Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 868 patients admitted with pancreatitis between 1971 and 1976, coexisting hyperbilirubinemia was noted in 125 (14%). The patient population was primarily composed of alcoholics (84%) with chronic pancreatic disease (75% Marsielles Class H or higher) which was of moderate severity (77% fewer than three prognostic signs). The hyperbilirubinemia in these 125 patients was due to extrahepatic obstruction in 22%, hepatocelluar disease in 31%, and was idiopathic in 47%. Transient hyperbilirubinemia (< 10 days duration) occurred most commonly in the idiopathic group. Transitory periductular pancreatic edema may account for the elevated bilirubin in some of these cases. Liver biopsy should be done whenever hyperbilirubinemia persists longer than ten days in patients with pancreatitis. If hepatocellular disease is not found, transhepatic or endoscopic retrograde cholangiography are indicated. If common bile duct obstruction is demonstrated, a brief trial of medical therapy is in order. Persistent conservative treatment, however, exposes the patient to the risk of cholangitis and biliary cirrhosis. In 13 of the 125 cases (10%), persistent extrahepatic obstruction proved to be due to compression of the common bile duct by inflammatory pancreatic tissue. In these circumstances, choledochoduodenostomy is recommended as the procedure of choice. In patients requiring biliary decompression, concommitant procedures upon the pancreas are occasionally indicated.
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PMID:Hyperbilirubinemia in inflammatory pancreatic disease: natural history and management. 71 87

The authors have studied the frequency of an abnormal lipoprotein (LP-X), by the method presented by YAE e col. (21). The LP-X test is useful in differentiating of a cholestatic process from a non-cholestatic one, but it is not adequate to distinguish an intrahepatic cholestasis from an extrahepatic biliary obstruction. Out of the 41 icteric patients who were studied, a frequency of the presence of the LP-X was observed in 68.3% thus distributed: viral hepatitis 90,5% obstructive jaundice 85,7%, jaundice of uncertain etiology 37.6%; it was not present in 5 patients with hepatic cirrhosis and in the serum of 21 healthy volunteers. A significant association was found between the presence of LP-X and an abnormal curve of lipoproteins.
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PMID:[Frequency of lipoprotein-X (LP-X) in icteric patients. Comparison with some bioquimical data (author's transl)]. 74 47

Numerous interactions between hormonal contraceptives and liver function have been described. Changed laboratory results do not represent obligatory pathologic conditions or hepatotoxi effects. Some of these changed results are transient, suggesting that liver cells are capable of adaptation. The use of oral contraceptives is contraindicated in the following liver diseases: - recurrent intrahepatic cholestasis (recurrent jaundice of pregnancy, Dubin-Johnson syndrome, Rotor syndrome); - acute disturbances of liver function. In general it is recommended that hormonal contraceptives should not be used by patients with biliary cirrhosis although some authors have stated that chronic disturbances of liver function did not appear to be aggravated by these agents. Impairment of carbohydrate and lipid metabolism needs careful control of the laboratory tests concerned. Due to its low frequency the increased risk of gallstones does not necessitate the withdrawal of the medication. Up to now the interrelationship between the use of contraceptive steroids and the induction of hepatic tumours has not been proven.
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PMID:[Liver function in hormonal contraception]. 82 25

An epidemic of jaundice probably due to toxic hepatitis occurred in three adjoining districts of Northwest India during the period November and December, 1974. The dogs of the villages were affected first, then the human beings. Detailed clinical features, appropriate laboratory tests, and liver biopsies were studied. A retrospective epidemiological survey was carried out. The disease had a subacute onset starting with high fever, followed by rapidly progressive jaundice. Ascites appeared simultaneously and soon became quite massive. Hepatomegaly was recorded when ascites decreased. Liver function tests suggested cholestatic jaundice. The mortality rate in the hospital was 10%. Clinical features in dogs were similar, but mortality was almost 100%. Liver histology was characterized by (1) edema and collagenization of the central veins, never with thrombosis, (2) cholangiolar proliferation, (3) moderate to severe ballooning of the hepatocytes, (4) perisinusoidal fibrosis, (5) cholestasis, and finally, (6) cirrhosis with reverse lobulation. Etiology of this epidemic of hepatitis could not be unequivocally established. Critical analysis of the data suggests that some food toxin may have been a factor in the outbreak of this unusual epidemic of toxic hepatitis.
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PMID:Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India. 83 97

