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)

Blood coagulation and lysis system was studied with other biochemical serum analysis in three groups of mongrel dogs; laparotomy without hepatic resection (group I), with 50% hepatic section (group II), and 70% hepatic resection (group III). In clinical studies, six cases of hepatic tumors and one case of hepatoma with cirrhosis were selected for examinations. All the data examined in group I were restored toward normal within 48 hours. Total serum protein level was significantly decreased after hepatic resection. The protein level in group III was lower than in group II on the 4th postoperative day (P less than 0.01). In clinical studies, low serum protein levels did not reach a preoperative value even 3 weeks after extended right hepatic lobectomy. Time course of Al-P and transaminase changes in clinical studies was similar to that in experimental study with dogs. Al-P and transaminase showed an abnormally high level in the patient with hepatic cirrhosis. Serum bilirubin levels were not increased after hepatic resection. In blood coagulation and lysis system, serum fibrinogen levels were markedly decreased: 50% reduction in group III and 30% reduction in group II on the first postoperative day. The degree of decrease in the fibrinogen level was proportional to the size of resected volume of the liver. On the other hand, in clinical studies fibrinogen levels were slightly decreased. In the case of hepatic resection with cirrhosis, however, the values were markedly decreased: 40% reduction on the 4th and 25% on the 21st postoperative days. Fibrinolysis system was accelerated group II and III. The acceleration continued until 3 weeks after hepatic resection. From these results it may be concluded that analysis of blood coagulation and lysis system after hepatic resection is useful in evaluating a residual hepatic function after partial resection and in selecting a treatment suitable for hepatic insufficiency.
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PMID:[Experimental and clinical studies on blood coagulation and lysis system after hepatic resection (author's transl)]. 23 Oct 2

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

Serum concentrations of 3,3',5'-triiodothyronine (reverse T3, rT3) were measured in adult patients with several systemic illnesses whose serum total and/or free T3 were low, serum total T4 was low or normal, and free T4 was either normal or elevated. The mean serum rT3 was 76, 46, and 77 ng per 100 ml in patients with hepatic cirrhosis, chronic renal failure, and acute febrile illnesses, respectively; the values in patients with hepatic cirrhosis and acute febrile illness were significantly higher than, and values in patients with renal failure did not differ significantly from, the mean serum rT3 (41 ng per 100 ml) in normal subjects. The mean serum rT3 in another group of patients from Calcutta, India, who had severe protein calorie malnutrition (PCM), was 53 ng per 100 ml; it was significantly higher than the corresponding value, 22 ng per 100 ml, in the same patients after feeding treatment. Mean serum rT3 in patients with systemic illnesses was not so high as that (151 ng per 100 ml) in the normal newborn, who also has low serum T3 and normal or high T4. High serum rT3 in patients with systemic illness could not be attributed to increased serum protein binding of rT3; whenever studied, the dialyzable fraction of rT3 was not decreased but actually increased. The mean serum-free rT3 was 450,207, and 366 pg per 100 per 100 ml in patients with hepatic cirrhosis, chronic renal failure, and acute febrile illnesses, respectively; each of these values was significantly higher than the corresponding value, 98 pg per 100 ml, in normal subjects. The mean serum free rT3, 516 pg per 100 ml, in newborn cord sera was similar to that in patients with hepatic cirrhosis but was higher than that observed in patients with chronic renal failure and acute febrile illnesses. High serum rT3 and low serum T3 in patients with PCM improved to normal or towards normal after feeding treatment. Since the peripheral metabolism of T4 is normally the predominant source of T3 as well as rT3 in man, our data, demonstrating reciprocal changes in serum rT3 and T3 and no consistent change in serum T4, suggest that body metabolism of T4 may be so altered in systemic illness that the conversion of T4 to rT3 may be increased while that to T3 is decreased. The mechanism or the biological significance of such a diversion of T4, from the normally occurring conversion to highly potent T3, to the generation of poorly calorigenic rT3 in systemic illness, is not clear at this time. The data in patients with PCM demonstrate, however, that such a change in the metabolism of T4 can be reversible.
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PMID:Reciprocal changes in serum concentrations of 3,3',5-triiodothyronine (T3) in systemic illnesses. 81 82

