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)

Plasma concentrations of atrial natriuretic peptide (ANP), aldosterone (PA), vasopressin (AVP) and plasma renin activity (PRA) were measured in 15 patients with decompensated cirrhosis of the liver during a control period and subsequently during intravenous administration of albumin. Infusion of hyperoncotic albumin increased diuresis, natriuresis, stimulated ANP secretion and tended to normalize other vasoactive hormone levels in 9 patients (responders), whereas it had no effect in 6 other patients (non-responders). Responders had significantly lower basal levels of ANP and higher ones of PRA, and AVP than non-responders, suggesting that responders had decreased effective intravascular volume. Our data suggest that cirrhotic patients with ascites formation do not represent a homogenous group. In some patients with decompensated cirrhosis a compromised circulatory state with decreased effective circulatory volume induces compensatory changes in several regulatory hormones. It appears that secondary alterations in the plasma concentrations of ANP of cirrhotic patients may occur according to the suspected change of intravascular fluid volume.
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PMID:Atrial natriuretic peptide in patients with decompensated hepatic cirrhosis. 214 34

Desmopressin (1-deamino-8-D-arginine vasopressin, DDAVP) is a synthetic analogue of the antidiuretic hormone L-arginine vasopressin. Because it can raise circulating levels of Factor VIII and of von Willebrand's factor, DDAVP is used for nontransfusional treatment of mild and moderate hemophilia and von Willebrand's disease. DDAVP also shortens the prolonged skin bleeding time in patients with uremia, liver cirrhosis, and platelet dysfunctions and is given to prevent or stop excessive bleeding in such conditions. Finally, there is evidence that DDAVP can reduce blood loss and transfusion requirements during and after surgical operations in which blood losses are unusually large. Hence DDAVP is useful as a nontransfusional hemostatic agent in many of the bleeding disorders frequently encountered in clinical practice.
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PMID:Desmopressin: a nontransfusional hemostatic agent. 218 48

The haemostatic effect of terlipressin (triglycyl-lysine vasopressin; Glypressin) on bleeding from oesophageal varices was evaluated in a placebo-controlled, double-blind, randomized clinical trial. Patients with clinically suspected liver cirrhosis were included in the study if they had been admitted to hospital with an extensive haemorrhage within the last 24h before diagnostic endoscopy. The patients randomized after stratification for severity of liver disease. Terlipressin or placebo was administered as intravenous bolus injections every 4th h during a period of 24 to 36 h or until the clinical course necessitated active intervention (failure or withdrawal). Sixty patients entered the study; 31 patients were allocated to receive terlipressin, and 29 patients to receive placebo. Bleeding from varices was arrested in 28 of the 31 receiving terlipressin, as compared with 17 of the 29 receiving placebo (p less than 0.01). Patients receiving active drug required significantly fewer blood transfusions (p less than 0.05). Most of the side effects were classified as mild and were registered in the terlipressin group.
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PMID:Terlipressin (triglycyl-lysine vasopressin) controls acute bleeding oesophageal varices. A double-blind, randomized, placebo-controlled trial. 219 77

Patients with cirrhosis and esophagogastric varices have a 25% to 33% risk of initial variceal bleeding, a risk of up to 70% for recurrent variceal bleeding, and an associated mortality of up to 50%. Based on a review of prospective randomized trials, control of acute variceal bleeding should involve vasopressin plus nitroglycerin as indicated for minor bleeding episodes, sclerotherapy for more severe bleeding episodes, and staple transection of the esophagus for patients who do not respond to these initial measures. Emergency portasystemic shunt surgery cannot be recommended at this time. For prevention of recurrent variceal hemorrhage, the data support the use of nonselective beta-adrenergic blockers (propranolol or nadolol) for patients with good liver function (Child's class A and B) and the use of chronic sclerotherapy to obliterate esophageal varices for patients with decompensated cirrhosis (Child's class C). Surgical procedures should be reserved for failures of medical management. The use of beta-adrenergic blockers offers the most promise for prevention of initial variceal bleeding.
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PMID:A hepatologist's view of variceal bleeding. 219 10