Eleven patients with hepatic cirrhosis or cholestasis were treated with rifampicin for 7 to 132 days. Ten patients received hexobarbital (7.32 mg/kg) and five received tolbutamide (20 mg/kg) by i.v. infusion prior to and after rifampicin treatment; plasma concentrations of the two test compounds were determined during and after infusion. The average elimination half-life of hexobarbital had decreased from 624 to 262 min and that of tolbutamide from 292 to 160 min following rifampicin treatment. It was calculated that the metabolic clearance of hexobarbital had increased more than two-fold and that of tolbutamide almost two-fold. The results suggests that rifampicin is able to stimulate hepatic drug metabolism in patients with liver disease. It was apparent in general that the induction did not lead to improvement of hepatocellular function during disease as judged by laboratory findings.
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PMID:Stimulation of drug metabolism by rifampicin in patients with cirrhosis or cholestasis measured by increased hexobarbital and tolbutamide clearance. 86 50

Hepatocellular diseases, such as hepatitis, cirrhosis, or hepatic neoplasm, are associated with impaired metabolism of certain drugs, including aminopyrine, whereas cholestasis produced variable effects on aminopyrine metabolism. Reasons for the variable effects of cholestasis on hepatic aminopyrine metabolism were sought by performing in patients with hyperbilirubinemia the aminopyrine breath test (ABT), which consists of measurements of 14CO2 in breath 2 hr after oral administration of [14C]aminopyrine. Hyperbilirubinemia (total serum bilirubin less than 1.2 mg/100 ml) in these patients was due to hepatocellular disease or cholestasis. The ABT, defined as the percentage of the administered dose of 14C excreted in breath for 2 hr after [14C]aminopyrine administration, was 6.2 +/- 0.8% (mean +/- SD) in 107 control patients with normal total serum bilirubin. The ABT was severely abnormal (less than 3.1%) in 54 of 77 hyperbilirubinemic patients (70%) with hepatocellular disease and normal (greater than 4.5%) in only 5 of these patients (6%). In contrast, the ABT was severely abnormal in only 1 of 40 cases of cholestasis with hyperbilirubinemia and normal in 70% of these patients. Thus, aminopyrine metabolism is normal in most cases of hyperbilirubinemia due to cholestasis and is only rarely severely abnormal in these patients. On the other hand, severe abnormality in aminopyrine metabolism occurs in the majority of patients with hyperbilirubinemia due to hepatocellular disease. It therefore appears that the ABT may be useful in hyperbilirubinemia to distinguish patients with hyperbilirubinemia due to cholestasis form most patients with hyperbilirubinemia due to hepatocellular disease.
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PMID:Aminopyrine metabolism in the presence of hyperbilirubinemia due to cholestasis or hepatocellular disease. Combined use of laboratory tests to study disease-induced alterations in drug disposition. 87 Feb 74

