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)

Endotoxaemia was investigated by the Limulus assay in 42 cirrhotic patients with ascites and in 33 without ascites. The incidence of endotoxaemia in the former group (59.5%) was significantly (P less than 0.05) higher than in the latter (36.4%). Correlation between endotoxaemia and specific gravity and concentrations of total protein, albumin, and globulin in ascitic fluid was studied in the group with ascites. The specific gravity of ascites in 25 patients with endotoxaemia was significantly greater than that in 17 patients without endotoxaemia (P less than 0.01). The concentration of total protein in patients with endotoxaemia (13.95 +/- 7.18 milligram, mean +/- SD) was nearly twice as high (P less than 0.01) as in patients without endotoxaemia (7.49 +/- 3.60 milligram). The protein content of those who showed reactions greater or equal to 2(+) in the Limulus assay (16.78 +/- 7.14 milligram) was a significantly (P less than 0.05) higher than in those with 1(+) reaction (11.26 +/- 6.33 milligram). Moreover, the concentration of albumin in patients with endotoxaemia (7.68 +/- 4.60 milligram) was more than twice that of the patients without endotoxaemia (3.39 +/- 1.58 milligram, P less than 0.01). On the other hand, globulin concentration in patients with endotoxaemia was 1.6 times that of patients without endotoxaemia (P less than 0.01). Similar differences were noted between endotoxaemic and non-endotoxaemic patients in the ascites-to-serum ratio in protein, albumin, and globulin. These results suggest that in liver cirrhosis endotoxaemia may cause an increase in protein concentrations in ascitic fluid, and that it may be a precipitating factor in the formation of ascites.
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PMID:Relationship between endotoxaemia and protein concentration of ascites in cirrhotic patients. 43 53

The influence of renal failure and of hepatic cirrhosis on the plasma protein binding of etomidate, an intravenous anaesthetic agent of basic nature, has been investigated. The percentage of free etomidate in plasma containing 1 microgram/ml was markedly increased in patients with renal failure and in patients with hepatic cirrhosis, when compared with a group of healthy volunteers (43.4 +/- 2.9% and 44.2 +/- 2.1 versus 24.9 +/- 1.4%). This decrease in binding correlated inversely with serum albumin levels in both conditions (r = -0.88 and r = 0.72, respectively) but a slight decrease in the amount bound per mole of albumin was also apparent in both types of disease.
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PMID:Plasma protein binding of etomidate in patients with renal failure or hepatic cirrhosis. 45 72

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

Plasmapheresis together with immunosuppressive drug therapy has been used in the treatment of 17 patients with glomerulonephritis [Goodpasture's syndrome (4), systemic lupus erythematosus (4), mesangiocapillary glomerulonephritis (2), glomerulonephritis associated with cirrhosis (2), nonspecific mesangial proliferative glomerulonephritis (3), Henoch-Schoenlein purpura glomerulonephritis (1) and glomerulonephritis associated with infective endocarditis (1)]. Use of the Haemonetics Model 30 blood cell separator, exchanging two liters of plasma with 5% albumin in Hartmann's solution has provided a safe, effective but relatively expensive procedure, capable of producing a marked reduction of fibrinogen, complement components, anti-glomerular basement membrane antibody and immune complex concentrations. Removal of one or more of these factors is felt to be at least partly responsible for the improvement in renal function and clinical well-being demonstrated in patients with Goodpasture's syndrome, systemic lupus erythematosus and other forms of glomerulonephritis associated with the presence of circulating immune complexes.
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PMID:Plasmapheresis in glomerulonephritis. 50 88

Twenty-one of 30 patients with essential mixed cryoglobulinemia (EMC) had evidence of liver involvement. The liver disease was characterized by the absence of clinical symptoms, hepatosplenomegaly, mild elevation of enzymes, abnormal BSP retention and low albumin levels. Histology, available in 12 patients, showed either chronic persistent or chronic active hepatitis or liver cirrhosis; 44% of the patients had HBsAg or HBsAb in sera and/or cryoglobulins, confirming the high frequency of exposure to hepatitis B virus (HBV) infection in EMC. However, liver lesions were similar in all patients, regardless of HBV exposure. Since other factors usually associated with chronic liver diseases were absent or apparently irrelevant, it is temptative to speculate that a 'cryoglobulinemic hepatitis' may exist as a distinct syndrome. The characteristic complement profile of the patients with EMC (low CH50 and C4, normal C3PA), not related to albumin levels, can help to differentiate this disease from chronic liver disease without cryoglobulins.
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PMID:Liver involvement in essential mixed cryoglobulinemia. 54 44

The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices.
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PMID:Association of abnormal fibrin polymerisation with severe liver disease. 59 Aug 52

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

Despite regular long-term parenteral vitamin D2 treatment, four patients with biliary cirrhosis had multiple symptoms of bone disease and bone biopsy specimens showed osteomalacia without osteoporosis. Three patients also had a proximal myopathy. Plasma calcium values (after correction for albumin), phosphorus, magnesium, and serum 25-hydroxy-vitamin D were within normal limits. Treatment with 1,25-dihydroxy-cholecalciferol (1,25-(OH)2D3) relieved symptoms in three of the four patients and improved those in the fourth. Histological examination of bone showed improvement in all four patients, but serum and urinary biochemical changes were not pronounced. We conclude that 1,25-(0H)2D3 treatment has a beneficial effect on bone and muscle in hepatic osteomalacia, either because vitamin D 1-hydroxylation fails in biliary cirrhosis or because hepatic osteomalacia is resistant to vitamin D2 metabolites.
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PMID:Parenteral 1,25-dihydroxycholecalciferol in hepatic osteomalacia. 62 Feb 4

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

Hypoxemia is a frequent occurrence in patients with severe hepatic disease. Multiple mechanisms have been implicated in the production of such hypoxemia. The case of a 35-year-old man with cyanosis, clubbing, and cirrhosis is presented. Physiologic data from this patient revealed normal pulmonary function, except for a low diffusing capacity and a 28 percent shunt while the patient was breathing 100 percent oxygen. A perfusion scan with radioactive 99mtechnetium-labelled macroaggregated albumin revealed 67 percent of the labelled macroaggregated albumin in the systemic circulation. Post-mortem examination demonstrated normal pulmonary parenchyma, markedly dilated intraparenchymal capillaries and arterioles, subpleural angiomata, and cirrhosis. No anatomic arteriovenous connections were demonstrated before or after death. We conclude that the arterial hypoxemia of some patients with hepatic cirrhosis results from dilated gas-exchanging blood vessels. These widened vessels prevent end pulmonary capillary oxygen tension from reaching equilibrium with alveolar gas, perhaps because of the widened distance for diffusion.
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PMID:Alveolar-capillary oxygen disequilibrium in hepatic cirrhosis. 63 Sep 68


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