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)

This study was undertaken to determine the pathogenesis of muscle atrophy that frequently accompanies liver disease. Hepatic injury was induced in rats by giving weekly intragastric doses of carbon tetrachloride (CCl4) in combination with phenobarbital in the drinking water. Muscle protein catabolism was assessed during three stages of liver injury and compared with pair-fed controls: group A had hepatic necrosis and inflammation without significant fibrosis; group B had cirrhosis as well as necrosis and inflammation; and group C had cirrhosis with minimal necrosis and inflammation. In group A, vastus lateralis white muscle, which contained predominantly fast glycolytic fibers, showed a significant increase in protein catabolic rates compared with pair fed controls (0.95 +/- 0.05 nmol tyrosine released.mg-1.2 h-1 vs. 0.86 +/- 0.04; P less than 0.05). In group B, protein catabolic rates were significantly increased in vastus lateralis white muscles, as well as two muscles that have a mixed fiber composition, diaphragm, and triceps. Protein catabolic rates were not increased in soleus muscle that predominantly contained slow oxidative fibers in either group A or B. In group C rats there was no increase in catabolic rates in diaphragm or vastus lateralis white muscle. None of the muscles from group B had any impairment in protein synthesis. In diaphragms from group B animals, there was a selective reduction in the cross-sectional areas of fast glycolytic fibers (3725 +/- 224 mm2 control vs. 2926 +/- 208 mm2 experimental; P less than 0.01). This study indicated that liver injury characterized by inflammation and hepatocyte necrosis, with or without cirrhosis, was associated with muscle atrophy that selectively affected fast glycolytic fibers. This muscle atrophy was caused by an increase in protein catabolism and was not the result of an inhibition of protein synthesis.
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PMID:Increased muscle protein catabolism caused by carbon tetrachloride hepatic injury in rats. 156 80

Ascites formation in patients with cirrhosis of the liver is dependent on local factors that preferentially localize any fluid retention to the peritoneal space and systemic factors that favor renal retention of salt and water. The local factors are largely related to adaptive changes in the hepatic sinusoids and mesenteric capillaries in response to an increase in hydrostatic pressure. The systemic factors reflect the disturbance in volume homeostasis evident in patients with cirrhosis and are largely explained by the neurohumoral consequences of a decreased peripheral vascular resistance.
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PMID:Pathophysiology of ascites formation. 156 74

Water immersion was used as the treatment method in a patient with ascites caused by liver cirrhosis resistant to therapy. Application of water immersion caused only a short improvement; it was probably connected with the shortterm natriuretic effect. The joint effect of a diuretics and of the water immersion was beneficial.
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PMID:[Therapeutic use of the method of water immersion in a patient with ascites in uncompensated cirrhosis of the liver]. 164 67

In order to investigate the possible risk factors of primary hepato-carcinoma (PHC) in Tianjin, 122 clinical diagnosed PHC patients and matched hospital controls were interviewed and 99 pairs of their blood samples were examined for HBV. The findings confirmed the strong association between HBV infection and PHC. The individual's immune state during HBV infection might be an important factor for PHC development. Histories of hepatitis and cirrhosis and family history of PHC were risk factors of PHC. Cigarette smoking might have association with PHC. Smoking for more the years of, the higher the risk of PHC. The present study did not find association between PHC and drinking water, dietary habits, alcohol consumption, histories of blood transfusion and injection, exposure to pesticides and poison.
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PMID:[A study on aetiological factors of primary hepato-carcinoma in Tianjin China]. 166 80

Evaluation of postoperative disturbance in the sodium and water balance was made in eight patients with compensated liver cirrhosis who had undergone segmental hepatectomy for hepatocellular carcinoma and had received unrestricted administration of sodium and water to maintain a normal urine output. On postoperative day 3, a significantly higher plasma atrial natriuretic peptide level and a significantly lower plasma aldosterone level were noted compared with postoperative day 1: the hormonal levels on postoperative day 3 were similar to the postinfusion levels obtained by the preoperative saline-loading test, which was performed to assess the physiological control of effective extracellular fluid and blood volume. Pulmonary artery and pulmonary wedge pressures were slightly, but significantly, higher on postoperative day 3 than on postoperative day 1. These results suggest that unrestricted fluid management prevents the depletion of effective extracellular fluid and blood volume on postoperative day 1, and permits their slight excess on postoperative day 3.
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PMID:Evaluation of preoperative and postoperative sodium and water loading in patients undergoing hepatectomy for liver cirrhosis complicated by hepatocellular carcinoma. 166 78

The malnourished alcoholic patient requires frequently hospitalization for treatment and an adequate nutritional support is necessary for recovery of their health. The objective of the present study was to evaluate the nutritional value of an enteral diet based on "soya milk", corn sugar, coconut oil and water. Seven alcoholics, males, with 36.4 year mean age, without any clinical evidence of hepatic cirrhosis and/or pancreatitis, were submitted to three periods of metabolic nitrogen balance (NB), with multiple levels of protein intake (0.4, 0.6 and 0.8 grams of proteins/kg of body weight/day). The nitrogen intake (NI), the fecal nitrogen (FN) and the urinary nitrogen (UN) were determined, and the NB and protein digestibility value were calculated. The net protein utilization (NPU) was calculated by correlation studies between the NI and NB, with a value of 101.3%. The mean true digestibility was 100.1% and the mean requirement for that population was 0.5g protein/kg of body weight/day. Using a 97.5% confidence limit, the protein requirement of the enteral diet was calculated to be 0.8g protein/kg of body weight/day. The enteral diet based on "soya milk" can be profitable for this group of patients. It is a good alternative for use in enteral nutrition, easily available, well tolerable, and of high biological value.
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PMID:[Nutritional value of soya milk in the treatment of malnourished alcoholic patients]. 166 22

