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 paper describes a case of jaundice in a three-year-old bassett hound. The illness was accompanied by hyperbilirubinaemia and raised serum levels of alkaline phosphatase and glutamic pyruvic transaminase, indicating the presence of both biliary obstruction and hepatocellular damage. Examination of liver biopsies on two occasions showed intrahepatic cholestasis and mild inflammatory change. The dog was treated with corticosteroid. The jaundice regressed after three months, hepatic functions returned to normal and the dog recovered. The cause of the jaundice was not determined.
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PMID:Intrahepatic cholestasis in a dog: a clinicopathological study. 120 93

Clinical and laboratory findings from 15 patients with icteric viral hepatitis during pregnancy (VHP) and from 22 patients with intrahepatic cholestasis during pregnancy (CJP) were evaluated statistically in order to find out which parameters might help in order to find out which parameters might help in differentiating the two diseases. Diagnosis was established by needle liver biopsy in all cases. The following data were considered: history, physical examination, erythrocyte sedimentation rate (ESR) serum cholesterol, prothrombin time, total serum bilirubin, SGOT, SGPT, serum alkaline phosphatase, serum protein, serum flocculation tests, BSP blood clearance and serum HB Ag. Vomiting, high GOT and GPT serum levels, and serum HB Ag positivity suggest VHP diagnosis. Otherwise a severe itching with scratching lesions, high ESR, elevated total cholesterol and serum alkaline phosphatase values mainly if occurring in the later stage of pregnancy are consistent with CJP diagnosis. When clinical and laboratory data from a jaundiced pregnant female do not allow diagnosis, this can be established only on the basis of needle liver biopsy.
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PMID:The differential diagnosis between intrahepatic cholestatic jaundice and viral hepatitis during pregnancy. 122 May 7

Among 179 patients with various chronic diseases of the liver the authors found in 20 cases histological evidence of intrahepatic cholestasis and in all these cases lipoproteid X (LP-X) was present in the serum. In the group of 159 patients without evidence of cholestasis in microscopic examination of liver tissue LP-X was demonstrated only in two cases (1.3%). The results of investigations confirm the view that detection of LP-X in the serum is a specific and sensitive index of cholestasis and its value in the diagnosis of this condition is greater than that of determinations of alkaline phosphatase, gamma-glutamyl-transpeptidase, leucinamino-peptidase activity or cholesterol in the serum.
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PMID:Significance of serum lipoproteid-X (LP-X) determination for the diagnosis of cholestasis in chronic liver diseases. 122 4

This study characterizes a syndrome of partial common bile duct obstruction and marked elevation in serum alkaline phosphatase in 6 male alcoholic patients with calcific pancreatitis. In each patient, a marked elevation in serum alkaline phosphatase was associated with minimal, if any, elevation in serum bilirubin. In all cases, the alkaline phosphatase was hepatic in origin, and intravenous or operative cholangiography showed a dilated common bile duct. Liver biopsy showed canalicular bile stasis in 4 patients and bile duct proliferation in 2 patients. This study demonstrates that calcific pancreatitis may cause partial bile duct obstruction which differentially increases serum alkaline phosphatase without altering bilirubin or bromsulphthalein excretion.
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PMID:Marked alkaline phosphatase elevation with partial common bile duct obstruction due to calcific pancreatitis. 124 86

Report of a 10-year-old boy with congenital hypoplasia of the intrahepatic bile ducts, the socalled MacMahon-Thannhauser-Syndrome. The patient had been suffering from a varying degree of jaundice since his 2nd day of life and from pruritus since his 21st month of life. Furthermore, he had hepatomegaly, a systolic cardiac murmur, hypogenitalism, retarded growth, and finally hypertension. Transitory xanthomas existed between 1 3/4 and 2 3/4 years of age. Signs of persistent intrahepatic cholestasis was manifested by increased levels of bilirubin and bile acids in serum as well as raised activities of leucine aminopeptidase, gamma-glutamyl transpeptidase and alkaline phosphatase. Pathological values of serum glutamic dehydrogenase pointed to a persistent destruction of liver cells. Without treatment, the activities of vitamin K dependent clotting factors were decreased. Cholesterol, phosphatides and triglycerides in serum were increased and lipoprotein-X was detectable. Aortography revealed stenosis of both renal arteries. An exploratory laparotomy and 5 liver biopsies led to the diagnosis of hypoplasia of the intrahepatic bile ducts. Therapeutic trials with steroids and the anion exchange resin "cholestyramine" were ineffective. Phenobarbital relieved the pruritus. Parenteral administration of fat soluble vitamins restored the activity of vitamin K dependent clotting factors to normal. The high blood pressure fell significantly due to treatment with adelphan. The etiology of hypoplasia of the intrahepatic bile ducts is unknown. It may be a malformation or an obliteration secondary to inflammation. In our patient, narrowing of the renal arteries, increase of plasma-renin activity and hypertension were probably secondary to hyperlipidemia. It has been suggested that hyperlipemia secondary to cholestasis may be due to a disturbance of lipoprotein metabolism. A review of reports on 118 patients suffering from intrahepatic bile ducts hypoplasia is included.
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PMID:[Hypertension and bilateral stenosis of the renal artery associated with congenital hypoplasia of the intrahepatic bile ducts (author's transl)]. 124 84

