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)

When disease impairs clearance of drugs, multiple-dose therapy may result in cumulation. The disposition of chlordiazepoxide (CDX), 50 mg infused intravenously over 10 min, was studied in 14 normal subjects and in 11 patients with biopsy-proven cirrhosis. In the normal subjects, mean (+/- SE) kinetic parameters were: t 1/2 beta, 10.0 (+/- 0.9) hr; Vd, 0.38 (+/- 0.04) l/kg; clearance, 0.54 (+/- 0.13) ml/min/kg. Clearance of total drug correlated inversely with serum albumin concentration in normal subjects (r = -0.63). Values in cirrhotic patients were: t 1/2 beta, 34.9 (+/- 8.7) hr; Vd, 0.34 (+/- 0.024) 1/kg; and clearance, 0.185 (+/- 0.34) ml/min/kg. Desmethylchlordiazepoxide (DMCDX), the major metabolite of CDX, appeared in blood of cirrhotic patients less rapidly than in normal subjects. Severity of liver disease did not indicate the impairment of CDX clearance. In 5 of the same cirrhotic patients, mean t 1/2 beta for oxazepam (7.1 +/- 1.0 hr) was 27% longer than in control subjects (5.6 +/- 0.7 hr); the difference is not significant. On kinetic grounds oxazepam may be preferable to chlordiazepoxide in cirrhotic patients since its elimination kinetics are not greatly altered in cirrhosis.
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PMID:Chlordiazepoxide and oxazepam disposition in cirrhosis. 45 93

Ten male patients with cirrhosis of the liver (three with portacaval anastomosis [PCA]) and eight sex- and age-matched controls underwent an arginine infusion test followed by an intravenous glucose tolerance test. Plasma glucose and growth hormone (GH) levels were measured during a period of three hours. In the normal subjects, the peak GH response to arginine occurred 60 minutes after the start of the infusion and was followed by a progressive decline in GH concentration; dextrose injection resulted in a further rapid fall in GH concentration. In cirrhotic patients, both fasting and postarginine GH concentrations were significantly higher than in controls; in addition, the dextrose injection, after causing a transitory drop in plasma GH levels, resulted in a marked increase in plasma GH concentration. In the patients with PCA, the plasma GH increase after arginine and after dextrous was more marked. In these cirrhotic patients, the plasma GH levels correlated directly with the magnitude of the portal hypertension and inversely with the serum albumin concentration, suggesting that the abnormality of GH secretion was a reflection of the derangement in liver function.
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PMID:Altered control of growth hormone secretion in patients with cirrhosis of the liver. 48 48

Extracellular water (EWC; 82-bromide), total body water (TBW; 3-THO), intracellular water (ICW = TBW-ECW), plasma volume (PV; 51-Cr), and total body potassium (TBK; 40-K) were studied in patients with cirrhosis of the liver (n = 12) and in controls (n = 12). ECW (39%), TBW (28%), ICW (19%), and PV (24%) increased, TBK (28%) however, decreased in cirrhosis. The results indicate that it is less the lean body mass, but rather the intracellular potassium concentration that is lowered (cirrhosis: 84 +/- 21 mmol/l ICW; controls: 115 +/- 23 mmol/l ICW). Decreased potassium per cell (mmol) and increased intracellular water are discussed as possible reasons for this. The correlation between TBK (%) and serum potassium (mmol/l) was found to be r = 0.56 (p less than 0.002). Correlations between the biochemical parameters gamma-globulins, cholin esterase, serum sodium and serum albumin (g/l PV) and characteristic fluid disturbances in cirrhosis are highly significant whereas albumin (g/kg bodyweight) was the same in both groups. We can support the 'overflow theory' of ascites formation.
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PMID:Total body water, extracellular water, plasma volume, and total body potassium in cirrhosis of the liver. 49 99

In 38 patients with chronic hepatitis and 53 patients with liver cirrhosis the portal vein pressure was determined by wedged hepatic vein pressure (WHVP). There were significant differences among chronic persistent, chronic active hepatitis and liver cirrhosis. The wedged hepatic vein pressure increased in chronic active hepatitis according to the rate of hepatic connective tissue. The platelet count and the thromboplastin time were correlated to the values of wedged hepatic vein pressure not only in chronic active hepatitis but in liver cirrhosis as well. The correlation among serum albumin level, bromsulphalein retention and systolic blood pressure after Riva-Rocci and wedged hepatic vein pressure was significant in liver cirrhosis exclusively. Even if the determination of wedged hepatic vein pressure does not permit an absolute statement on the risk of hemorrhage of esophageal varicosis it is nevertheless suited for follow-up controls in chronic hepatitis and liver cirrhosis and renders possible an outlook on the progress of the disease.
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PMID:[The diagnostic value of wedged hepatic vein pressure in chronic hepatitis and liver cirrhosis (author's transl)]. 55 23

