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)

Total body potassium (40K) and leucocyte potassium measurements were carried out on 19 patients with stable but decompensated cirrhosis maintained on diuretics for previous ascites. Of 13 patients receiving spironolactone alone none had a total body potassium below the expected lower limit of normal, whereas, of six receiving additional frusemide, two had low values. The results for leucocyte potassium were in agreement and simultaneous measurements of leucocyte magnesium showed a close correlation, those with intracellular potassium depletion also having magnesium depletion. One such patient was treated with magnesium supplements without effect on the potassium, although intracellular magnesium was improved. It is concluded that spironolactone alone is the treatment of choice in the maintenance management of such patients; that additional potassium would be unnecessary; and that additional frusemide should be avoided if possible.
Gut 1977 Sep
PMID:Potassium and magnesium depletion in patients with cirrhosis on maintenance diuretic regimens. 60 88

Serum vitamin B12 and vitamin B12 binding proteins (transcobalamins, TCS) were determined in patients with malaria, amoebic liver abscess, carcinoma of the liver, infectious hepatitis, cirrhosis and chronic myelocytic leukemia (CML) as well as in 60 blood donor subjects. Serum vitamin B12 in patients with infectious hepatitis, cirrhosis and CML were higher than that of the normal subjects. The values of unsaturated vitamin B12 binding capacity (UBBC) in patients with carcinoma of the liver, infectious hepatitis, cirrhosis were lower while that of patients with CML were higher than that of the normal subjects. A markedly increased TCI and decreased TCII was observed in patients with CML while these changes was much less in patients with other liver diseases. The difference was possibly due to a flooding of vitamin B12 from damaged liver cells into the circulation and the decreased synthesis of transcobalamins in patients with liver diseases while the increased granulocytes, the source of TCI, was much increased in patients with CML.
Southeast Asian J Trop Med Public Health 1977 Sep
PMID:Vitamin B12 and vitamin B12 binding proteins in liver diseases. 60 23

In a review of 906 consecutive liver biopsies, sinusoidal dilatation, unrelated to passive congestion of the liver, sinusoidal infiltration, or cirrhosis, was found in 26 cases (2.9%). In 21 of them the final diagnosis was a neoplastic or granulomatous disease (tuberculosis, brucellosis, Crohn's disease), but in only half of them was there evidence of neoplastic or granulomatous infiltration of the liver. In the remaining cases, sinusoidal dilatation was either the only histological abnormality or it was associated with nonspecific changes. Although the pathogenesis of sinusoidal ectasia is not known, our findings indicate a definite relationship to the presence of tumor or granulomatous disease in the liver or elsewhere in the body. It is concluded that the finding of sinusoidal dilatation as an isolated histological change in a liver biopsy specimen should prompt the search for a tumor or a disease associated with granulomas.
Gastroenterology 1978 Sep
PMID:Incidence and clinical significance of sinusoidal dilatation in liver biopsies. 68 May 4

There is an increased incidence of unwanted sedation associated with chlordiazepoxide usage in the elderly and in patients with liver disease. To determine whether pharmacokinetic alterations could account in part for these observations we studied the disposition and elimination of intravenously administered chlordiazepoxide in 27 healthy controls aged 16 to 86 years, 8 patients with cirrhosis, and 5 patients with acute viral hepatitis. Both increasing age and parenchymal liver disease led to similar changes in chlordiazepoxide pharmacokinetics. Over the age range 20 to 80 years, elimination half-life (t1/2(beta)) increased from 7 to 40 hr (r, 0.67; P less than 0.001) attributable to a decrease in plasma clearance from 30 ml per min to 10 ml per min (r, -0.71; P less than 0.001) and an increase in volume of distribution from 0.26 to 0.38 liters per kg (r, 0.60; P less than 0.05). Similarly, a decrease in plasma clearance in cirrhosis (7.7 +/- 2.1 compared to 15.3 +/- 4.4 ml per min, P less than 0.01) and acute viral hepatitis (6.1 +/- 4.3 compared to 18.1 +/- 7.1 ml per min, P less than 0.01) relative to age-matched controls and an increase in the volume of distribution resulted in a prolongation of the elimination half-life in both forms of liver disease. Impaired elimination of chlordiazepoxide may account in part for the increased incidence of oversedation seen in the elderly and in patients with liver disease.
Gastroenterology 1978 Sep
PMID:Effect of age and parenchymal liver disease on the disposition and elimination of chlordiazepoxide (librium). 68 May 5