The isoenzymes of alkaline phosphatase were measured on admission to hospital, and then weekly over a 2 to 3 month period, in 40 patients presenting with uncomplicated acute hepatitis, 12 patients with cholestatic hepatitis, and 10 patients with histologically confirmed chronic persistent hepatitis. In acute uncomplicated hepatitis the increase in total alkaline phosphatase is not due to a cholestatic reaction of the damaged liver, but reflects the impaired catabolic capacity of the liver cells to degrade alkaline phosphatases from intestine and bone, as well as that of hepato-biliary origin. The isoenzyme distribution pattern is the same as found in normal healthy subjects. The increase in total alkaline phosphatase in patients with cholestatic hepatitis results from this impaired catabolic capacity for degradation of all isoenzymes, together with an increase in cholestatic reflux of hepato-biliary enzymes. In patients with chronic persistent hepatitis the raised total alkaline phosphatase activity at each point during the illness is due to this catabolic impairment of degradation of all isoenzymes. A cholestasis is not seen. The isoenzyme distribution pattern remains normal; only the enzyme activity due to the intestinal fraction, when compared with the acute hepatitis, is slightly, but significantly, raised.
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PMID:[Distribution pattern of isoenzymes of alkaline phosphatase in patients with various forms of hepatitis (author's transl)]. 125 32

Cholestatic hepatitis, whilst having a longer course than cytolytic forms, in general regresses in a few months. The authors report here seven cases of cholestatic hepatitis lasting for more than 18 months. These chronic forms have certain characteristic features: - female predominance (6 cases out of 7). - a severe degree of cholestasis with, in particular, marked elevation of lipids, cholesterol and alkaline phosphatase. - the absence of Australia antibody and antigen, together with the absence of anti-smooth muscle antibody and anti-mitochondrial natibody. - a decrease in the number of permeable biliary canaliculi in the portal spaces. - a decrease in the number of permeable biliary canaliculi in the portal spaces. - a course which appears to be little influenced by various therapeutic measures. Although the final course seems satisfactory on the majority of cases, the possibility of a slow cirrhogenic transformation cannot be excluded in certain instances.
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PMID:[Cholestatic hepatitis with a chronic course. 7 cases]. 125 18

Thirty patients are described who developed jaundice during the course of severe bacterial infection. Although the infecting organism was variable, as was the site of infection, the patients were generally ill and pyrexial. The group had a very high mortality rate (43%). A positive blood culture was obtained in 11 patients. Biochemical abnormalities noted were those of an increased concentration of conjugated bilirubin in the serum with only a modest increase in alkaline phosphatase and transaminase levels. Serum cholesterol was found to be normal. The mean serum urea level was significantly elevated, as were creatine phosphokinase and lactic dehydrogenase. Most patients exhibited a neutrophil leukocytosis and an elevated sedimentation rate, and the mean hemoglobin level was low. Liver histology was studied in 13 patients. There was evidence of mild bile stasis in 5 and moderate bile stasis in 2. Findings were otherwise nonspecific and were characterized by fatty change and/or inflammatory cells in the portal areas. There was no correlation between degree or duration of juandice and prognosis, although all patients who died remained jaundiced until death. It is suggested that this syndrome is not one of true cholestasis in that all biliary substances were not shown to be elevated in the serum, but that it is rather a selective defect in the excretion of conjugated bilirubin.
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PMID:Jaundice in severe bacterial infection. 127 54

Surgical jaundice can be easily induced by ligation of bile duct, but it is not easy to reverse the ligation in rats. Therefore, a simple method was designed in our laboratory to address the problem. Obstruction of bile duct can be achieved by the compression by two arms of a fine silicon tube enveloped in an outer bigger silicon tube. Both silicon tubes are then fixed and sutured to the abdominal peritoneum. Therefore, if the releasing of the obstruction is required, removal of the inner fine silicon tube by removing off the previous suture tire of silicon tube which had settled under the skin. Thus, the reversing of obstruction could be achieved without extensive exploration into the abdominal cavity. One week after obstruction the bile duct of rats were dialated 6.10 +/- 1.26 mm (Mean +/- SD) in rats. The serum bilirubin and alkaline phosphatase were 6.29 +/- 1.26 mg% and 229.30 +/- 82.22 IU respectively. The dilated bile duct decreased into 3.00 +/- 0.98 mm one week after decompress with this method. Serum bilirubin and alkaline phosphatase were 1.80 +/- 0.79 mg% and 90.50 +/- 19.60 IU respectively. It proved that this animal model was simple and had the benefit of being able to sample the bile without contamination with intestinal contents after decompression.
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PMID:A simple animal model for inducing and releasing surgical jaundice in rats. 129 29

A prospective study of 113 patients with jaundice and 20 patients with unjaundiced cholestasis was carried out to evaluate the value of serum tumour markers, carcinoembryonic antigen (CEA) and monoclonal antibodies CA 50 and CA 242, in the distinction between benign and malignant diseases causing jaundice and/or cholestasis. In the patients with malignant disease (n = 37) the serum values of all tumour markers were significantly higher than in the patients with benign disease (n = 96). The sensitivities of CEA, CA 50 and CA 242 in detecting malignancy were 70.2%, 94.5% and 56.7%, respectively, while the specificities were 57.2%, 33.3% and 77.0%, respectively. Serum alkaline phosphatase and bilirubin levels had a high positive correlation with CA 50, and CA 242 correlated positively with serum bilirubin levels. No correlation was seen between CEA and alkaline phosphatase or bilirubin levels. The CEA, CA 50 and CA 242 tests may be used as useful complements to other investigative methods in the distinction between benign and malignant causes of jaundice and/or cholestasis. In particular, the rather high specificity of the CA 242 test for malignant diseases seems promising.
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PMID:Clinical value of serum tumour markers CEA, CA 50 and CA 242 in the distinction between malignant versus benign diseases causing jaundice and cholestasis; results from a prospective study. 133 81


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