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)

Hepatic encephalopathy in liver cirrhosis is due to several factors, including amino acid imbalance and hyperammonemia. Lactitol [correction of lactilol], a non adsorbable disaccharide, improves hepatic encephalopathy increasing bowel movements, modifying colonic bacteria and pH, and reducing blood ammonium. Ten patients with liver cirrhosis and longstanding stable hepatic encephalopathy were treated, after a period of drugs wash-out, with lactitol. A significant improvement of hepatic encephalopathy was observed, with a significant decrease of blood ammonium, related with the increase of stool frequency/day. Atrial natriuretic peptide decreased as well. Moreover, an increase of the ratio of plasma aliphatic amino acids (valine, leucine and isoleucine)/aromatic amino acid (tyrosine and phenylalanine) was observed. Lactitol is an effective drug in the treatment of chronic hepatic encephalopathy; its mechanism of action involves not only a decrease of blood ammonium but also modifications of the degree of plasma amino acid imbalance, and fluid and circulatory adjustments.
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PMID:Effects of lactitol [correction of lactilol] on hepatic encephalopathy and plasma amino-acid imbalance. 756 87

Little is known about the effect of posture on the circulatory abnormalities of advanced cirrhosis. We evaluated the systemic hemodynamics, measured by Doppler-echocardiography, atrial natriuretic factor, plasma renin activity and plasma norepinephrine, in 10 patients with cirrhosis and ascites and 10 healthy controls, after 2 h of standing and during lying down for a further 2 h. Standing hemodynamic patterns of controls and patients with cirrhosis did not differ significantly. The latter, however, showed higher plasma renin activity, norepinephrine and atrial natriuretic factor. The assumption of the supine position led to greater increases in cardiac index and atrial natriuretic factor, and reduction in systemic vascular resistance in patients with cirrhosis. Norepinephrine and plasma renin activity declined in both groups to a similar extent, while heart rate only slowed in controls. Thus, after 2 h in the supine position, patients with cirrhosis showed hyperdynamic circulation with increased cardiac index and heart rate and reduced systemic vascular resistance. Norepinephrine, plasma renin activity and atrial natriuretic factor were also elevated. The hyperdynamic circulation in advanced cirrhosis appears during or is enhanced by lying down. This finding suggests that this syndrome is, at least in part, attributable to excessive blood volume translocation towards the central area. However, the persistent activation of renin-angiotensin and sympathoadrenergic systems suggests that a concomitant reduced vascular sensitivity to vasoconstrictors concurs in its development.
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PMID:Hyperdynamic circulation of advanced cirrhosis: a re-appraisal based on posture-induced changes in hemodynamics. 760 82

The study investigated the hemodynamic and neurohumoral effects of albumin infusion after total paracentesis in 18 patients with cirrhosis and tense ascites. Measurements of systemic and splanchnic hemodynamics, and vasoactive neurohumoral systems were performed before and immediately after total paracentesis. The patients were then randomized to receive albumin or not, and hemodynamic and humoral measurements were repeated at 24 hours. Hemodynamic and humoral changes just after paracentesis were similar in patients later randomized to receive albumin infusion or not. Twenty-four hours after total paracentesis, patients nor receiving albumin had total significant reductions in cardiac index (-13%; P = .005), femoral blood flow (-17%; P = .004), and pulmonary capillary pressure (-16%; P = .02), which were accompanied by significant increases in plasma renin activity (PRA) and plasma aldosterone (PA) and by significant decreases in atrial natriuretic factor (ANF) and plasma sodium. By contrast, there was no significant changes in patients receiving albumin, except for an increase in ANF and a further decrease in PA. In both groups, hepatic venous pressure gradient (HVPG) and azygos blood flow decreased just after paracentesis returning to baseline at 24 hours. This study shows that albumin infusion prevents the impairment in systemic hemodynamics, vasoactive neurohumoral systems, and plasma sodium after a large-volume paracentesis, without detrimental effects on portal pressure and portocollateral blood flow.
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PMID:Beneficial effects of intravenous albumin infusion on the hemodynamic and humoral changes after total paracentesis. 765 79

