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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the sodium retention of cirrhosis is attributable primarily to enhanced tubular reabsorption of sodium, the precise nephron sites responsible remain the subject of continuing controversy. Since changes in phosphate clearance may be used as an index of proximal sodium reabsorption, we undertook to characterize the effects of immersion-induced volume expansion on renal sodium and phosphate handling in order to clarify further the nephron sites of enhanced Na reabsorption. 18 cirrhotic patients were studied twice while in balance on a 10-mEq sodium. 100-mEq potassium diet during a control period and during water immersion. Cirrhotic patients manifested a wide continuum of responses characterized by either a sluggish or barely discernible natriuretic response (group I, n = 5) or an appropriate natriuretic response (group II, n = 13). Despite widely varying natriuretic responses, group I patients manifested a phosphaturic response to water immersion which was virtually identical to that of group II patients. The current findings indicate that distal sodium reabsorption contributes importantly to the sodium content of the final urine in cirrhotic patients with sodium retention.
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PMID:Interrelationship of renal sodium and phosphate handling in cirrhosis. 716 92

The intracellular potassium content of leukocytes, the extracellular fluid volume (82Br space), and exchangeable potassium were determined in 28 patients with cirrhosis of the liver (18 with ascites) and in 15 hospitalized controls. No intracellular potassium depletion could be identified in these patients. Leukocyte potassium was similar in cirrhotic patients with and without ascites (355.9 +/- 25.3 and 348.1 +/- 31.9 mEq/kg of dry solids, respectively) and in hospitalized controls (359.7 +/- 27.4) (mean +/- SD). The extracellular fluid volume was similar in controls and cirrhotics without ascites, but markedly increased in cirrhotics with ascites. The exchangeable potassium (mEq/kg of body weight) was similar in nonascitic cirrhotics and in hospitalized controls, but significantly lower in patients with cirrhosis and ascites. However, when the estimated weight of the extracellular fluid volume was substrated from the total body weight, thus obviating the influence of the increased extracellular fluid volume of ascitic patients in the body weight, the exchangeable potassium (mEq/kg of "corrected" body weight) was similar in cirrhosis with ascites (52.9 +/- 6.7 mEq/kg), nonascitic cirrhotics (55.8 +/- 6.1 mEq/kg) and hospitalized controls (55.0 +/- 8.3 mEq/kg), and a significant correlation was obtained between the exchangeable potassium and the leukocyte potassium content. In five patients, the measurements were repeated after relieving ascites with diuretics. No change was observed in the leukocyte potassium, but exchangeable potassium (mEq/kg of body weight) increased, reaching values not significantly different from controls or nonascitic cirrhotics. The exchangeable potassium (mEq/kg of "correct" body weight) did not change. Our results strongly suggest that potassium depletion was not present in the series of cirrhotic patients studied.
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PMID:Intracellular and exchangeable potassium in cirrhosis. Evidence against the occurrence of potassium depletion in cirrhosis with ascites. 726 37

Previous studies have demonstrated abnormalities of intracellular electrolyte content and sodium transport in leukocytes of patients with fulminant hepatic failure. The current study was undertaken to establish whether similar abnormalities were present in patients with encephalopathy from advanced cirrhosis. Results from 19 patients with advanced cirrhosis showed values for the leukocyte total sodium efflux-rate constant were significantly reduced in patients, 3.02 +/- 1 SEM 0.12 h-1, compared to control values, 3.80 +/- 0.06 h-1. This reduction was due primarily to a lowering of the ouabain-sensitive component of sodium efflux, a measure of Na,K-ATPase activity. In comparison, leukocytes from patients with fulminant hepatic failure show a greater inhibition of the ouabain-sensitive component of sodium efflux with a raised ouabain-insensitive efflux. Although cirrhosis has generally been associated with potassium depletion, the intracellular potassium content of the cirrhotic patients' leukocytes was normal. Since the leukocyte is considered to be a good cell model and because abnormalities of sodium transport have been shown in the leukocytes of these patients, it is likely that similar abnormalities of sodium transport are present in other organs, including the brain.
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PMID:Abnormalities in the leukocyte sodium pump in advanced cirrhosis. 726 13