The elimination of para-aminosalicylic acid (PAS) after the intravenous injection of 20 mg PAS sodium/kg was estimated in patients with liver disease, in uremic patients and in volunteers without damage of the liver or kidneys. The drug was estimated with a colorimetric and fluorometric method. In the volunteers, the half-lives obtained with the fluorometric method were significantly longer than those estimated with the colorimetric method. This is caused by the estimation of more PAS metabolites by the used fluorometric method. In the patients with renal insufficiency (dialysis patients) the elimination rate of unchanged PAS--estimated with the colorimetric method--was not altered, whereas the elimination of PAS and its metabolites extractable by ethyl acetate was markedly slowed in comparison with the results obtained with the volunteers. The clearance of the unchanged PAS was even increased in the uremic patients. The serum protein binding of PAS was lowered significantly in the serum of uremic patients. In patients with liver cirrhosis, acute virus hepatitis and cholangitis the elimination rate of the drug was not altered in comparison with the volunteers. The results show that the dose of PAS in patients with renal insufficiency may not be reduced. The therapeutic level of the drug cannot otherwise be reached in these patients.
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PMID:Elimination of para-aminosalicylic acid in patients with liver disease and renal insufficiency. 92 30

The protein content in serum and peritoneal fluid has been determined and analysed electrophoretically in patients with Crohn's disease and ulcerative colitis and the data obtained compared with previously published data on serum and ascites content in liver cirrhosis, heart failure and intestinal tuberculosis. Ascites fluid in liver cirrhosis and heart failure, representing a true transudate, had a comparatively low protein content while the ascites fluid in inflammatory bowel diseases including Crohn's disease had high protein content. There was no difference in ascites protein content or ascites/serum protein ratio between patients with Crohn's disease and patients with ulcerative colitis. An exudative nature of both these inflammatory bowel conditions appears to be the main cause to the peritoneal fluid often observed at laparotomy. It cannot be excluded, however, that a lymphatic stasis, which is thought to be involved in Crohn's disease, might at least partly contribute to the development when larger quantities of ascitic fluid are at hand in this disease.
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PMID:Protein patterns in serum and peritoneal fluid in Crohn's disease and ulcerative colitis. 93 40

The determination of plasma viscosity in 37 patients with liver disease allowed their subdivision into three groups. Firstly, decreased viscosity (hypoviscosity) was found in patients with cirrhosis, marked portal hypertension and esophageal varices. Secondly, normal viscosity (normoviscosity) was found in patients with inactive cirrhosis without portal hypertension, and thirdly, increased viscosity (hyperviscosity) was found in patients with active cirrhosis and chronic progressive hepatitis. The concentrations of total serum protein, of fibrinogen and of IgG were found to influence plasma viscosity. A detailed differentiation revealed that increased plasma viscosity is caused by increased levels of IgG while decreased viscosity correlates with low fibrinogen levels. Furthermore a close correlation exists between plasma viscosity and the enzymatic activity of SGOT, SGPT and GLDH. In 5 patients with chronic progressive hepatitis treated with corticosteroids the plasma viscosity normalized in parallel with improvement of the hepato-cellular damage. These findings will be discussed in detail. Hyperviscosity might possibly serve as an additional parameter to characterize chronic progressive hepatitis and to indicate steroid treatment.
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PMID:[Changes of blood-flow properties in patients with chronic liver disease (author's transl)]. 113 47

Duodenal and jejunal absorption of a nutrient solution at two different caloric loads (1.32 and 3.96 kcal/min = 5.6 and 16.8 kJ/min) was compared in chronic alcoholics without malnutrition, liver cirrhosis, obvious small-bowel dysfunction, and exocrine pancreatic insufficiency and in an age-matched control group, by means of the intestinal perfusion technique. In chronic alcoholics duodenal net absorption of water (p < 0.025), sodium (p < 0.02), potassium (p < 0.005), total nitrogen (p < 0.02), carbohydrates (p < 0.05), and lipids (p < 0.05) was lower than in controls when both caloric loads were administered, but jejunal absorption rates were not decreased. Biliopancreatic secretion did not differ between alcoholics and controls. Higher serum protein leakage in alcoholics was indicated by an increased (p < 0.01) duodenal alpha 1-antitrypsin clearance under low caloric load infusion. It is concluded that the absorptive function of the duodenum is impaired in alcoholics, whereas the upper jejunum is not affected.
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PMID:Absorption of a nutrient solution in chronic alcoholics without nutrient deficiencies and liver cirrhosis. 147 18