We recently showed that patients with compensated cirrhosis can dispose of their fluid overload while reclining. In contrast, patients with ascites fail to develop supine-induced natriuresis. To assess the effect of reclining on renal sodium handling in patients with advanced cirrhosis and the mechanisms blunting natriuresis in this situation, renal function and plasma concentrations of atrial natriuretic factor, aldosterone and norepinephrine were evaluated in 10 nonazotemic patients with cirrhosis and ascites and 10 healthy controls standing for 2 h and reclining for 2 h. While standing, all patients showed marked sodium retention and significantly elevated plasma atrial natriuretic factor levels, aldosterone and norepinephrine. Glomerular filtration rate did not differ from healthy controls. The reclining increased renal sodium excretion in both groups, but this change was far less marked in patients; natriuresis only rose to the control range in two of them. An increase in atrial natriuretic factor and a depression of plasma aldosterone and norepinephrine was seen in both controls and patients. In the latter, despite the greater change in atrial natriuretic factor and aldosterone, the aldosterone to atrial natriuretic factor ratio, which was inversely correlated with natriuresis during both standing and reclining remained significantly elevated. In the two patients who achieved normal natriuresis during reclining, reclining was associated with both the normalization of the aldosterone/atrial natriuretic factor ratio, and with an increase in glomerular filtration rate. The supine-induced increase in atrial natriuretic factor was not only preserved but was even enhanced in cirrhosis with ascites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal sodium handling in cirrhosis with ascites: mechanisms of impaired natriuretic response to reclining. 769 37

We measured the plasma levels of atrial natriuretic factor (ANF) during orthotopic liver transplantation (OLT) in eight adult patients with cirrhosis and ascites. The aim of this study was to determine whether significant differences in ANF concentration may be detected during the individual phases of OLT and to correlate these changes with hemodynamics. In each patient a hemodynamic assessment was achieved using a Swan-Ganz fiber optic catheter for continuous monitoring of cardiac output (CO), systemic vascular resistance index (SVRI), right filling pressure as assessed by central venous pressure (CVP), and left filling pressure by means of pulmonary arterial wedge pressure (PAWP). During reperfusion a clear-cut increase in ANF values was observed (P < 0.05). Concurrently, an increase in CVP (P < 0.05) and a decrease in SVRI were observed without any significant increase in diuresis. These data suggest that ANF might play a role in the development of the reperfusion syndrome.
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PMID:Human natriuretic factor in cirrhotic patients undergoing orthotopic liver transplantation. 788 52

The authors subjected 10 healthy subjects and 13 patients inflicted by liver cirrhosis in the stage of vascular decompensation (ascites and/or oedemas) to water immersion (WI). The group of healthy subjects responded during WI by a significant increase of diuresis and sodium diuresis at its maximum in the third hour, which was accompanied by a decrease of plasma aldosterone (PA) and a decrease of atrial natriuretic factor (ANF) and digoxin-like activity (DLA). The decrease of plasma vasopressin (PAVP) was not statistically significant. In patients with liver cirrhosis a significant increase of diuresis and sodium diuresis took place, whilst the response was significant already in the first hour of WI. Only 3 non-respondents were among the ill patients. In the group of liver cirrhotics also a significant decrease of AVP, PA, and an increase of ANF and DLA were recorded, the response of humoral factors was not significant due to great variability. A long term administration of diuretics (Spirolakton+Furosemid) did not decrease the serum K in ill patients. Hence, WI by means of supervention of volume expansion evokes an increase of diuresis and natriuresis in both healthy and ill subjects, the latter with decompensated liver cirrhosis which is associated with a controversial reaction of sodium diuresis and sodium retention factors. It is possible to use it as a supplementary method in the therapy of oedemas due to liver cirrhosis besides diuretic therapy. (Tab. 2, Fig. 3, Ref. 22.)
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PMID:[The effect of water immersion on humoral and urinary parameters in healthy persons and in patients with liver cirrhosis]. 792 22

Plasma atrial natriuretic factor concentrations and different hemodynamic parameters, including the evaluation of femoral arteriovenous shunting by measuring the arteriovenous difference of oxygen content (Ca-vO2), were determined in eight healthy subjects and 24 patients with cirrhosis without renal failure (group I: seven patients without ascites, group II: nine patients with ascites and UNaV > 10 mEq/24 h and group III: eight patients with ascites and UNaV < or = 10 mEq/24 h). Atrial natriuretic factor was 34 +/- 4.7 pg/ml in the control group and 44.28 +/- 5.4, 67.89 +/- 8.8 and 84 +/- 10.8 pg/ml in groups I, II and III respectively (p < 0.001. group III vs. I and control and II vs. control). Atrial natriuretic factor directly correlated with cardiac index (p < 0.01), blood volume (p: 0.01), femoral blood flow (p < 0.01) and inversely with systemic and femoral vascular resistances (p < 0.02), Ca-vO2 (p < 0.01), serum albumin (r: -0.61; p < 0.01) and prothrombin index (r: -0.63; p < 0.02). These results indicate that plasma atrial natriuretic factor is increased in patients with cirrhosis, especially in those with advanced disease and marked renal sodium retention. This suggests that in cirrhosis, arteriolar vasodilation and peripheral arteriovenous shunting influence renal function while inducing a state of overflow at the central venous compartment leading to increased atrial natriuretic factor secretion. Increased production of this vasodilatory hormone may thus contribute to the hyperkinetic circulation of cirrhosis.
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PMID:Atrial natriuretic factor in cirrhosis: relationship to renal function and hemodynamic changes. 798 11

