Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the addition of clonidine to diuretics on the mobilization of ascites in the short term (diuretic response and requirement of diuretics) and the long term (readmissions for tense ascites and requirement of diuretics) were examined in patients with cirrhosis and with increased sympathetic nervous system (SNS) activity. We also studied neurohormonal, hemodynamic effects and side effects of clonidine and diuretics. Patients were randomized to receive placebo (group 1, n = 32) or clonidine (0.075 mg) twice daily (group 2, n = 32) for 3 months. After 8 days and for 10 days duration, spironolactone (200 mg/day) was added in both groups. After this period, the dosages of diuretics were individually increased until diuretic response. Responding patients were discharged and followed at the outpatient clinic. During the first hospitalization, the time needed for diuretic response was shorter in group 2 than in group 1. The mean requirement for diuretics was significantly higher in group 1 than in group 2, and the diuretic complications (hyperkalemia and renal impairment) were significantly lower in group 2. Clonidine induced a permanent decrease in SNS activity and delayed decrease in renin/aldosterone levels. During the follow-up, the time to the first readmission for tense ascites was shorter in group 1 than in group 2. Readmissions related to tense ascites or diuretic complications were significantly lower in group 2. The mean requirement for diuretics was significantly higher in group 1 than in group 2. In conclusion, the additional administration of clonidine to diuretics induced an earlier diuretic response associated with fewer diuretic requirements and complications.
 ...
PMID:Effects of clonidine on diuretic response in ascitic patients with cirrhosis and activation of sympathetic nervous system. 1808 Mar 35

Ascites is the most common complication of cirrhosis and is associated with 50% mortality at 2 years if patients do not receive orthotopic liver transplantation. Recently the International Ascites Club defined ascites into three groups: In grade I ascites fluid is detected only by ultrasound; in grade II, ascites is moderate with symmetrical distention of the abdomen; and in Grade 3 ascites is large or tense with marked abdominal distention. About 10% of patients with ascites are refractory to treatment with diuretics. In refractory ascites, patients do not respond to highest doses of diuretics (spironolactone 400 mg/day and furosemide 160 mg/ day) or develop side effects (hyperkalemia, hyponatremia, hepatic encephalopathy, or renal failure) that prohibit their use. Patients may be treated either by repeated large volume paracentesis plus albumin or transjugular intrahepatic portosystemic shunts (TIPS). Dilutional hyponatremia in cirrhotic patients is defined as serum sodium < or = 130 mEq/L in the presence of an expanded extracellular fluid volume, as indicated by the presence of ascites and/or edema. This complication of cirrhotic patients with ascites has recently gained attention given that several reports indicate that when serum sodium concentration is combined with the Model for End-Stage liver disease (MELD) it improves the prognostic accuracy of MELD score in patients awaiting orthotopic liver transplant (OLT). The first step in the management of dilutional hyponatremia is fluid restriction and discontinuation of diuretics. Water restriction at 1,000 mL/day helps prevent the progressive decrease in serum sodium concentration but usually does not correct hyponatremia in most cases. Actually are developing drugs that are active orally and act by selectively antagonizing the specific receptors (V2 receptor) of arginine vasopressin. These agents act in the distal collecting ducts of the kidneys, by increasing solute free water excretion and, thus, improving serum sodium concentration in hyponatremic patients.
 ...
PMID:[Refractory ascites and dilutional hyponatremia: current management and new aquaretics]. 1706 87

Tense ascites is one of the most disabling and distressing manifestation of liver cirrhosis. In the presence of ascites alteration in ventricular function is marked. Renin-angiotensin-aldosterone and sympathetic nervous system, whose activation is marked when tense ascites develops, could be involved as pathogenic factors causing increased left ventricular wall thickness. Large volume paracentesis (LVP) is an old but safe and effective procedure to mobilize ascitic fluid in cirrhotic patients. The study evaluated the left ventricular function in patients with liver cirrhosis and tense ascites and determine the effect of total abdominal paracentesis on cardiac performance and correlated between cardiac performance and some humoral factors (renin, aldosterone, nor-epinephrine and epinephrine) in cirrhotic patients with ascites. Fifty cirrhotic patients with tense ascites, besides 20 normal persons matched with patients in age and gender as a control group were included in our study. All patients were hospitalized and, submitted to a 4 days bed rest, low sodium diet and subjected to full investigations clinically and laboratory. Abdominal paracentesis was done to all patients (mean volume 7.5 + 11.7 L) with dexran-70 infusion. Blood samples were taken before and immediately after paracentesis for neurohormonal assay (plasma rennin activity PRA, plasma aldosterone PA, plasma nor-epinephrine and epinephrine). The plasma renin activity, plasma aldosterone, plasma epinephrine, and plasma nor epinephrine was significantly higher than control. They showed significant reduction after paracentesis but still significantly higher than control levels. The results showed that sudden abdominal decompression could play a role in the post paracentesis systemic haemodynamic changes through mechanical decompression of the splanchinic vascular bed. Total paracentesis with albumin infusion causes immediate favorable effects; increasing cardiac output, suppressing plasma renin activity and plasma aldosterone, decreasing serum createnine and blood urea nitrogen and reducing portal pressure and Porto collateral blood flow.
 ...
PMID:Large volume abdominal paracentesis effect on some humoral factors and cardiac performance in patients with liver cirrhosis and tense ascities. 1798 89

