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

Eighteen patients with hepatic cirrhosis or nephrotic syndrome and having edema and/or ascites were treated during successive periods with metolazone 5 to 40 mg/day, spironolactone 100 mg/day, and with both diuretics concurrently. Metolazone alone produced a marked diuresis, natriuresis, and weight loss in 8 patients. Spironolactone alone had little effect, but the addition of metolazone renewed diuresis and natriuresis and resulted in additional substantial weight losses in all patients responsive to metolazone alone. Concurrent spironolactone and metolazone also induced moderate diuretic effects in some patients who failed to respond to either drug alone. The drugs were well tolerated; the administration of spironolactone with metolazone prevented decreases in serum potassium, which had occurred during treatment with metolazone alone.
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PMID:Metolazone and spironolactone in cirrhosis and the nephrotic syndrome. 31 37

The activity of demeclotetracyclin, and ADH antagonist, is studied in 11 ethylic patients with cirrhosis of the liver, under a large hydric diet (1500 cm3). The prescription of the cyclin (600 mg daily) is always determined by a fall of the urinary osmolarity (-36%) and by a dramatic improvement of the free water clearance (+ 60%); consecutively, we observe an increase of natremia in 8 out of 9 cases. Associated with Spironolactone (200 mg daily) the anti-ADH activity persists (the free water clearance becomes positive in 5 out of 10 patients), in spite of the natriuretic activity of anti-aldosterone ; a minimal fall of the natremia is observed in only 2 cases. The indication of Demeclotetracyclin in the curative or preventive treatment of the hyponatremia of the liver cirrhosis is discussed.
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PMID:[Use of demeclotetracycline in the treatment of hyponatremia in cirrhotic ascitis]. 40 86

The dynamic excretion of aldadiene, the principal metabolite of spironolactone with biological activity, was studied in normal subjects and patients with liver cirrhosis following administration of spironolactone. Aldadiene appeared in the three-days urine collection in around 3% of the dose. There was no significant difference in the biological half-life, calculated from the urinary pattern, and in the rate of excretion in patients with hepatopathy and hospitalized controls. Healthy volunteers without hospitalization exhibited the most rapid elimination of the metabolite. An increase of spironolactone dose enhanced the per cent rate of aldadiene excretion, while the biological half-life did not change. Spironolactone decreased the rate of dehydroepiandrosterone and androsterone excretion even after a single dose. Determination of total 17-ketosteroids is of no value on evaluation of adrenal function during spironolactone therapy, due to a Zimmermann-positivity of spironolactone metabolites.
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PMID:Spironolactone metabolism in normal subjects and in patients with liver cirrhosis. 57 59

A review of the aldosterone antagonist spironolactone is presented. It is effective both as monotherapy and in combination with other hypotensive agents in the control of both essential and hyperaldosterone-induced hypertension. It is useful as a diuretic in conditions such as cirrhosis and congestive heart failure, and is most commonly employed because of its potassium- and magnesium-sparing qualities. Spironolactone also has been used as an antiandrogenic agent in managing hirsutism. Its adverse effect profile, considered somewhat prohibitive in the past, is generally not significant when reasonably low doses (less than 150 mg/d) are used.
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PMID:Spironolactone: a re-examination. 240 87

The pathogenesis and diagnosis of cirrhotic ascites are reviewed, and the treatment options are described, focusing on pharmacologic management. The major theories on the pathogenesis of cirrhotic ascites are the underfill and overflow theories. The underfill theory states that ascites formation results in decreased plasma volume leading to renal sodium and water retention. The overflow theory states that the initial event in ascites formation is renal sodium retention. Evidence suggests that the formation of ascites is a continuum involving both overflow (early) and underfill (late) mechanisms. Although the most frequent cause of ascites is hepatic cirrhosis, analysis of the ascitic fluid is important to exclude other causes (e.g., neoplasm, peritonitis, pancreatitis). Patients who do not respond to treatment with sodium restriction and bed rest require diuretic therapy. Spironolactone is the agent of choice for treatment of the nonazotemic patient with cirrhotic ascites. Combination therapy with spironolactone and furosemide or spironolactone and metolazone may be used in those patients who do not respond to spironolactone. Patients with impaired renal function should not be treated with spironolactone because of the risk of hyperkalemia. Paracentesis with albumin replacement has been used successfully for treatment of patients with tense cirrhotic ascites. Initial management of cirrhotic ascites is conservative, with sodium restriction and bed rest. Spironolactone is a good first-choice drug for treatment of ascites. Daily weight, serum electrolytes, and renal function should be monitored to assess the effectiveness and potential adverse effects of diuretic therapy.
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PMID:Management of cirrhotic ascites. 267 16

