Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 22 normal subjects and 22 patients suffering from liver cirrhosis and ascites, sodium, potassium and water concentrations in the red blood cell and plasma were determined. In patients with liver cirrhosis complicated by ascites (compared with control subjects) we found out: Red blood cell sodium concentration was significantly increased in cirrhotic patients (p less than 0.001). The potassium and water content in red blood cells was not significantly different in the 2 groups. Sodium concentration in the plasma of cirrhotic patients was significantly decreased (p less than 0.01).
 ...
PMID:Some red blood cell abnormalities in patients with liver cirrhosis and ascites. I. Red blood cell sodium, potassium and water content. 398 58

Ten patients with compensated cirrhosis of the liver, 7 patients with portal decompensated cirrhosis of the liver and 10 patients with intact liver function were investigated. After intravenous injection of 40 mg furosemide elimination half-life, total and excretory clearance were not significantly different in the 3 groups investigated, but renal clearance was enhanced in the 2 cirrhosis groups and nonrenal clearance diminished in patients with decompensated cirrhosis of the liver. In those patients distributional volumes were significantly higher than in the control group. According to the increased urinary excretion of unchanged furosemide in patients with cirrhosis of the liver, the pharmacodynamic effect of the drug is enhanced: In the first 4-h-collecting period the excretion of water, chloride and sodium is significantly more increased than in the control group. After a period of 24 h this effect is still noticeable. The effect of furosemide on the excretion of potassium, creatinine and urea nitrogen is not significantly influenced by liver disease. Doubling the dose from 40 to 80 mg furosemide did not enhance the diuretic effect of the drug despite the doubled urinary excretion of unchanged furosemide.
 ...
PMID:Pharmacokinetics and pharmacodynamic effects of furosemide in patients with liver cirrhosis. 399 98

Renal excretion, skeletal muscle content and plasma concentration of electrolytes were studied in 108 patients on long-term diuretic therapy for congestive heart failure and/or arterial hypertension. As reference populations served a group of 16 healthy volunteers and a group of 22 patients with liver cirrhosis, but not on diuretic therapy. Diuretic therapy was found to deprive the patients of their ability to conserve potassium and magnesium when there was a simultaneous cellular depletion of these ions. Magnesium excretion was found to be correlated to the skeletal muscle magnesium content. An inverted Na/K ratio in urine and a low magnesium excretion were fair indicators of cellular magnesium depletion.
 ...
PMID:Renal excretion of electrolytes in patients on long-term diuretic therapy for arterial hypertension and/or congestive heart failure. 409 Oct 44

Measurements of total body potassium (T.B.K.) were made by whole-body counting in four groups of patients receiving oral frusemide for one year. Patients in group 1 had essential hypertension and normal renal function and received 40 mg frusemide daily without potassium supplements. Patients in group 2 were similar but received oral potassium supplements for the first four months of treatment. Patients in group 3 had hypertension associated with renal disease and received 120 mg frusemide daily without potassium supplements. Patients in group 4 also had hypertension and renal impairment and in addition to 120 mg frusemide daily they received oral potassium supplements for four months. No evidence of depletion of T.B.K. was found in any of the groups after continuous treatment with frusemide for one year. It is questioned whether potassium supplementation in long term diuretic therapy with frusemide is necessary unless there is evidence of pre-existing potassium depletion or of some other factor such as cardiac failure, cirrhosis of the liver, or the nephrotic syndrome.
 ...
PMID:Total body potassium in long-term frusemide therapy: is potassium supplementation necessary? 421 34

In a significant percentage of examined cases of fulminant hepatitis, subacute hepatitis, chronic aggressive hepatitis, liver cirrhosis and chronic persistent hepatitis, Australia (hepatitis-associated) antigen (Au HAA) was identified in the liver and in extrahepatic locations. The several immunofluorescent patterns of Au HAA localization in hepatocytes strongly suggested various stages of Au HAA accumulation and release. Deposits of a mixture of immunoglobulins G and M and occasionally beta1C-globulin were found in the cytoplasm of Au HAA containing hepatocytes, on their plasma membranes, on or in the nuclei, in the cytoplasm of Kupffer cells and, rarely, in the sinusoids. The accompanying tissue changes were hepatocellular degeneration and necrosis. These intra- and extracellular complexes of Au HAA and immunoglobulins displayed strong affinity for guinea pig complement in the immunohistochemical complement fixation reaction. When tested by immunodiffusion in agar, IgG dissociated from these complexes by potassium thiocyanate (KSCN) treatment showed anti-Au HAA specificity. In fulminant hepatitis neither Au HAA nor immunoglobulins and complement were found in the liver. In chronic aggressive hepatitis and subacute hepatitis the amount of the Au HAA immune complexes identified in the liver was approximately inversely proportional to the extent and severity of the parenchymal lesions. In liver cirrhosis and chronic persistent hepatitis there was a positive correlation between the amount of the Au HAA immune complexes found in the liver and the degree of hepatocellular damage. The deposits of Au HAA, identified in extrahepatic locations including germinal centers of lymph nodes and spleen, kidney glomeruli and blood vessel walls, were as a rule accompanied by deposits of IgG, IgM, beta1C-globulin and fibrin. All these deposits showed strong affinity for guinea pig complement in the immunohistochemical reaction of complement fixation. Germinal center activation, chronic membraneous glomerulonephritis, panarteritis and simple arteriolar hyalinosis were found at sites of localization of these deposits.
 ...
PMID:Tissue localization of Australia antigen immune complexes in acute and chronic hepatitis and liver cirrhosis. 462 11