Accumulation of fluid as ascites is the most common complication of cirrhosis. This is occurring in about 50% of patients within 10 years of the diagnosis of cirrhosis. It is a prognostic sign with 1-year and 5-year survival of 85% and 56%, respectively. The most acceptable theory for ascites formation is peripheral arterial vasodilation leading to underfilling of circulatory volume. This triggers the baroreceptor-mediated activation of renin-angiotensin-aldosterone system, sympathetic nervous system and nonosmotic release of vasopressin to restore circulatory integrity. The result is an avid sodium and water retention, identified as a preascitic state. This condition will evolve in overt fluid retention and ascites, as the liver disease progresses. Once ascites is present, most therapeutic modalities are directed on maintaining negative sodium balance, including salt restriction, bed rest and diuretics. Paracentesis and albumin infusion is applied to tense ascites. Transjugular intrahepatic portosystemic shunt is considered for refractory ascites. With worsening of liver disease, fluid retention is associated with other complications; such as spontaneous bacterial peritonitis. This is a primary infection of ascitic fluid caused by organisms originating from large intestinal normal flora. Diagnostic paracentesis and antibiotic therapy plus prophylactic regimen are mandatory. Hepatorenal syndrome is a state of functional renal failure in the setting of low cardiac output and impaired renal perfusion. Its management is based on drugs that restore normal renal blood flow through peripheral arterial and splanchnic vasoconstriction, renal vasodilation and/or plasma volume expansion. However, the definitive treatment is liver transplantation.
 ...
PMID:Fluid retention in cirrhosis: pathophysiology and management. 1818 68

Patients with cirrhosis who develop tense ascites and hepatorenal syndrome have a very high mortality and present a management challenge. Current debate stems from a lack of studies evaluating changes in effective arterial blood volume following paracentesis or targeting fluid replacement with appropriate vascular physiological measures to ensure no paracentesis-related circulatory dysfunction. The study by Umgelter and colleagues addresses a goal-directed approach to fluid management in hepatorenal syndrome and raises several mechanistic questions, the answers to which are likely to improve our understanding of the pathophysiology in hepatorenal syndrome and to guide future management.
 ...
PMID:Towards goal-directed therapy of hepatorenal syndrome: we have the tools but we need the trials. 1819 61

Ascites is a classic complication of advanced cirrhosis and it often marks the first sign of hepatic decompensation. Ascites occurs in more than 50% of patients with cirrhosis, worsens the course of the disease, and reduces survival substantially. Portal hypertension, splanchnic vasodilatation, liver insufficiency, and cardiovascular dysfunction are major pathophysiological hallmarks. Modern treatment of ascites is based on this recognition and includes modest salt restriction and stepwise diuretic therapy with spironolactone and loop-diuretics. Tense and refractory ascites should be treated with large volume paracentesis followed by plasma volume expansion or transjugular intrahepatic portosystemic shunt. Ascites complicated by spontaneous bacterial peritonitis requires adequate treatment with antibiotics. New potential treatment strategies include the use of vasopressin V(2)-receptor antagonists and vasoconstrictors. Since formation of ascites is associated with a poor prognosis, and treatment of fluid retention does not substantially improve survival, such patients should always be considered for liver transplantation.
 ...
PMID:Ascites: pathogenesis and therapeutic principles. 1947 32

