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)

Patients with a metabolic block in the conversion of THCA to cholic acid develop cirrhosis and hemolysis. Tauro-THCA has been shown to distort hepatic architecture and cause hemolysis in bile-fistula rats. In this study, the critical micellular concentration of tauro-THCA was found to be one fourth of that measured for the primary human bile salt, taurocholate. In short-term incubations with intact red cells, tauro-THCA was more effective than taurocholate in removing red cell membrane lipid, inducing morphological red cell sphering, and decreasing functional cellular membrane surface area. These detergent biological membrane effects were most apparent at a concentration above the critical micellar concentration, with the membrane toxicity of the two bile salts roughly paralleling their differences in critical micellar concentration. The lower critical micellar concentration, greater hydrophobicity, and enhanced surface-active properties of tauro-THCA are speculated on as possible factors contributing to the bile salt's toxicity in vivo.
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PMID:Micellar properties of 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholestan-26-oyl taurine and relationship to in vitro red cell disruption. 47 69

Bile acid metabolism was studied in rats with cirrhosis induced by carbon tetrachloride (CCl4). Although the typical histologic features of cirrhosis were seen, cholestasis was not present in these animals as evidenced by a normal total serum bilirubin concentration and by a normal hepatic capacity to remove taurocholate infused intravenously. The cirrhotic rats also secreted taurocholate into bile at a normal rate. The total bile salt pool size in the cirrhotic rats was not significantly different from the pool size in normal rats (10.59 +/- 1.19 mumoles per gm. of liver (+/- 1 standard error of the mean) and 10.43 +/- 0.92 mumoles per gm. of liver, respectively). When the bile was drained externally through a chronic bile fistula, the normal rats increased the bile salt synthetic rate approximately 3-fold after 48 hours of drainage. However, the cirrhotic rats failed to significantly increase the synthetic rate for bile salts in response to biliary drainage. The normal rats also had a significant increase in cholic acid synthesis at the maximal synthetic rate, whereas the cirrhotic rats did not. These findings indicate that (when feedback inhibition is removed) CCl4 cirrhotic rats lack the ability to normally increase the activity of 7 alpha-hydroxylase and 12 alpha-hydroxylase, rate-limiting enzymes in the synthesis of bile salts.
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PMID:Bile acid metabolism in the cirrhotic rat. 51 42

Experimental cirrhosis was produced in dogs by the sporadic feeding of dimethylnitrosamine for the purpose of studying the temporal relationships between urinary sodium retention, plasma volume expansion, and ascites formation. Sodium retention started about 16 days following the onset of cirrhosis and preceded ascites formation by about 10 days. Plasma volume increased by 9% (P less than 0.05) within 3-4 days of sodium retention and expanded further as ascites accumulated. Splanchnic plasma volume was greater by 161 ml in 10 cirrhotic dogs with ascites than in 14 normal dogs. Nonsplanchnic volume was greater by 96 ml (P less than 0.05). Thus, the "effective" as well as the splanchnic component of the vascular space was expanded. Paracentesis did not cause the re-formation of ascites in five dogs as long as dietary salt was denied. Refeeding permitted reaccumulation of ascites and further plasma volume expansion. Renal perfusion remained constant as dogs became progressively cirrhotic. We conclude that ascites formation depends on the prior retention of urinary sodium, and occurs as an "overflow" phenomenon. A contracted effective plasma volume does not appear to be necessary for continuing sodium retention.
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PMID:Sodium retention and ascites formation in dogs with experimental portal cirrhosis. 59 55

Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). This contrasts with the conspicuous tendency of patients with Laennec's cirrhosis to retain salt and water. In an attempt to clarify this clinical observation, renal handling of sodium was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone in five patients with PBC. These PBC patients were compared with two control populations: five edema-free patients with Laennec's cirrhosis and nine healthy volunteers. The natriuretic and diuretic response to ECVE was significantly greater in the patients with PBC as compared with the two control groups. CH2O for given rates of urine flow were similar in PBC patients as compared with normal subjects. The data suggest that a supranormal rejection of sodium at the proximal tubule in response to ECVE underlies the exaggerated natriuresis of PBC. The augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this variety of cirrhosis.
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PMID:Exaggerated natriuretic response to volume expansion in patients with primary biliary cirrhosis. 60 57

Renal handling of sodium was studied in five dogs where an end-to-side portacaval fistula was constructed prior to the induction of cirrhosis with DMN. Such a model permits the effects of cirrhosis to be studied separately from the consequences of portal hypertension. Three control animals without cirrhosis maintained normal liver and kidney function and remained in sodium balance for as long as 8 weeks following surgery. In the five cirrhotic dogs, urinary sodium retention preceded ascites formation and was independent of hyperaldosteronism, hypoalbuminemia, hepatic ischemia, or decreased renal perfusion. Portal venous pressure remained normal in all cirrhotic dogs, and the splanchnic area remained free of venous collaterals. Plasma volume expansion also preceded ascites formation, and this variable increased by 8.4% (p less than 0.05) following 6 days of sodium retention. These temporal relationships between sodium retention, expanded plasma volume, and ascites formation are similar to those observed in ordinary cirrhotic dogs previously studied in this laboratory. Total plasma volume increased by 13.2% (p less than 0.05) when measured during the ascitic phase of cirrhosis. However, when the splanchnic and nonsplanchnic ("effective") components of plasma volume were measured by an exclusion technique, the ratio of these components to total plasma volume was not different from that observed in normal dogs. Thus no preferential consignment of retained salt and water had occurred. We conclude that urinary sodium retention in cirrhotic dogs occurs independently of portal hypertension or augmented splanchnic vascular capacity and is associated with expansion of the effective plasma volume, even though ascites is present.
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PMID:Renal sodium retention and ascites formation in dogs with experimental cirrhosis but without portal hypertension or increased splanchnic vascular capacity. 62 53

Twelve patients with cirrhosis, refractory ascites, and varying degrees of renal failure (creatinine clearance, 5 to 44 ml/min) were studied before and up to 2 weeks following peritoneovenous shunt. Creatinine clearance increased 60% or more in seven patients (group I) and 22% or less in five patients (group II). There were no significant differences in maximum urine output or sodium excretion between groups (group I, 4,272 ml/14 hr, 372 mEq/24 hr; group II, 3,722 ml/24 hr, 255 mEq/24 hr). Aldosterone and renin concentrations were higher in group I and showed a greater decrease after shunting. Renin substrate levels also were higher in group I and rose following shunt insertion, while group II remained low. Ascitic fluid was found to contain renin substrate in concentrations of approximately 25% to 50% of plasma concentrations. Patients with the greatest increase in creatinine clearance showed the largest rise in substrate concentration and fall in renin and aldosterone secretion, suggesting a dynamic relationship between these factors. That a diuresis could occur without significant change in these parameters in five of 12 patients suggests independent control mechanisms for renal salt and water excretion and glomerular filtration in the ascitic patient.
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PMID:Improved renal function and inhibition of renin and aldosterone secretion following peritoneovenous (LeVeen) shunt. 66 20

The labeled bile salt tolerance test is the measure of the decrease in plasmatic radioactivity after intravenous injection of carboxyl-14C-labeled chenic acid. The label is distributed in the blood, taken up by hepatocytes and then secreted in the bile. The decrease in plasmatic radioactivity during the 4 h following the injection follows a bi-exponential curve. It has been studied in 6 normal subjects, 4 patients equipped with "T tube", 3 cases of acute viral hepatitis, 4 cases of hepatic steatosis, and 6 cases of hepatic cirrhosis. The first slope (b1) represents the hepatic uptake of the label. It is lowered in cases of viral hepatitis and in cirrhosis. The second slope (b2) represents hepato-biliary secretion of the label. It is lowered in patients equipped with a "T tube". From 100 min after the injection, the plasma concentration of radioactivity remains constant. This is the residual value (R), and it is very low in normal subjects. It is increased in cases of acute viral hepatitis and cirrhosis, indicating displacement of a fraction of the bile salt pool into peripheral blood. After a standard meal, the R value is not modified in the normal subject. In cases of steatosis and cirrhosis, a temporary peak may be seen, indicating recirculation of the label towards the periphery due to a porto-systemic shunt or a hepatocyte lesion.
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PMID:[Clinical application of the radiolabeled bile salt tolerance test]. 67 9

