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)

Sodium retention and peripheral vasodilatation are common consequences of portal hypertension secondary to cirrhosis. Although peripheral vasodilatation has been extensively documented in prehepatic portal hypertension, it is not known whether sodium retention is also a feature of this entity. The aim of this study in portal vein-constricted rats was to evaluate (a) whether sodium retention is a feature of prehepatic portal hypertension and (b) if sodium retention is present in this model, what its temporal relationship with peripheral vasodilatation might be. It was proposed that an understanding of the temporal interplay between peripheral vasodilatation and sodium retention could shed light on the current theories of sodium retention in portal hypertension. Rats were studied 1, 2, 3, and 4 days after partial portal vein ligation (n = 80) or sham operation (n = 63). Sodium retention was evaluated by changes in the size of the sodium space measured by the volume of distribution of 22Na. Systemic vascular resistance was calculated from mean arterial pressure (measured by arterial catheterization) and cardiac index (measured by thermodilution). A decrease in systemic vascular resistance was already observed on day 1 after constriction of the portal vein (4.2 +/- 0.2 vs. 5.2 +/- 6.1 mm Hg.min.mL-1.100 g; P less than 0.01). However, an expansion of the sodium space, which indicates sodium retention, was not observed until day 2 after induction of portal hypertension (37.1 +/- 0.8 vs. 32.6 +/- 0.7 mL.100 g-1; P less than 0.01). Therefore, sodium retention should be considered along with peripheral vasodilatation among the characteristic features of prehepatic portal hypertension. Because the reduction in systemic vascular resistance preceded the expansion of the sodium space by at least 24 hours, the finding of this study indicates that sodium retention follows peripheral vasodilatation.
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PMID:Vasodilatation and sodium retention in prehepatic portal hypertension. 153 1

The susceptibility of the gastric mucosa to injury by topical sodium taurocholate (40 mmol/l) in hydrochloric acid (150 mmol/l) was studied in prehepatic and cirrhotic rat models of portal hypertension. Portal venous pressure was increased in rats who had undergone partial portal vein ligation compared with rats that had undergone sham operation on days 3, 7, and 28 after operation (20.6 (0.9), 14.8 (0.8), and 11.3 (0.5) mm Hg v 7.3 (0.7), 7.3 (0.6), and 8.2 (0.2) mmHg respectively (mean (SEM)). At day 3 gastric mucosal injuries were increased in rats with partial portal vein ligation compared with sham operated rats (55.3 (9.4) vs 22.3 (10.5) mm2, p = 0.006), but at the later time intervals there was no significant difference in injuries between the two groups. In rats with carbon tetrachloride induced hepatic cirrhosis, portal pressure was increased (15.6 (1.0) v 6.7 (0.6) mmHg), but again there was no significant difference in mucosal injuries relative to control animals. We conclude that gastric mucosal defence mechanisms are impaired in acute but not chronic experimental portal hypertension.
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PMID:Taurocholate induced gastric mucosal injuries in experimental portal hypertension. 154 11

The reliability of lithium clearance as an index of distal fluid delivery in cirrhosis with ascites and in other clinical conditions characterized by low fractional sodium excretion has not yet been proven. In particular, lithium reabsorption in the amiloride-sensitive segment of the distal tubule, as evidenced in experimental studies, has not been excluded in such clinical conditions. Thus the acute effect of amiloride on renal lithium handling in 15 nonazotemic ascitic cirrhotic patients with avid sodium retention was evaluated after at least 5 days of controlled sodium intake. Renal plasma flow, glomerular filtration rate, fractional sodium excretion, fractional lithium excretion, fractional potassium excretion, fractional excretion of uric acid, plasma renin activity, plasma aldosterone and human atrial natriuretic peptide were evaluated before and for 6 hr after the administration of amiloride (20 mg/os). After amiloride administration a volume replacement scheme was enacted with intravenous amounts of saline solution, determined by the diuretic and natriuretic effect of the drug, to avoid volume depletion. Amiloride induced a prompt and sustained increase in fractional sodium excretion (from 0.28% +/- 0.09% to 1.0% +/- 0.41%, p less than 0.001) and a decrease in fractional potassium excretion (from 9.38% +/- 5.98% to 3.28% +/- 2.24%, p less than 0.0025), whereas it did not affect fractional lithium excretion and fractional excretion of uric acid. No change was observed in renal plasma flow, glomerular filtration rate, plasma renin activity, plasma aldosterone and human atrial natriuretic peptide. It was concluded that lithium is not reabsorbed in the amiloride-sensitive segment of the distal tubule in nonazotemic ascitic cirrhotic patients with avid sodium retention.
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PMID:Effects of amiloride on renal lithium handling in nonazotemic ascitic cirrhotic patients with avid sodium retention. 155 43