Diuretic drugs have historically been developed for the treatment of sodium and water retention in edematous disorders. The latter have traditionally been an amalgam of congestive heart failure, nephrotic syndrome, cirrhosis and chronic renal failure. With a > 50-year tradition of this approach to development, diuretic drugs have not been evaluated specifically for their safety and efficacy profile in patients with congestive heart failure. Yet, they are the most frequently prescribed drug class for this disorder. Furthermore, they remain the only drug class in congestive heart failure not subjected to large scale clinical trials. Sodium and water retention within this group of patients is related primarily to functional rather than to structural renal abnormalities. The reduction of glomerular filtration rate, increase in aldosterone secretion and abnormal profile of atrial natriuretic factor, all produce sodium retention and can be related to the severity of heart failure. Diuretic drugs have not been scrutinized in a manner similar to that of other drugs for the management of heart failure. Controversy persists regarding direct vascular effects, objective end points of assessment and the magnitude of adverse effects such as activation of neurohormonal pathways. These issues may be addressed by the establishment of reasonable objective end points, better stratification of patients in clinical trials and prospective trials in large clinical series. Even mortality studies should be considered.
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PMID:Clinical trials of diuretic therapy in heart failure: research directions and clinical considerations. 810 3

To test a possible effect of blood flow change on disposal of atrial natriuretic factor: ANF99-126 (ANF), we determined renal, azygos, hepatic and cubital venous, and arterial plasma concentrations of ANF in 18 patients with cirrhosis before and after ingestion of propranolol 80 mg. Arterial ANF was similar to that of controls (9.4 vs. 10.9 pmol l-1, NS) and was positively correlated to cardiac output (r = 0.49, p < 0.02) and to right atrial pressure (r = 0.44, p < 0.01). All the vascular beds examined extracted ANF significantly. The renal (n = 17), hepato-enteric (n = 16), and splanchnic superior collateral (azygos) beds (n = 13) had significantly higher extraction ratios (0.34-0.39) than that observed in the cubital vein (0.24, n = 15, p < 0.05). Arterial ANF showed no significant change (9.6-11.0 pmol l-1, NS) after reduction of cardiac output (-25%, p < 0.001) by propranolol. Only insignificant changes in ANF extraction and a small decrease in azygos and hepato-enteric clearance occurred during beta-adrenergic blockade. Our results show a substantial extraction of ANF in the kidney, in the splanchnic bed drained through superior portosystemic collaterals, and in the hepato-enteric bed. Only minor effects on ANF extraction were observed after reduction of the blood flow with propranolol.
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PMID:Disposal of atrial natriuretic factor (ANF99-126) in patients with cirrhosis: effect of beta-adrenergic blockade. 826 99

Resistance to the natriuretic action of atrial natriuretic factor (ANF) in cirrhosis with ascites has been correlated with rising levels of antinatriuretic factors, such as renin, angiotensin II (AII), and aldosterone, as well as increased sympathetic nerve activity. To determine whether AII can serve as a mediator rather than only as a marker of the antinatriuresis, a nonpressor dose of AII (5 ng/kg/min) was given during an ANF infusion in eight patients with cirrhosis and ascites who responded to ANF infusion with a natriuresis. Patients were maintained in metabolic balance and measurements of para-aminohippuric acid, inulin, and lithium clearance were taken before and during infusion of ANF with or without AII. Atrial natriuretic factor infusion was associated with a natriuretic response accompanied by an increase in glomerular filtration rate, filtration fraction, and lithium clearance compared with baseline. The addition of AII was associated with a return of the glomerular filtration rate to baseline, with no change in filtration fraction. This was reversible on withdrawal of AII infusion. Natriuresis induced by ANF occurred despite baseline elevations of the renin angiotensin aldosterone system and was associated with an increase in distal delivery of sodium and a decrease in fractional reabsorption of distally delivered sodium as estimated by lithium clearance parameters. Angiotensin II infusion exerted effects on both proximal and distal nephron sites to abrogate ANF-induced natriuresis. These results suggest that AII may serve as a mediator as well as a marker of resistance to the natriuretic effect of ANF in patients with cirrhosis and ascites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin II modulates atrial natriuretic factor-induced natriuresis in cirrhosis with ascites. 848 14


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