Forty-two patients with autoimmune liver disease have been investigated. Renal tubular acidosis was detected in 60% of the patients with primary biliary cirrhosis, in 30% with active chronic hepatitis, and in one out of seven cases with cryptogenic cirrhosis. The presence of the defect of renal acidification was not related to the level of plasma potassium, copper, or total globulin, nor to the pattern of immunological abnormalities detected in the serum. It is suggested that autoimmune liver disease and renal tubular acidosis may be part of a systemic disorder in the pathogenesis of which immunological mechanisms are involved.
 ...
PMID:Renal tubular acidosis and autoimmune liver disease. 554 62

Twelve cirrhotic patients with portal hypertension and esophageal varices were treated with nadolol for 1 month, and the effects on renal and hepatic hemodynamics and function were studied. A significant decrease in cardiac output, portohepatic gradient, and effective hepatic blood flow was found, whereas mean arterial pressure, liver function, effective renal blood flow, glomerular filtration rate, and urinary sodium and potassium excretions were not affected. In seven patients esophageal varices were also reduced. A significant correlation was found between the decrease in portohepatic gradient and that in cardiac output. The percentage of cardiac output distributed to the kidneys was significantly increased after nadolol treatment. In conclusion, nadolol seems to have properties useful for the treatment of portal hypertension in patients with liver cirrhosis.
 ...
PMID:Effects of nadolol treatment on renal and hepatic hemodynamics and function in cirrhotic patients with portal hypertension. 614 80

Thirty-seven patients with liver cirrhosis (16 without ascites: group 1; 21 with untreated ascites at the first onset: group 2) were studied during controlled sodium intake (40 mmol/day). Renal plasma flow, glomerular filtration rate, urinary sodium excretion, plasma sodium and potassium, plasma renin activity, plasma aldosterone concentration, blood volume, and arterial pressure were evaluated. All the patients had normal renal perfusion, plasma sodium and potassium, and arterial pressure. Mean plasma renin activity and plasma aldosterone concentration were significantly depressed in group 1 (p less than 0.001, p less than 0.005 respectively) compared with 21 normal controls in identical experimental conditions. This was possibly a consequence of expanded blood volume (p less than 0.001 compared with controls) which was directly correlated with plasma aldosterone concentration (p less than 0.001). In group 2 plasma renin activity and plasma aldosterone concentration were normal in over 50% of cases. Blood volume was lower than in group 1 (p less than 0.002), but again related to plasma aldosterone concentration (p less than 0.01). In both groups plasma aldosterone concentration was hyperbolically and inversely correlated with urinary sodium excretion, but the two curves were progressively shifted to the left in respect to controls suggesting an enhanced renal tubular sensitivity to the hormone. The results suggest that aldosterone related renal sodium retention, with consequent blood volume expansion, occurs before ascites formation. The mineralocorticoid activity of aldosterone is amplified by an enhanced sensitivity of renal tubules which appears to increase as the disease progresses.
 ...
PMID:Aldosterone related blood volume expansion in cirrhosis before and during the early phase of ascites formation. 634 31

The management of ascites is a serious postoperative problem in patients with liver cirrhosis. The present study reports the effect of potassium, glucose and insulin treatment (P.G.I. treatment) applied before and after surgery in such patients. Twenty-two patients who underwent trans-abdominal esophageal transection received P.G.I. treatment, and the volume of postoperative ascites was compared with that seen in 62 cases who underwent the same operation without P.G.I. Ascites was assessed on the 21st postoperative day by physical examination. Of the 22 cases who had undergone P.G.I., 72.7% were without ascites and 27.3% with ascites. For the 63 cases who did not receive P.G.I., however, the figures were 48.4% and 51.6% respectively. The rate of ascites development is significantly different (P less than 0.05) between the two groups. This suggests that P.G.I. treatment tends to prevent the development of ascites after trans-abdominal esophageal transection, in patients with liver cirrhosis.
 ...
PMID:Potassium, glucose and insulin in the management of ascites after esophageal transection. 635 Feb 9

Piretanide is a high-ceiling, loop-active diuretic that has been developed for treatment of congestive heart failure, hypertension and edematous states caused by renal and hepatic diseases. Piretanide is structurally related to furosemide and bumetanide; when administered orally, 6 mg of piretanide is as effective as 40 mg of furosemide, and when administered intravenously, 12 mg of piretanide is as effective as 40 mg of furosemide. Piretanide enhances water and sodium excretion in patients with congestive heart failure, with nephrotic syndrome and with cirrhosis and ascites. Adverse effects reported to date are limited to those attributable to excess loss of fluid and electrolytes. Under some conditions, piretanide appears to be less potassium wasting than thiazide diuretics or other loop-active diuretics.
 ...
PMID:Piretanide: a loop-active diuretic. Pharmacology, therapeutic efficacy and adverse effects. 638 44


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>