The medical treatment of ascites in cirrhosis is based on sodium restriction and the administration of diuretics. Because the natriuretic potency of spironolactone is greater than that of loop diuretics (i.e., furosemide) in patients with marked sodium retention, spironolactone is the basic drug for the treatment of ascites. The simultaneous administration of spironolactone and furosemide increases the natriuretic effect of each drug and diminishes their effects on potassium metabolism. Recent studies indicate that large-volume paracentesis associated with intravenous albumin infusion is more effective than diuretic therapy in eliminating the ascitic fluid; is associated with a lower incidence of complications (hepatic encephalopathy, renal impairment, and hyponatremia); and considerably reduces the duration of hospital stay. Therapeutic paracentesis associated with intravenous albumin infusion is therefore the treatment of choice for cirrhotic patients with tense ascites. The mobilization of the ascitic fluid by paracentesis without plasma volume expansion is constantly associated with a deterioration of effective circulating blood volume and may induce renal impairment and severe hyponatremia. Dextran 70 and polygeline appear as effective as albumin in preventing these abnormalities. Cirrhotic patients treated with paracentesis require the administration of diuretics to avoid reaccumulation of ascites. Peritoneovenous shunt, a prosthesis capable to correct most abnormalities involved in the accumulation of fluid in the abdominal cavity, is an effective treatment of ascites in cirrhosis. It is especially indicated in patients who do not respond to diuretics and develop repeated episodes of ascites despite adequate treatment. The use of peritoneovenous shunting is limited by the high incidence of complications induced by the procedure, however. In addition, approximately 40% of patients develop an obstruction of the prosthesis within the first postoperative year.
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PMID:Treatment of ascites in cirrhosis. Diuretics, peritoneovenous shunt, and large-volume paracentesis. 156 75

Eighty unselected cases of hyponatremia complicating liver cirrhosis were analysed. Of these cases, 20 had sodium levels less than 135 mmol/L, 48 less than or equal to 130 mmol/L and 12 less than or equal to 125 mmol/L. 5 cases developed acute hyponatremic syndrome after abdominal paracentesis and high-dose of diuretics. Of these 5 cases, 1 died and 4 recovered after immediate infusion of 3% sodium chloride (200-300 ml/d intravenously for 7-10 days). Both the crystal and colloid pressure of blood determined in 10 cases were less than normal. The sodium level of the ascitic fluid determined in 5 cases was higher than that of serum. Respiratory alkalosis complicated with metabolic alkalosis or acidosis were the main features of acid-base disorders. These might be due to alkalinizing agents therapy, infection and hepato-renal syndrome. Based on these clinical studies, it was shown that paracentesis and diuretics are the main causes of acute hyponatremic syndrome, so these measures should be taken carefully in patients with hyponatremic state previously, especially in patients with poor general, hepatic and renal conditions.
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PMID:[Hyponatremia in patients with ascites complicating liver cirrhosis]. 158 43

Failure to escape from mineralocorticoids in compensated cirrhosis is considered a major argument supporting the overflow theory of ascites. To assess the frequency and mechanism of mineralocorticoid escape in cirrhosis, 9-alpha-fluorohydrocortisone (0.6 mg/day) was administered to 19 patients with compensated cirrhosis, portal hypertension, and no history of ascites who were able to maintain sodium balance on a 250 mmol Na+ diet. Fifteen patients (78.9%) escaped from mineralocorticoids, while 4 patients (21.1%) did not escape and developed ascites. Patients who did not escape had significantly higher cardiac index (4.97 +/- 0.42 vs 3.46 +/- 0.21 L.min-1.m-2) and lower peripheral vascular resistance (485.9 +/- 37.5 vs. 665.8 +/- 32.9 dyne.s.cm-5/m2) than those who escaped. Hepatic venous pressure gradient was not significantly different. The escape phenomenon was associated with a significant increase in mean arterial pressure, creatinine clearance, and atrial natriuretic factor and suppression of plasma renin activity. All of these parameters showed minimal or no changes in patients who did not escape. These results indicate that failure to escape from mineralocorticoids is uncommon in patients with compensated cirrhosis, is related to an inadequate expansion of effective plasma volume due to the accumulation of ascites, and occurs in patients with marked peripheral arteriolar vasodilation.
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PMID:Mineralocorticoid escape in patients with compensated cirrhosis and portal hypertension. 153 59