The RBF was measured by means of the 133Xe washout method in seventy patients with cirrhosis. The average RBF in controls was 3.72 ml/g-min compared with 2.34 in the patients without ascites, 1.82 in the decompensated patients, 1.47 in the patients with azotaemia and 1.13 in the patients with additional oliguria. The RBF was not significantly correlated to changes in the systemic or portal haemodynamics. Likewise it was not correlated to any biochemical test of liver function except the serum albumin concentration (P less than 0.01). From the present results it can be concluded that a reduction in RBF in cirrhosis frequently is present before sodium and water retention is clinically evident and before laboratory proof of impairment of renal function, and that a subnormal serum albumin concentration may be a factor among several leading to renal hypoperfusion in cirrhosis.
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PMID:Renal blood flow in cirrhosis: relation to systemic and portal haemodynamics and liver function. 59 43

The transcapillary escape rate of albumin (TERalb), i.e. the fraction of intravascular mass of albumin that passes to the extravascular space per unit time, was determined from the disappearance of intravenously injected 125I-labelled human serum albumin during the first 60 min after injection in nine patients with cirrhosis of the liver. Six of the patients had ascites. The wedged hepatic venous pressure or splenic pulp pressure ranged from 20 to 30 mmHg, mean 26 mmHg. Plasma albumin concentration was low, but plasma volume was slightly enlarged, and thus the intravascular mass of albumin was only moderately reduced. The transcapillary escape rate of albumin was significantly elevated in all the cirrhotics, mean 10.2%/h, range 8.8 to 12.3%/h, in comparison to values for twenty-eight normal subjects 5.4%/h, range 3.5-7.2%/h. Our results can best be explained by increased filtration out of the vessels in the portal system, due to the increased portal venous pressure. The increased TERalb probably contributes to the formation of oedema and ascitic fluid.
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PMID:Increased transcapillary escape rate of albumin in patients with cirrhosis of the liver. 59 44

To clarify the involvement of tryptophan in the pathogenesis of hepatic coma, plasma and cerebrospinal fluid (CSF) tryptophan was studied in three patient groups (hepatic coma, stable cirrhosis, and control). An assessment of free fatty acids, some of the amino acids reported to compete with tryptophan for brain uptake, and albumin was also made. The data demonstrated that, whereas the elevated CSF tryptophan levels in cirrhotic patients compared to controls may have been attributable to decreased plasma branched chain amino acids, the elevated CSF tryptophan levels in hepatic coma compared to stable cirrhotic patients were probably attributable to increased plasma free tryptophan concentrations. Associated with the elevated plasma free tryptophan in coma patients was an increase in plasma free fatty acids and a marked decrease in serum albumin levels. Of all the amino acids investigated in the CSF, only tryptophan was significantly increased in patients in hepatic coma compared to cirrhotic patients not in coma.
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PMID:Tryptophan and hepatic coma. 62 Aug 92

The serum protein changes occurring in liver disease associated with parenchymal damage are characteristically decreased in serum albumin and increased in gamma globulin levels. Beta-gamma bridging in the electrophoretogram is highly characteristic of hepatic cirrhosis. Variation of alpha 1, alpha 2 and beta fractions is inconstant and is not of great diagnostic or prognostic value. The increase in gamma fraction is polyclonal in nature and is due first to increase in IgM fraction followed by an increase in IgG fraction. Elevation of IgA fraction is not as constant or prominent.
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PMID:Serum proteins in hepatic disease. 63 17

The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.
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PMID:[1-14C]Ethanol breath test in alcoholic liver disease. 65 31

The behaviour of albumin during the development of chronic progressing liver damages was investigated on the model of the thioacetamide cirrhosis in Wistar-rats. Simultaneous estimations of the albumin concentrations in extractable liver protein and in the serum as well as accompanying measurements of the total protein and of the transaminases SGOT and SGPT in the serum allow a complex judgment. The albumin concentration in the liver significantly decreased after 4 and 8 weeks and reached highly normal values in fully developed cirrhosis. In each case the serum level changed in the same sense, but less expressed. The total protein in liver and serum showed an analogous course of the curve, whereas the albumin-total protein-quotient in the liver remained unchangedly low. The relative proportion of albumin in the serum did not show a diminution in every phase. The simultaneous decrease of albumin and total protein are explained as an expression of an inhibition of the synthesis due to destruction of protein-synthesizing subcellular structures. The normalisation of the serum levels and of the highly normal albumin contents despite the developed cirrhosis become understandable by the loss of efficiency of the foreign substance thioacetamide in consequence of structural and biochemical adaptation. The thioacetamide cirrhosis of the rat in the investigated phase despite the microscopically provable so-called degenerative parenchymal damages is accompained by parameters of the increased protein metabolism. The relative serum albumin content apparantly in the first place undergoes the oncotic pressure regulation and is not suited as the measure of a hepatocellular lesion. From the diagnostic point of view the reduction of the albumin concentrations seems to be of importance in the developmental phase to cirrhosis.
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PMID:[The behavior of albumin in acute and chronic liver diseases. I. The behavior of albumin during the development of rat thioacetamide cirrhosis]. 68 33


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