Liver biopsy was done at the time of operation in 125 consecutive upper abdominal procedures to assess the incidence of unsuspected or undiagnosed hepatic abnormalities. Specifically excluded were hepatic lesions unexpectedly identified at laparotomy. Sixty-seven percent of the liver biopsy specimens were abnormal, the most frequent findings being fatty metamorphosis, cholestasis, triaditis, fibrosis, inflammatory infiltrate, cholangitis, cirrhosis, and hepatitis. The most frequent operation performed was cholecystectomy. In 63 patients with chronic cholecystitis, there was a 51% incidence of abnormal liver histology, while in nine patients with acute cholecystitis, the incidence was 78%. In 83% of all other operations, abnormal liver biopsy specimens were identified. Bile leakage, hemorrhage, and infection did not occur in this series, despite inclusion of patients with severe biliary obstruction, abnormal clotting factors, and intra-abdominal sepsis. New techniques of histochemical enzyme analysis and electron microscopy are expected to enhance the clinical correlation of occult hepatic lesions. We conclude that liver biopsy in a safe, informative adjunct to all upper abdominal procedures.
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PMID:'Routine' liver biopsy in upper abdominal surgery. 88 45

Patients with a metabolic block in the conversion of THCA into cholic acid develop cirrhosis and hemolysis, and die of hepatic failure. In these patients, THCA is largely conjugated to taurine (tauro-THCA) and excreted instead of being converted into cholic acid. In the present study, the effects of tauro-THCA on hemolysis, bile flow, and hepatic morphology were evaluated in bile fistula rats. All rats infused with tauro-THCA at rates of 0.25, 0.50 or 0.75 micronmol/min developed hemolysis with hemoglobinuria. A direct toxic effect of tauro-THCA on washed human red blood cell membranes was demonstrated at a concentration of 8 X 10(-4) M. Liver biopsy sections from rats infused for a 2 hr period with tauro-THCA were examined by electron microscopy and showed dilation of the rough endoplasmic reticulum and distortion of mitochondrial membranes. Cholestasis was not induced, since tauro-THCA actually caused a greater choleretic response for a given rate of bile salt excretion than did taurocholate. This study raises the possibility that the clinical liver disease seen in patients with a metabolic block in the conversion of THCA into cholic acid may be caused by tauro-THCA.
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PMID:Hepatic lesions and hemolysis following administration of 3alpha, 7alpha, 12alpha-trihydroxy-5beta-cholestan-26-oyl taurine to rats. 89 5

Liver specimens from 68 cases of biliary atresia were histologically studied in reference to postoperative prognosis. The histological findings were classified into 4 to 5 groups by the degree of fibrosis, bile duct proliferation, bile plugs, giant cell transformation, and intralobular cholestasis. Furthermore, morphometrical studies of interstitial area, bile duct (ductules), intrahepatic portal vein, and intrahepatic artery were done and correlated with the age of patients and with operative results. From this study, it was shown that 1) marked fibrosis (cirrhosis) and interstitial areas occupying more than 35% of the sectional area of the liver specimen, 2) severe ductular proliferation, shown by proliferated bile ducts occupying more than 20% of interstitial areas, 3) no or slight intralobular cholestasis and 4) marked interlobular cholestasis are considered to predict poor postoperative bile excretion.
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PMID:Histopathological studies on the prognosis of biliary atresia. 91 63

A patient who developed chronic cholestatic jaundice during the 1st year of life and eventually died of liver cell failure at the age of 18 years is described. During the terminal illness Kayser-Fleischer-like rings were observed and the serum concentrations of total copper and ceruloplasmin were elevated. At autopsy, a mixed macronodular and micronodular cirrhosis was found and cholangiography and dissection of bile ducts revealed no obstructive lesion of the biliary tract. There was no family history of hepatobiliary disease. Liver biopsies obtained at the ages of 5 and 7 years showed accumulation of bile droplets in hepatocytes, normal-appearing bile ducts, no significant fibrosis, and intact lobular architecture. Striking features of the terminal cirrhosis were the presence of Mallory bodies and a marked excess of copper in the liver (2,175 mug per g dry weight). The latter two findings, as well as the elevated serum concentrations of total copper and ceruloplasmin, may be attributable to chronic cholestasis per se. This study emphasizes the clinical and therapeutic problems posed by chronic cholestasis of unknown etiology in childhood.
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PMID:Progressive intrahepatic cholestasis of infancy and childhood. A clinicopathological study of patient surviving to the age of 18 years. 95 55


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