After rapid intravenous injection of furosemide 40 mg (Fu), plasma levels were determined in 7 healthy volunteers, 8 patients with liver cirrhosis with ascites and 7 patients with end-stage renal disease (ESRD). The diuretic response was evaluated by measuring the urinary excretion of sodium and potassium and the urine volume. The mean elimination half life (t 1/2 beta) of Fu averaged 51 +/- 7.7 (+/- SD) min in healthy subjects, 52 +/- 7.7 min in cirrhosis and 200 +/- 57 min in ESRD. The non-renal clearance (Clnr) in healthy subjects (56 +/- 28 ml/min) corresponds to the total plasma clearance in functionally anephric patients (54 +/- 18 ml/min). In cirrhosis there was no significant change in the disposition parameters of Fu in comparison to the healthy volunteers, but there was a significant reduction in urine sodium and volume, whereas potassium excretion remained unchanged. Fu "excretion rate--response" curves showed diminished tubular sensitivity to Fu in cirrhosis.
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PMID:Influence of hepatic cirrhosis and end-stage renal disease on pharmacokinetics and pharmacodynamics of furosemide. 730 69

Red cell sodium and potassium contents were investigated in 57 patients with histologically proven liver cirrhosis and were compared with 13 controls without clinical evidence of liver disease. Patients with normal serum electrolytes (and without digoxin treatment) had normal red cell sodium content indicating no influence of the cirrhosis per se on the sodium-potassium pump or membrane permeability for sodium. Red cell potassium content was elevated, possibly as a consequence of subclinical hemolysis and a relatively young cell population. Hypokalemia was correlated to increased red cell sodium. Hyponatremia was correlated to low red cell sodium indicating reduced influx due to a decreased concentration gradient. According to the concept of the "sick cell syndrome," membrane failure and cellular gain of sodium and loss of potassium can lead to hyponatremia. Our findings of normal or low red cell sodium contents provide evidence against this mechanism as explanation for the often sever hyponatremia in terminal liver failure. The abnormalities found in the red cells could be attributed to secondary complications to the cirrhosis.
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PMID:Red cell sodium and potassium contents in liver cirrhosis. 735 Dec 91

The combination of furosemide-amiloride was used in the management of fluid retention in 16 cirrhotic patients. The study lasted 60 days. In 15 out of the 16 patients a clinical response was observed, namely increased urinary volumen and reduction of abdominal girth. The body weight was reduced by a mean of 7.7 Kg. Serum potassium rose, within normal limits, in 14 patients and a reduction of urinary potassium elimination was observed. Mild hepatic encephalopathy was noticeable in 3 cases, rapidly responding to treatment reduction or withdrawal. The combination of furosemide-amiloride seems to be of value in the management of fluid retention in liver cirrhosis and is uncommonly associated to side effects.
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PMID:[Furosemide-amiloride combination in the treatment of ascitic-edema in patients with hepatic cirrhosis]. 740 64

Twenty patients with cirrhosis and ascites but no renal failure were given piretanide, a new loop diuretic, in order to investigate its efficacy and to relate the diuretic response with the pretreatment plasma aldosterone concentration. Eleven patients responded to piretanide 12 mg/day (equivalent in potency to 80 mg furosemide); there was no response in nine patients. Both groups were similar with regard to liver function, plasma urea, serum creatinine, plasma electrolytes, urine volume, and urine potassium concentration. The basal urinary sodium excretion was significantly higher in those patients who responded (23.6 +/- 5.7 mmol/day vs. 4.3 +/- 1.42 mmol/day; P < 0.01) (M +/- SE). Plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were normal or only slightly increased in patients who responded to piretanide (PRA = 1.22 +/- 0.20 ng/ml/h; PAC = 12.25 +/- 2.20 ng/100 ml) and very high in patients who did not respond (PRA = 8.71 +/- 1.18 ng/ml/h; PAC = 84.6 +/- 16.2 ng/100 ml) (P < 0.001). Patients unresponsive to piretanide 12 mg/day also failed to respond when the dose was increased to 24 mg/day. However, the addition of spironolactone, 150 mg/day, to piretanide was followed in these patients by a marked increase in diuresis and natriuresis. These results strongly suggest that the pre-treatment level of aldosterone is an important factor influencing the response to loop diuretics in patients with non-azotaemic cirrhosis and ascites.
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PMID:Use of piretanide, a new loop diuretic, in cirrhosis with ascites: relationship between the diuretic response and the plasma aldosterone level. 743 5