A study was done on the action of splenohepatoplasty upon intrahepatic and prehepatic portal hypertension. Portal hypertension was induced Wistar rats following the establishment of cirrhotic conditions. Hepatic cirrhosis was obtained in these rats by an oral, daily dose of tioacetamide during a four and five month period. Prehepatic hypertension was produced in dogs by the installation of a rubber cylinder, completely covered by cellophane paper, around the trunk of the vena porta. This procedure brought about a progressive compression of the vena porta. The application of splenoheptoplasty is a highly valuable treatment for portal hypertension as a derivative system and for intrahepatic portal hypertension as a derivative regenerative system.
Surg Gynecol Obstet 1978 Sep
PMID:Simultaneous treatment of portal hypertension and hepatic cirrhosis by splenohepatoplasty. 68 92

During computed tomography (CT) scanning of the liver, the inferior vena cava can be identified as a separate structure of lesser density adjacent to the caudate lobe in two-thirds of patients without known hepatocellular disease. In patients with alcoholic (portal) cirrhosis of moderate to severe degree, intrahepatic portal veins may not be identified on CT scans, even though their inferior vena cavas can be definitely distinguished from the caudate lobe. Portal cirrhosis causes distortion and obliteration of the portal triads, which is presumably reflected by lack of visualization of intrahepatic portal veins during CT scanning.
J Comput Assist Tomogr 1978 Sep
PMID:Lack of visualization of the portal venous tree in cirrhosis of the liver: a computed tomography finding with possible diagnostic significance. 70 18

The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices.
Z Gastroenterol 1978 Sep
PMID:[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)]. 70 17

The pharmacokinetics of chlormethiazole were studied in eight patients with advanced cirrhosis of the liver and in six healthy volunteers after oral and intravenous administration of the drug. In the patients the systemic bioavailability of oral chlormethiazole was increased about tenfold, whereas its elimination was only slightly retarded. The increased bioavailability was clearly due to decreased first-pass metabolism of chlormethiazole in the cirrhotic liver. The results indicate that chlormethiazole should be used in reduced dosage when given by mouth to patients with cirrhosis of the liver.
Br Med J 1978 Sep 23
PMID:Effect of cirrhosis of the liver on the pharmacokinetics of chlormethiazole. 70 96

The morphology of red blood cells was studied in 30 patients with severe liver cirrhosis, in 10 patients with extrahepatic jaundice, and in 10 control subjects. In all the patients with extrahepatic jaundice more than 30% of red blood cells were target cells with increased resistance to osmotic lysis. In 12 patients with liver cirrhosis more than 30% of red blood cells were spur cells. The cholesterol: phospholipids (C/PL) molar ratio was 0.89 in target cells, 1.33 in spur cells, and 0.74 in normal red blood cells. The red blood cell membrane cholesterol and phospholipids exchanged with plasma lipoproteins, the lipid composition of which was studied in eight patients with spur cells; the free cholesterol: phospholipid (FC/PL) molar ratio was 0.33 (0.16 in the controls) in high density lipoproteins (HDL) and 1.40 (0.82 in the controls) in low density lipoproteins (LDL); in these patients the polyunsaturated fatty acid content was low in both phospholipids and cholesterol esters of lipoproteins. The irregular folds of the spur cells regressed when polyunsaturated lecithin was infused (2 g daily for five days) in eight patients with spur cell anaemia; the infusions decreased both C/PL ratio in RC to 0.88 and the concentration of unconjugated bilirubin (104.3 to 82.0 mumol/l (6.1 to 4.8 mg%)), whereas the activity of the plasma lecithin:cholesterol acyltransferase (LCAT) increased from 31.2 to 54.4 mumol/l/h. Polyunsaturated fatty acid content of RC lecithin increased after the infusion as it did in HDL, the FC/PL ratio of which decreased to 0.23.
Gut 1978 Sep
PMID:Membrane lipid composition of red blood cells in liver disease: regression of spur cell anaemia after infusion of polyunsaturated phosphatidylcholine. 71 Sep 73

In 27 male patients (age 31--60 years) with chronic hepatic diseases--10 of which with alcohol-toxic cirrhosis (ACi), 10 with hepatitic cirrhosis (HCi) and 7 with chronic aggressive hepatitis (CHAH)--total testosterone (T) and total oestradiol-17 beta (E2) in plasma were determined before and after HCG i.m. as well as LH and FSH before and 30 min and 60 min after LH-RH i.v. T, E2, LH and FSH were evaluated by specific RIA. Basal T was significantly decreased in ACi in comparison to normals and to HCi and CHAH. The increase after stimulation with HCG was reduced in all patient groups. Mean E2 before stimulation was altered in none of the groups compared to controls. After HCG there was an inadequate response only in ACi. Before as well as after stimulation with LH-RH, LH and FSH were increased in all patient groups. Our results point to the following: In males with chronic hepatic failure a testes insufficiency often occurs, which may depend on the etiology and the stage of the liver disease. An additional pituitary insufficiency appears not to exist.
Klin Wochenschr 1978 Sep 15
PMID:[Investigations on pituitary-testes axis in males with chronic liver diseases (author's transl)]. 71 23


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