Six patients with chronic uremia in whom ascites developed during maintenance hemodialysis are described. Their clinical and biochemical findings are reviewed and compared with data of 10 hemodialyzed patients without ascites. Liver cirrhosis was the origin of ascites in only one case. Hypoalbuminemia, liver cirrhosis, congestive heart failure, peritonitis, peritoneal tuberculosis and carcinomatosis were uniformly absent in the other patients. Long-term and marked overhydration seems to be at the origin of ascites. Lack of peripheral edema, probably due to ascites compartmentalization, was a constant finding in every noncirrhotic patient with ascites. When long-term overhydration was stopped after successful kidney transplantation or by means of diminished water and salt ingestion, reversal of the syndrome was attained. Nevertheless, ascites because of liver cirrhosis was not influenced by means of kidney transplantation. In three patients with ascites who did not receive a transplant, a significant reduction in water and salt ingestion was reached after intensive psychotherapy which led to reversal of the ascitic syndrome. In one anephric patient ascites did not develop despite water overloading. Survival has not been influenced by the formation of ascites. Further research is needed to determine the mechanism of sodium transfer across the peritoneal membrane. Influence of humoral factors can be considered, if an active transport mechanism could be demonstrated.
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PMID:Ascites in patients undergoing maintenance hemodialysis. Report of six cases and physiopathologic approach. 78 11

The object of this study was to localize increased sodium resorption in rats with chronic hepatic cirrhosis. Cirrhosis was induced by the administration of phenobarbital and carbon tetrachloride. The animals retained salt and water after loading and showed edema and ascites. Salt and water balance, clearance, and micropuncture tests were performed. Five or six weeks after the start of procedures to induce injury, the rats were unable to excrete salt and water loads promptly. Urine flow and sodium concentration were significantly less in cirrhotic rats with edema and ascites than in the normal controls. The glomerular filtration rate was slightly lower in the right, nonmicropunctured kidney but was the same in the left. The nephron glomerular filtration rates of surface nephrons were equal in both the experimental and control rats. The fractional proximal resorption rate was notably greater in cirrhotic rats, as was the total proximal nephron resorption rate. That increased proximal resorption alone might account for diminished sodium and water excretion cannot be demonstrated from this study, although we believe that major evidence is provided of the importance of proximal resorption in this phenomenon.
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PMID:A micropuncture study of salt and water retention in chronic experimental cirrhosis. 85 Nov 88

After a short survey on the history of the therapy of liver cirrhosis the importance of the prevention of alcoholism is emphasized. A "liver diet" is regarded as unnecessary, prednisolone is recommended for the treatment of the active cirrhosis. After a short description of the principles of the therapy of biliary cirrhoses, of haemochromatosis and of Wilson's hepatocerebral degeneration the use of restriction of salt, saluretics and aldosterone antagonists in the treatment of ascites is discussed in detail. After description of the conservative therapy of the haemorrhage from varices with the compression sound, intraarterial octapressin infusion and combat against consumption coagulopathy finally the prophylaxis of the hepatoportal encephalopathy with reduction of the protein intake and the restriction of the formation of toxic products of protein metabolism in the intestine by application of neomycin or lactulose, respectively, is described.
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PMID:[Conservative therapy of liver cirrhosis]. 85 44


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