We evaluated the changes in the hepatic hemodynamics and blood ketone body ratio (KBR) induced by vasopressin in 40 patients with chronic liver diseases to clarify the effect of hepatic blood flow on hepatic energy charge expressed by KBR. Following infusion of vasopressin, the rate of decrease in portal blood flow in liver cirrhosis (LC) was significantly lower than that in chronic hepatitis (CH). Moreover, the blood flow in the hepatic artery after vasopressin infusion was greater in LC than in CH. As a result, the total hepatic blood flow, which was the sum of the flow in the above two vessels, after vasopressin infusion was greater in LC than in CH but the decrease in the blood KBR was not significant in LC. Thus, vasopressin appears to be hemodynamically safe in patients with LC, but caution is needed since it may decrease blood pressure, total hepatic blood flow and KBR in some LC patients.
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PMID:[The changes in hepatic hemodynamics and hepatic energy charge (blood ketone body ratio) induced by vasopressin infusion in chronic liver disease]. 225 Mar 79

The mechanism of hyponatremia associated with pneumonia has been debated. In particular, the responsibility of inappropriate antidiuretic hormone secretion has been questioned. We have shown that inappropriate antidiuretic hormone secretion is a nearly constant finding during pneumonia and is roughly proportional to the extent of pneumonia. Nevertheless, it must be emphasized that extracellular fluid volume may be increased, diminished or normal during pneumonia, depending on the underlying condition (congestive heart failure, cirrhosis) or on the importance of extrarenal losses (sweats, fever). Careful clinical and laboratory assessment of extracellular fluid volume should enable adequate therapy.
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PMID:[Hyponatremia of acute pulmonary infections]. 226 57

Refractory ascites (or diuretic-resistant ascites), i.e. ascites that cannot be mobilized by medical treatment (low sodium diet and high doses of furosemide and spironolactone) is an infrequent phenomenon in cirrhosis. It usually occurs in patients with functional renal failure as a consequence of alteration in both pharmacokinetics and pharmacodynamics of diuretics. Peritoneovenous shunting, a procedure which improves systemic hemodynamics and renal function and suppresses the plasma levels of renin, aldosterone, norepinephrine and antidiuretic hormone in cirrhotics with ascites, has been proposed as the treatment of choice in patients with refractory ascites. Unfortunately it is associated to a high rate of severe complications and does not prolong the survival of these patients. Moreover, in approximately one third of the patients the shunt becomes occluded within the first year after operation. Recent studies have shown that repeated large volume paracentesis (4-64 per day until disappearance of ascites) or total paracentesis (complete mobilization of ascites in only one paracentesis session) associated to i.v. albumin infusion are an effective and safe therapy of ascites. At present, there is only one controlled trial comparing therapeutic paracentesis versus peritoneo-venous shunt in the management of patients with refractory ascites. In this study, there were no significant difference between both therapeutic groups with respect to survival. However, the incidence of readmission to hospital for the treatment of ascites was higher in the paracentesis group. Therefore, both procedures are valid therapeutic alternatives for that type of patients. Future studies are necessary to investigate if there are subsets of cirrhotics with refractory ascites in which one of these two types of treatment is especially indicated.
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PMID:Diuretic-resistant ascites in cirrhosis. Mechanism and treatment. 226 4