In the United States, approximately one million patients each year develop a pleural effusion. Pleural effusions have classically been divided into transudative and exudative pleural effusions. A transudative pleural effusion occurs when the systemic factors influencing pleural fluid formation and reabsorption are altered so that pleural fluid accumulates; an exudative pleural effusion occurs when the local factors influencing pleural fluid formation and reabsorption are altered, allowing accumulation of pleural fluid. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis with ascites. The leading causes of exudative pleural effusions are pneumonia, malignancy, and pulmonary embolization. Transudative pleural effusions can be differentiated from exudative pleural effusions by measurement of the pleural fluid protein and lactic dehydrogenase (LDH) levels. The ratio of the pleural fluid protein to the serum protein is less than 0.5, the ratio of the pleural fluid LDH to the serum LDH is less than 0.6, and the absolute value of the pleural fluid LDH level is less than two thirds of the upper normal limit for serum with transudative pleural effusions while at least one of these criteria is not met with exudative effusions. Most patients who have a pleural effusion with congestive heart failure have left ventricular failure. It is believed that the transudation of the pulmonary interstitial fluid across the visceral pleura overwhelms the capacity of the lymphatics to remove the fluid. Most patients with cirrhosis who have a pleural effusion also have ascites. It is also believed that the pleural effusions form when fluid moves directly from the peritoneal cavity into the pleural cavity through pores in the diaphragm. Approximately 40% of patients with pneumonia will have a pleural effusion. If these patients have a significant amount of pleural fluid, a diagnostic thoracentesis should be performed. Chest tubes should be inserted if the pleural fluid is gross pus, if the Gram stain of the pleural fluid is positive, if the pleural fluid glucose level is below 40 mg/dl, or if the pleural fluid pH level is less than 7.00. If drainage with the chest tubes is unsatisfactory, either streptokinase or urokinase should be injected intrapleurally. If drainage is still unsatisfactory, a decortication should be considered. The three leading malignancies that have an associated pleural effusion are breast carcinoma, lung carcinoma, lymphomas and leukemias. The diagnosis of pleural malignancy is made most commonly with pleural fluid cytology; in recent years immunohistochemical tests have proved invaluable in differentiating benign from malignant pleural effusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pleural diseases. 157 32

To evaluate abnormal secretion of growth hormone (GH) in cases of liver diseases, the authors performed a loading test of growth hormone-releasing factor (GRF) and approximately one week later, a loading test of thyrotropin-releasing hormone (TRH), and measured serum GH in 15 cases of liver cirrhosis (LC), 5 with chronic active hepatitis (CAH), and 5 controls. In the TRH test, 8 of 15 LC patients showed a peak GH value of 6 ng/ml or more and were classified as the TRH-responder group (LC-R). Seven other LC patients showing a peak GH value of less than 6 ng/ml were classified as the TRH-non-responder group (LC-NR). None of the CAH cases or controls showed a peak GH value of 6 ng/ml or more. In GRF test, the response of GH was poor in all 8 in the LC-R group. The responses in the LC-NR group were significantly greater than those in the LC-R group from 15 to 90 minutes after the GRF loading. In the LC-R group, greater impairment of liver function was indicated by total bilirubin, serum protein and cholinesterase values compared to the LC-NR group. Fischer's ratio was significantly lower in the LC-R group. In cases of liver diseases, Fischer's ratios negatively correlated with the peak GH values in the TRH test (r = -0.679, P less than 0.01). These results suggest that in LC cases showing a paradoxical GH response to TRH, the GH response to GRF which is a GH stimulatory hormone, is decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal GH secretion in liver cirrhosis: evaluation of using GRF test and TRH test. 162 79

Thirty four patients with peritoneoscopy and/or biopsy proven uncomplicated cirrhosis of liver with ascites were studied for the effect of diuretic therapy on ascitic fluid protein and cell count. Renal function tests, liver function tests, ascitic fluid protein concentration and cell count were estimated prior to diuretic therapy and once every week till the end of therapy. There was no change in mean total serum protein (5.71 +/- 0.58 g/dl to 5.72 +/- 0.63 g/dl). The rise in mean ascitic fluid protein from 1.55 +/- 0.77 g/dl to 1.76 +/- 0.79 g/dl was not significant (P greater than 0.05). Twenty one patients (Group I) showed a rise in ascitic fluid protein concentration while 13 patients (Group II) did not show a rise or showed a fall in protein concentration during diuretic therapy. The rise in ascitic fluid protein concentration in Group I from 1.62 +/- 0.69 g/dl to 2.05 +/- 0.67 g/dl was statistically significant (P less than 0.05). Group I patients had a mean weight loss of 6.21 +/- 3.66 kg as compared to 3.15 +/- 2.00 kg in Group II patients (p less than 0.05). There was no other difference between Group I and Group II patients. Only 5 patients showed a rise in ascitic fluid cell count (more than 50 cell/mm3). It is concluded that diuretic therapy alters ascitic fluid protein concentration in a majority of patients but has no significant effect on cell count.
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PMID:Ascitic fluid protein and cellular changes during diuretic therapy in cirrhosis of liver. 188 96


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