Micro- and macronodular experimental cirrhosis-like liver lesion was induced in female rats by administration of 0.03% thioacetamide (TAA) in drinking water for 3 or 6 months. The activity of gamma-glutamyltranspeptidase (GGT) and the distribution pattern of this enzyme within the liver structure were investigated 14 d after withdrawal of TAA in comparison to neonatal and adult normal liver. GGT activity was extremely high at birth. Chronic TAA administration led to a strong increase in hepatic GGT activity in dependence on duration of TAA administration in comparison to adult controls. In accordance to these results we observed by enzyme-histochemistry a small to moderate hepatocellular GGT activity after 3 months of TAA treatment. GGT activity was also demonstrable in epithelia of proliferated ductuli biliferi of single enlarged portal tracts. After 6 months of TAA administration the hepatocellular GGT activity was moderate to strong. It was demonstrable both in parenchymal (preneo-plastic) nodules and in cholangiocellular/cholangioductular proliferates. A GGT activity of mesenchymal cells was not demonstrable. We conclude that the increased hepatic GGT activity after chronic TAA administration can be correlated with the process of development of preneoplastic nodules. A relation between increased GGT activity and the process of cirrhogenesis does not seem to be probable in this animal cirrhosis model.
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PMID:Gamma-glutamyltranspeptidase (GGT) in experimental liver cirrhosis induced by thioacetamide: a biochemical and enzymehistochemical study. 168 70

Changes in the major component of renal cortical membranes as well as membrane fluidity and Na+, K+, ATPase activity have been studied in membranes from the renal cortex of rats with experimental liver cirrhosis, which show renal sodium and water retention, and in normal animals. Rats with cirrhosis of the liver show a decrease in cholesterol, phospholipid and protein content, without changes in cholesterol/phospholipid molar ratio. In addition there is a small decrease in 14:0 and 18:2 and an increase in 20:4 content, without differences in unsaturation degree. Membrane fluidity was decreased in renal membranes from cirrhotic rats when compared with normal ones. Na+, K+, ATPase activity was higher in cirrhotic than in normal renal membranes could be related with the changes in renal water and electrolyte changes shown by cirrhotic rats.
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PMID:Alterations in the physicochemical properties of renal cortical membranes in rats with experimental cirrhosis of the liver. 170 76

Torasemide (torsemide) is a high-ceiling loop diuretic which acts on the thick ascending limb of the loop of Henle to promote rapid and marked excretion of water, sodium and chloride. Like furosemide (frusemide), its major site of action is from the luminal side of the cell. Torasemide is at least twice as potent as furosemide on a weight-for-weight basis, produces equivalent diuresis and natriuresis at lower urinary concentrations and has a longer duration of action, allowing once-daily administration without the paradoxical antidiuresis seen with furosemide. Torasemide also appears to promote excretion of potassium and calcium to a lesser extent than furosemide. In trials of up to 48 weeks' duration in patients with mild to moderate essential hypertension, torasemide, administered as a single daily dose, has been shown to achieve adequate blood pressure control reaching steady-state within 8 to 12 weeks. Those patients not responding initially have generally responded to a doubling of the dose. Comparative trials of up to 6 months show torasemide is as effective as indapamide, hydrochlorothiazide or a combination of triamterene/hydrochlorothiazide in maintaining control of blood pressure. Torasemide has also been used successfully to treat oedematous states associated with chronic congestive heart failure, renal disease and hepatic cirrhosis. In short term trials control of blood pressure, bodyweight and residual oedema has been sustained. Torasemide appears to be a useful alternative to furosemide in these patients, providing potent and long-lasting diuresis while being relatively potassium and calcium sparing. In clinical trials to date torasemide has been well tolerated with adverse effects of a mild, transient nature reported by only small numbers of patients. Changes in biochemical parameters have been common, including decreases in plasma sodium and potassium levels and increases in plasma creatinine and uric acid levels. These changes are typical of loop diuretics. No changes were clinically significant nor were clinically relevant changes noted in glucose metabolism, cholesterol or triglyceride levels or in haematological values. Thus, torasemide is an interesting new loop diuretic with potential use in the treatment of mild to moderate essential hypertension and of oedematous states in which diuretic therapy is warranted. Preliminary studies suggest it to be as efficacious as other diuretics in common use and to have some advantage over furosemide in duration of action and in effects on potassium and calcium. However, further long term trials in larger groups of patients are needed to delineate the place of torasemide in therapy fully, both as a single agent and in combination with other currently accepted drug regimens.
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PMID:Torasemide. A review of its pharmacological properties and therapeutic potential. 170 90

Current concepts of the pathophysiology of ascites formation in cirrhosis of the liver have become more complex. Traditionally, the initiating event of renal sodium and water retention in cirrhosis was considered to be ascites formation ("underfilling" hypothesis) or primary renal dysfunction ("overflow" hypothesis). Changes in systemic, splanchnic and renal hemodynamics, as well as of volume regulating hormones observed in cirrhosis are compatible with a decrease in effective blood volume as suggested by the "underfilling" hypothesis. These changes, however, have been shown to precede ascites formation. This observation, together with the demonstration of an increase in total blood volume in cirrhosis prompted the "overflow" hypothesis. However, many studies are incompatible with this concept and, in addition, the agent causing primary renal sodium retention in cirrhosis still remains to be defined. The recently proposed "vasodilation" hypothesis reconciles the most salient features of both theories, proposing peripheral arterial vasodilation as the initiating event of decreased effective blood volume and renal sodium retention. Further studies are needed to elucidate the temporal relationship and more precisely define the character of hemodynamic, humoral and renal changes in cirrhosis of the liver.
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PMID:Pathophysiology of ascites formation in cirrhosis of the liver. 176 51


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