A prospective randomized double-blind study was conducted to evaluate the efficacy of sodium benzoate in the treatment of acute portal-systemic encephalopathy. Seventy-four consecutive patients with cirrhosis or surgical portasystemic anastomosis and hepatic encephalopathy of less than 7 days duration were randomized to receive lactulose (dose adjusted for 2 or 3 semiformed stools/day) or sodium benzoate (5 gm twice daily). Assessment of response included mental status, asterixis, arterial ammonia level, electroencephalogram and number-connection test. Each was given a score between 0 and 4+. A portal-systemic encephalopathy index was calculated with these scores. Visual, auditory and somatosensory evoked potentials and a battery of psychometric tests for intelligence and memory were also performed to assess improvement. Thirty-eight patients received sodium benzoate; 36 took lactulose. Thirty patients (80%) receiving sodium benzoate and 29 (81%) receiving lactulose recovered; the remaining patients died. Improvement in portal-systemic encephalopathy parameters occurred in both treatment groups and was similar (p greater than 0.1). Electroencephalogram and evoked potentials were not as helpful as mental status in assessing of recovery. Psychometric test scores remained abnormal after recovery of mental status (21 to 42 days) and were probably too sensitive for monitoring of these patients. The incidence of side effects was similar in the two treatment groups. The cost of lactulose for one course of therapy was 30 times that of sodium benzoate. We conclude that sodium benzoate is a safe and effective alternative to lactulose in the treatment of acute portasystemic encephalopathy.
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PMID:Sodium benzoate in the treatment of acute hepatic encephalopathy: a double-blind randomized trial. 161 65

Plasma levels of brain natriuretic peptide, a recently identified cardiac hormone with natriuretic activity, were measured in 11 healthy subjects, 13 cirrhotic patients without ascites, 18 nonazotemic cirrhotic patients with ascites and 6 patients with cirrhosis, ascites and functional kidney failure. Plasma levels of brain natriuretic peptide were similar in healthy subjects and cirrhotic patients without ascites (5.56 +/- 0.65 and 7.66 +/- 0.68 fmol/ml, respectively). In contrast, cirrhotic patients with ascites, with and without functional kidney failure, had significantly higher plasma concentrations of brain natriuretic peptide (19.56 +/- 1.37 and 16.00 +/- 1.91 fmol/ml, respectively) than did healthy subjects and patients without ascites (p less than 0.01); no significant difference was found between the two groups of cirrhotic patients with ascites with respect to this parameter. In the whole group of cirrhotic patients included in the study, brain natriuretic peptide level was directly correlated with the degree of impairment of liver and kidney function, plasma renin activity and plasma levels of aldosterone and atrial natriuretic peptide. The results of this study indicate that brain natriuretic peptide is increased in cirrhotic patients with ascites and suggest that sodium retention in cirrhosis is not due to deficiency of this novel cardiac hormone.
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PMID:Plasma levels of brain natriuretic peptide in patients with cirrhosis. 161 67

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

We studied the effects of fenoldopam, a selective dopamine DA1 agonist on systemic and splanchnic hemodynamics, renal blood flow and sodium excretion in 12 patients with alcoholic cirrhosis and ascites. Hepatic, azygos and renal veins were catheterized before and after intravenous administration of fenoldopam, 0.05 micrograms/kg/min for 1 hr and increased to 0.1 micrograms/kg/min for another hour. Mean arterial pressure progressively decreased (from 83 +/- 7 to a minimum of 77 +/- 8 mm Hg 100 min after starting the infusion) but returned to baseline level at 120 min. Plasma norepinephrine and renin activity increased (respectively from 567 +/- 297 to 919 +/- 375 pg/ml, p less than 0.05, and from 17 +/- 14 to 23 +/- 15 ng/ml/hr, p less than 0.05). Renal blood flow, urine output or sodium excretion did not change. Sodium output decreased at 1 hr from 6.9 mumol/min to 4.0 mumol/min, p less than 0.05. Both hepatic venous pressure gradient and azygos blood flow significantly increased by 21%. We conclude that the acute administration of fenoldopam did not improve renal hemodynamics or function in patients with cirrhosis and ascites. In addition, dopamine DA1 agonism caused further increases in norepinephrine concentration and plasma renin activity. Portal pressure also increased, probably because of an increase in mesenteric blood flow. These results question the renal benefit and raise concern about the use of dopamine agonists in patients with cirrhosis and ascites.
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PMID:Selective dopamine DA1 stimulation with fenoldopam in cirrhotic patients with ascites: a systemic, splanchnic and renal hemodynamic study. 167 Oct 29


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