The effects of spironolactone and cirrhosis on the measurement of serum digoxin levels by radioimmunoassay were studied in patients not receiving cardiac glycosides. Three groups of 10 patients each were studied. Groups 1 and 2 included patients with alcoholic cirrhosis, with Group 1 patients receiving spironolactone and Group 2 receiving no spironolactone. Group 3, the control group, included patients who were not receiving spironolactone and did not have cirrhosis. Apparent digoxin serum levels were measured by radioimmunoassay, and the mean levels of each group were compared. Group 1 had significantly higher apparent digoxin levels (1.3 +/- 0.62 ng/ml, p 0.05) than Groups 2 or 3. The apparent digoxin level of Group 2 (0.74 +/- 0.44 ng/ml) did not differ significantly from that of Group 3 (0.40 +/- 0.35 ng/ml). Significant correlations were found between apparent serum digoxin levels and daily spironolactone dose (Group 1), SGOT levels (Group 1), and prothrombin time/control ratios (Group 2 and all groups combined). Spironolactone appears to increase digoxin levels measured by radioimmunoassay. The effect of cirrhosis on digoxin radioimmunoassay has not been confirmed.
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PMID:Spironolactone interference with digoxin radioimmunoassay in cirrhotic patients. 721 55

To alleviate the risk of variceal bleeding, the portal pressure gradient--usually evaluated as the hepatic venous pressure gradient (HVPG)--must be reduced to < or = 12 mmHg. Although beta-blocking agents are accepted therapy for preventing first or subsequent bleeding episodes, propranolol therapy decreases final HVPG to < or = 12 mmHg in only 12% of patients, while only 24% of patients have a > or = 20% reduction in HVPG and nearly 40% show no reduction in HVPG. This has stimulated research on alternative or additional treatments. Nitrates such as isosorbide dinitrate reduce portal pressure by decreasing resistance to portal and collateral blood flow and by promoting reflex splanchnic vasoconstriction. However, while nitrates are effective in the acute situation, tolerance leading to refractoriness develops over the long term unless they are combined with diuretics or other agents in the treatment of portal hypertension. Propranolol and isosorbide-5-mononitrate combined cause a substantially greater reduction in HVPG than monotherapy with either drug in both acute and long-term use. Presumably concomitant isosorbide-5-mononitrate administration opposes the increase in portal resistance induced by propranolol. Spironolactone, which has been shown to lower HVPG in patients with cirrhosis, produces a reduction in plasma volume that attenuates the increased cardiac output associated with cirrhosis and triggers vasoactive mechanisms that decrease splanchnic blood flow. Potentially, spironolactone may maintain and enhance the decrease in portal pressure achieved by nitrates or propranolol. Triple therapy with a beta-blocker, a nitrate and spironolactone may be feasible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New approaches in the pharmacologic treatment of portal hypertension. 809 42