Ascites and hepatorenal syndrome (HRS) are the major and challenging complications of cirrhosis and portal hypertension that significantly affect the course of the disease. Liver insufficiency, portal hypertension, arterial vasodilatation, and systemic cardiovascular dysfunction are major pathophysiological hallmarks. Modern treatment of ascites is based on this recognition and includes modest salt restriction and stepwise diuretic therapy with spironolactone and loop diuretics. Tense and refractory ascites should be treated with a large volume paracentesis, followed by volume expansion or transjugular intrahepatic portosystemic shunt. New treatment strategies include the use of vasopressin V(2)-receptor antagonists and vasoconstrictors. The HRS denotes a functional and reversible impairment of renal function in patients with severe cirrhosis with a poor prognosis. Attempts of treatment should seek to improve liver function, ameliorate arterial hypotension and central hypovolemia, and reduce renal vasoconstriction. Ample treatment of ascites and HRS is important to improve the quality of life and prevent further complications, but since treatment of fluid retention does not significantly improve survival, these patients should always be considered for liver transplantation.
 ...
PMID:Pathogenetic background for treatment of ascites and hepatorenal syndrome. 1966 17

A 68-year-old man with hemophilia A and liver cirrhosis caused by hepatitis C virus was referred to our hospital to receive prophylactic endoscopic treatment for gastroesophageal varices (GOV). He had large, tense, and winding esophageal varices (EV) with cherry red spots extending down to lesser curve, predicting the likelihood of bleeding. Esophageal endoscopic injection sclerotherapy (EIS) was performed with a total 15 mL of 5% ethanolamine oleate with iopamidol (EOI). Radiographic imaging during EIS demonstrated that 5% EOI reached the afferent vein of the varices. He was administered sufficient factor VIII concentrate before and after EIS to prevent massive bleeding from the varices. Seven days after EIS, upper gastrointestinal endoscopy (UGIE) showed that the varices were eradicated almost completely. Eighteen months after EIS, the varices continued to diminish. We report a successful case of safe and effective EIS for GOV in a high-risk cirrhotic patient with hemophilia A.
 ...
PMID:Successful endoscopic injection sclerotherapy of high-risk gastroesophageal varices in a cirrhotic patient with hemophilia A. 2045 1

The cirrhotic patient with ascites presents unique challenges to the renal caregiver. This patient population has relative contraindications both to hemodialysis (HD) and to peritoneal dialysis (PD). Challenging hemodynamics and the bleeding risk from acquired coagulopathy make HD problematic. In PD, tense ascites can increase the risk of early catheter leak and complicate the initial instillation of dialysate. These patients are at increased risk of spontaneous bacterial peritonitis and would be suspected to have peritonitis rates different from those in non-cirrhotic patients. Ongoing protein losses in the dialysate may aggravate underlying malnutrition. Despite these concerns, available clinical reports suggest that patients with cirrhosis can be successfully managed on PD. The present review focuses on the application of PD therapy in the cirrhotic patient with ascites. Technical aspects of initiating PD are reviewed, and clinical reports, peritonitis risk, and infection control strategies are discussed. Dialysate increases intra-abdominal pressure and may oppose the formation of ascites; the impact of these mechanics on dialysate protein losses and portal hemodynamics are reviewed.
 ...
PMID:Peritoneal dialysis in patients with cirrhosis and ascites. 2134 86

Ascites is one of the major complications of liver cirrhosis and is associated with a poor prognosis. It is important to distinguish noncirrhotic from cirrhotic causes of ascites to guide therapy in patients with noncirrhotic ascites. Mild to moderate ascites is treated by salt restriction and diuretic therapy. The diuretic of choice is spironolactone. A combination treatment with furosemide might be necessary in patients who do not respond to spironolactone alone. Tense ascites is treated by paracentesis, followed by albumin infusion and diuretic therapy. Treatment options for refractory ascites include repeated paracentesis and transjugular intrahepatic portosystemic shunt placement in patients with a preserved liver function. Potential complications of ascites are spontaneous bacterial peritonitis (SBP) and hepatorenal syndrome (HRS). SBP is diagnosed by an ascitic neutrophil count > 250 cells/mm(3) and is treated with antibiotics. Patients who survive a first episode of SBP or with a low protein concentration in the ascitic fluid require an antibiotic prophylaxis. The prognosis of untreated HRS type 1 is grave. Treatment consists of a combination of terlipressin and albumin. Hemodialysis might serve in selected patients as a bridging therapy to liver transplantation. Liver transplantation should be considered in all patients with ascites and liver cirrhosis.
 ...
PMID:Diagnosis and therapy of ascites in liver cirrhosis. 2252 2


<< Previous 1 2 3 4 5 6 7 Next >>