Plasma levels of glucagon, secretin, norepinephrine, arginine-vasopressin, and prostaglandin biosynthesis in the gastric mucosa were determined in cirrhotic patients with gastric vascular ectasia associated with hypoacidity, in cirrhotics without this lesion, and in healthy controls. Plasma concentrations of glucagon, secretin, and norepinephrine were similar in cirrhotics with gastric vascular ectasia and cirrhotics without this lesion, these concentrations being significantly higher (p less than 0.05) than in healthy controls. However, there was no significant difference between plasma levels of arginine-vasopressin in patients with cirrhosis (with or without gastric vascular ectasia) and those in healthy controls. The biosynthesis of prostaglandin E2 in the antrum of the gastric mucosa was significantly higher in cirrhotics with gastric vascular ectasia than in cirrhotics without this lesion (p less than 0.05) and healthy controls (p less than 0.005). Prostaglandin E2 in the corpus was significantly higher (p less than 0.05) in cirrhotics with gastric vascular ectasia than in healthy controls. The biosynthesis of 6-keto PGF1 alpha (a stable metabolite of prostacyclin) and PGF2 alpha in the corpus and antrum of gastric mucosa was not significantly different in cirrhotics with gastric vascular ectasia, cirrhotics without this lesion and healthy controls. Since prostaglandin E2 has a vasodilator and acid-inhibitory effect, we speculate that high content of this prostanoid in the gastric mucosa may play a role in the pathogenesis of ectatic capillaries and acid inhibition present in some cirrhotic patients.
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PMID:Increased gastric PGE2 biosynthesis in cirrhotic patients with gastric vascular ectasia. 230 36

In this study, the author intended to examine the validity of the inhaled hydrogen gas clearance method (i-H2) for determination of the hepatic blood flow (HBF), and also to show some applicabilities of the method in experimental animals and patients with liver diseases. Simultaneous determinations of HBF by i-H2 and electromagnetic flowmetry in rabbits revealed an excellent correlation between the values obtained by the two methods. Moreover, HBF in rabbits measured by i-H2 varied in parallel with that by thermocouple flowmetry or laser Doppler velocimetry after administration of norepinephrine, propranolol or glucagon. In carbon tetrachloride-treated rats, HBF measured by i-H2 correlated better with the severity of damage in the sinusoidal structure than the severity of hepatic cell injury or the serum levels of transaminases. HBF as determined by i-H2 was significantly decreased in acute hepatitis (AH), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis (LC) and fatty liver. Reduced HBF in AH returned to normal during recovery of the disease. The ratio of HBF in tumor/normal tissue was greater than 1.0 for hepatocellular carcinoma in contrast to the ratio of less than 1.0 for metastatic liver carcinoma. Propranolol caused a decrease in HBF by 31%, and vasopressin by 39% in patients with CIH or LC. In contrast, glucagon induced its increase by 65%, 35% and 17%, respectively, in patients with CIH, AH and LC.
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PMID:[Measurement of hepatic blood flow by the hydrogen gas clearance method. Experimental and clinical observations]. 236 96

In patients with cirrhosis, vasopressin infusion induces sustained vasoconstriction and elevation of arterial pressure. The vasopressor effect could be caused by impairment of mechanisms normally aimed at buffering increases in arterial pressure (reflex bradycardia and decreases in arteriolar resistance). We studied the acute effects of continuous vasopressin infusion (0.4 IU/min) on systemic hemodynamics in seven patients with cirrhosis and in six patients without cirrhosis (controls). Vasopressin effects on systemic O2 consumption were also studied. In both groups, vasopressin infusion induced similar peak increases in arterial pressure, followed by similar decreases in heart rate and cardiac output. However, cirrhotic patients and controls differed 30 min after the start of vasopressin infusion. At 30 min, mean arterial pressure, diastolic arterial pressure and systemic vascular resistance remained significantly higher than preinfusion values in patients with cirrhosis. No decrease in systemic O2 consumption occurred in cirrhotic patients. In controls, at 30 min, mean arterial pressure and diastolic arterial pressure had returned to baseline. Systemic vascular resistance was not significantly higher than the preinfusion value and systemic O2 consumption had significantly decreased to below preinfusion values. We conclude that the vasopressor effect of vasopressin is abnormally sustained in patients with cirrhosis. This might be caused by insufficient buffering of vasopressin-induced arteriolar constriction rather than by abnormal vagal control of heart rate. In turn, as suggested by the lack of a decrease in systemic O2 consumption, persistent arteriolar constriction might be related to abnormally sustained sympathetic vascular tone in patients with cirrhosis.
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PMID:Abnormal pressor response to vasopressin in patients with cirrhosis: evidence for impaired buffering mechanisms. 237 86


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