The aim of this study was to investigate the hemodynamic effects of spironolactone associated with a low-sodium diet (n = 14) or a low-sodium diet alone (n = 9) in patients with compensated cirrhosis and portal hypertension. Spironolactone significantly reduced the plasma volume. This effect was associated with a significant reduction in the hepatic venous pressure gradient, from 17.6 +/- 3.6 mm Hg to 15.3 +/- 3.5 mm Hg (-13% +/- 13%; p < 0.01). Azygos blood flow (-20% +/- 20%), cardiac output (-16.2% +/- 10.5%) and mean arterial pressure (-9% +/- 9%) also decreased significantly. However, there were no significant changes in hepatic blood flow. Patients receiving low-sodium diet alone experienced a mild but significant reduction in hepatic venous pressure gradient (-6.3% +/- 6%) and in mean arterial pressure (-4% +/- 5%). There were no significant changes in cardiac output and in hepatic or azygos blood flows. This study indicates that low-sodium diet plus administration of spironolactone reduces portal pressure and azygos blood flow in patients with compensated cirrhosis. Low-sodium diet alone only produces mild effects that are likely to be clinically irrelevant.
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PMID:Effects of low-sodium diet and spironolactone on portal pressure in patients with compensated cirrhosis. 817 31

We studied the hemodynamic changes following a four-week administration of either low-dose transdermal nitroglycerin (a constant release of 5 mg of nitroglycerin/day) (N = 10) or low-dose transdermal nitroglycerin plus spironolactone (100 mg/day) (N = 9) in patients with cirrhosis and portal hypertension. Two patients in the latter group did not undergo repeat measurements after dropping out because of severe headaches or developing ascites during the study. Transdermal nitroglycerin induced a significant reduction in the hepatic venous pressure gradient (HVPG) (-11.7 +/- 14.9%, P < 0.05), which was associated with a significant reduction of cardiac output (-10.5 +/- 7.3%). Nitroglycerin plus spironolactone induced a significant reduction in the HVPG (-18.3 +/- 16.0%, P < 0.05) associated with a significant reduction of cardiac output (-13.8 +/- 5.6%), right atrial pressure (-35.0 +/- 30.0%), mean arterial pressure (-7.5 +/- 6.8%), and plasma volume (-10.2 +/- 7.0%). The difference of the mean HVPG reduction between the groups was insignificant. A decrease in the HVPG greater than 10% was observed in six of 10 patients (60%) and in five of seven patients (71.4%), defined as "responders," at four weeks. The difference in percentage of responders between the groups was insignificant. We found that in some cirrhotic patients, low-dose transdermal nitroglycerin is potentially useful in the treatment of portal hypertension. Spironolactone as an adjunct to low dose transdermal nitroglycerin did not demonstrate therapeutic advantages in the treatment of portal hypertension in cirrhotics. That there were nonresponders indicates that there are variable responses in splanchnic hemodynamics to these drugs.
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PMID:Chronic splanchnic hemodynamic effects of low-dose transdermal nitroglycerin versus low-dose transdermal nitroglycerin plus spironolactone in patients with cirrhosis. 907 34

The purpose of this study is to determine the hemodynamic effects of spironolactone administration associated with an unrestricted sodium diet (salt 10 g) in patients with compensated cirrhosis and portal hypertension. We studied the hemodynamic changes following eight weeks of administration of either placebo (N = 6) or spironolactone (100 mg/day) (N = 6 Pugh-Child's A and 6 B). No significant changes were observed after the administration of the placebo. Spironolactone induced a significant reduction in the hepatic venous pressure gradient (HVPG) (-10.1 +/- 13.3%, P < 0.05), which was associated with a significant reduction of cardiac output (-11.5 +/- 9.3%, P < 0.01), plasma volume (-8.1 +/- 4.7%, P < 0.01), and wedged hepatic venous pressure (-10.5 +/- 11.6%, P < 0.05). There was no significant change in hepatic blood flow and there was no significant correlation between the change in the HVPG and the change in circulating plasma volume. A decrease in the HVPG greater than 10% was observed in eight of 12 patients (67%), defined as responders, at eight weeks. Six of six (100%) grade A patients and two of six (33%) grade B patients responded. This study demonstrated that spironolactone with an unrestricted sodium diet decreased the HVPG in grade A patients but did not significantly decrease the HVPG in grade B patients.
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PMID:Chronic splanchnic hemodynamic effects of spironolactone with unrestricted sodium diet in patients with compensated cirrhosis. 955 49


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