A clinical pharmacological study was carried out with 11 patients suffering from hepatogeneous ascites. After pretreatment with spironolactone (twice daily 100 mg), 80 mg of a new loop diuretic, muzolimine, were administered orally in addition to 100 mg of spironolactone. The diuretic effect started rapidly, reached its maximum about 6 h after administration and declined slowly until 24 h. The electrolyte profile showed a pronounced excretion of sodium and chloride, whereas potassium excretion was distinctly lower. Sodium/potassium ratio was 5.9 during the first 8 hours, and the mean ratio was 5.2 during 24 hours. Urinary volume and sodium excretion were significantly correlated with plasma levels of muzolimine. Mean plasma half-life of muzolimine in these patients with liver cirrhosis was 7.9 h and was thus longer than in healthy volunteers.
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PMID:[Pharmacodynamic and pharmacokinetic studies of muzolimine in patients with hepatogeneous ascites (author's transl)]. 745 63

The efficacy and side effects of the combination therapy of thiazide and furosemide administered to patients with refractory heart failure, for a prolonged period of time, were assessed. Thirty-two patients were hospitalized during the years 1985-1991. Left heart failure (left ventricular ejection fraction (LVEF = 22.4% +/- 6.6%) was present in 26 patients, right heart failure in 3 patients, chronic renal failure, cirrhosis and bilateral pleural effusion were present each in one patient. Chlorothiazide 0.5 g daily was added to conventional therapy. Patients were monitored closely during hospitalization and later as outpatients. During hospitalization, addition of chlorothiazide caused a reduction of 4.8 +/- 4.0 kg in patients' weight, serum potassium decreased from 4.4 +/- 0.6 to 4.0 +/- 0.5 mmol/l (P < 0.005) and serum sodium from 139.0 +/- 4.7 to 136.8 +/- 5.5 mmol/l (P < 0.05). The duration of the combined therapy was 17.2 +/- 19.1 months. Thirteen patients had short treatment (1.6 +/- 0.8 months) and 19 patients had prolonged treatment (26.5 +/- 19.0 months). No specific characteristics distinguished patients in both groups. Thiazides were discontinued in 19 patients, 10 of which had side effects. In only 5 of the 19 patients treated for the prolonged period had thiazides to be discontinued because of side effects. Addition of thiazides to furosemide is efficacious in severe heart failure. The combination should be started during hospitalization. Many patients can be maintained on this combination for a prolonged period of time on an ambulatory basis.
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PMID:Prolonged therapy by the combination of furosemide and thiazides in refractory heart failure and other fluid retaining conditions. 759 35

The aim of this study is to observe the changes of bile elements in patients with cirrhosis of liver and to analyse the relationship with stone formation. The gallbladder bile in 24 patients with cirrhosis of liver was obtained with aspiration during operation. The levels of lipids, bilirubin and various metal elements such as potassium, sodium, calcium, magnesium, copper, iron, and zinc in the bile were determined. Elevated unconjugated bilirubin (UCB) level (P < 0.02) and decreased levels of total bile acid (TBA) (P < 0.001), total cholesterol (TC) (P < 0.001), phospholipids (PL) (P < 0.05) and bile viscosity (P < 0.001) were found. The levels of potassium, magnesium, copper and zinc in the bile decreased (all P values less than 0.001), while the level of iron increased (P < 0.02) significantly in cirrhotic patients. The results showed that there is an obvious tendency for gallbladder bile in cirrhotic patients to form pigment stones.
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PMID:[Changes in lipids, bilirubin and metal elements in the gallbladder bile in patients with cirrhosis of the liver]. 760 Aug 68


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