic nonsuppurative, destructive cholangitis of primary biliary cirrhosis was not present.
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PMID:Chronic intrahepatic cholestasis of sarcoidosis. 116 46

Carbenicillin disodium was temporally associated with eight episodes of a mild reversible anicteric hepatitis characterized by nausea, vomiting, and a tender, somewhat enlarged liver. Serum glutamic and oxaloacetic transaminase as well as alkaline phosphatase levels rose, but serum bilirubin values remained normal. There usually were no signs of concomitant allergy to penicillin, and other penicillins could be given subsequently without ill effects. Biopsy specimens of the liver showed spotty liver cell necrosis with no cholestasis.
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PMID:Anicteric carbenicillin hepatitis. Eight episodes in four patients. 117 85

The authors report the clinical, biochemical, histological and etiologic characteristics of 24 patients with the syndrome of benign intra-hepatic post-operative cholestasis. Jaundice appeared early in the post-operative period, from the first to the 12th post-operative day. All patients had received blood transfusions. In 23 patients, the post-operative course was complicated, chiefly by local infection or septicemia. Hyperbilirubinemia ranged from 2 to 28 mg per 100 ml and was mainly conjugated; serum alkaline phosphatase activity was normal or moderately elevated; in 3 patients, it was markedly elevated; serum glutamic-pyruvic transaminase activity was normal on 7 patients, moderatly increased in 15, and markedly increased in one. Liver histology was normal in 6 patients, and showed minimal lesions (cholestasis and slight portal inflammatory changes) in 3. Jaundice did not appear to modify the final outcome. It appears to be due both to increased production of bilirubin (as a result of blood transfusions) and to decreased excretion of bilirubin by the liver (as a result of the surgical operation and of infection).
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PMID:[Benign postoperative intrahepatic cholestasis]. 117 77


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