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

Massive ascites and hepatorenal syndrome (HRS) are frequent complications of liver cirrhosis. Thus, effective therapy is of great clinical importance. This concise review provides an update of recent advances and new developments. Therapeutic paracentesis can be safely performed even in patients with severe coagulopathy. Selected patients with a refractory or recurrent ascites are good candidates for non-surgical portosystemic shunts (TIPS) and may have a survival benefit and improvement of quality of life. Novel pharmaceutical agents mobilizing free water (aquaretics) are currently under test for the therapeutic potential in patients with ascites. Prophylaxis of hepatorenal syndrome in patients with spontaneous bacterial peritonitis is recommended and should be considered in patients with alcoholic hepatitis. Liver transplantation is the best therapeutic option with long-term survival benefit for patients with HRS. To bridge the time until transplantation, TIPS or Terlipressin and albumin are good options. Albumin dialysis can not be recommended outside prospective trials.
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PMID:Progress in treatment of massive ascites and hepatorenal syndrome. 1648 62

Hepatic hydrothorax is a complication of cirrhosis that is uncommon and difficult to treat. Diuretic therapy, thoracentesis, transjugular intrahepatic portosystemic shunt and liver transplantation are the main therapeutic options. Here, we report on a 47-year-old man with decompensated liver cirrhosis related to hepatitis B and D virus infections and who had complications of hepatic hydrothorax and hepatorenal syndrome. In this case, the hepatic hydrothorax, which was refractory to thoracic tube drainage and octreotide treatment, could be controlled with 5 days of terlipressin therapy associated with albumin. Terlipressin administration resulted in both improvement in renal function and successful resolution of hepatic hydrothorax. Splanchnic vasoconstrictor agents that reduce splanchnic blood flow, increase both central volume and effective renal blood flow. Thus they improve renal function. In our case, terlipressin, known to be beneficial in hepatorenal syndrome, was also effective in the treatment of hepatic hydrothorax probably by similar mechanisms. This is the first case in the literature.
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PMID:Treatment of hepatic hydrothorax with terlipressin in a cirrhotic patient. 1745 67

Cirrhosis associated with moderate and severe portopulmonary hypertension carries a poor prognosis. Optimal management has not yet been defined. Current treatment options, such as prostacyclin analogues, endothelin antagonists, and phosphodiesterase-5 inhibitors, are characterized by slow onset of action and various adverse effects, particularly in patients with advanced cirrhosis. Here, we report the significant reduction of pulmonary arterial pressure after 1-week terlipressin treatment in a patient with concomitant hepato-renal syndrome. Terlipressin could be a novel and safe treatment for portopulmonary hypertension.
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PMID:Significant improvement of portopulmonary hypertension after 1-week terlipressin treatment. 1828 Jun 5

Variceal bleeding is one of the most severe complications of portal hypertension related to liver cirrhosis. Primary prophylaxis is considered mandatory in patients with cirrhosis and high-risk oesophageal varices, and once varices have bled, every effort should be made to arrest the haemorrhage and prevent further bleeding episodes. In acute variceal bleeding, vasoactive drugs that lower portal pressure should be started even before endoscopy, and should be maintained for up to 5 days. The choice of vasoactive drug should be made according to local resources. Terlipressin, somatostatin and octreotide can be used; vasopressin plus transdermal nitroglycerin may be used if no other drug is available. In variceal bleeding, antibiotic therapy is also mandatory. In primary and secondary prophylaxis, beta-blockers are the mainstay of therapy. In secondary prophylaxis (but not in primary prophylaxis) these drugs can be combined with organic nitrates.
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PMID:Acute variceal bleeding: pharmacological treatment and primary/secondary prophylaxis. 1834 84

Terlipressin is a synthetic analogue of vasopressin, which has been used in the treatment of acute variceal hemorrhage. In contrast to vasopressin, terlipressin can be administered as intermittent injections instead of continuous intravenous infusion. Thus, it has a less adverse reaction than vasopressin. We report a case of ischemic skin complication in a cirrhotic patient treated with terlipressin. A 71-year-old man with liver cirrhosis was admitted because of hematemesis and melena. He was commenced on terlipressin at a dose 1 mg every 6 hours for the treatment of varicieal bleeding. After 36 hours of treatment, skin blistering and ecchymosis was noted on the skin of his upper thigh, scrotal area and trunk. We found that terlipressin was a possible cause of ischemic skin complication based on the skin biopsy finding. Terlipressin may induce a complication of the ischemic event. In spite of rarity, special attention needs to paid on the peripheral ischemic complication of terlipressin.
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PMID:[A case of ischemic skin necrosis after glypressin therapy in liver cirrhosis]. 1860 41

Terlipressin is an analog of the natural hormone arginine-vasopressin. It is used in the treatment of patients with cirrhosis and bleeding esophageal varices (BEV) and in patients with hepatorenal syndrome (HRS): two of the most dramatic and feared complications of cirrhosis. Terlipressin exerts its main pharmacological effect through stimulation of vasopressin-1 receptors. These receptors are located in vascular smooth muscle and mediate vasoconstriction. In patients with cirrhosis and portal hypertension, treatment with terlipressin increases mean arterial pressure and decreases portal flow and pressure within minutes of administration. Furthermore, in patients with ascites terlipressin improves glomerular filtration and excretion of sodium. Terlipressin decreases failure of initial hemostasis by 34%, decreases mortality by 34%, and is considered a first-line treatment for BEV, when available. Terlipressin in combination with albumin reverses type 1 HRS in 33%-60% of cases and is the only treatment with proven efficacy in randomized trials. The safety profile is favorable when considering the clinical efficacy and the high mortality of these clinical entities. Adverse events are mostly cardiovascular and related to vasoconstriction. Mortality and withdrawal of terlipressin due to adverse events occurs in less than 1% of cases. Mild adverse events related to terlipressin treatment occur in 10%-20% of patients. The benefit, however, of terlipressin on long-term survival in HRS remains to be determined. At present, treatment with terlipressin and albumin is considered the most efficient therapy and should therefore be recommended for the treatment of type 1 HRS-1.
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PMID:Efficacy and safety of terlipressin in cirrhotic patients with variceal bleeding or hepatorenal syndrome. 1901 83

Terlipressin, a vasopressin agonist, is a commonly used drug with different indications, particularly in patients with end-stage liver disease. As a V(1) receptor agonist, it increases systemic vascular resistance, particularly in the splanchnic area, resulting in a decrease of portal pressure. Besides the approved use for variceal bleeding, terlipressin also has beneficial effects in the treatment of hepatorenal syndrome and norepinephrine-resistant septic shock. In patients with cirrhosis and variceal bleeding, the use of terlipressin reduces the portal vein pressure and decreases the pressure in esophageal varices. This can save lives when skilled endoscopists are not immediately available. Hepatorenal syndrome is associated with vasodilation in the mesenteric circulation with arterial underfilling and consecutive renal vasoconstriction. Restoration of an effective arterial blood volume can be achieved by the combination of terlipressin and volume expansion. In some cases, a success rate of up to 75% is reported. The early use of terlipressin in catecholamine-resistant shock can improve organ perfusion.
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PMID:Pharmacology, clinical efficacy and safety of terlipressin in esophageal varices bleeding, septic shock and hepatorenal syndrome. 1907 11

Terlipressin is known to improve renal function in patients with liver cirrhosis and hepatorenal syndrome (HRS). This study investigated effects of duration and dose of terlipressin therapy and predictive factors for positive response to treatment. The clinical charts of 30 consecutive patients with HRS who received terlipressin and albumin based on a determined therapeutic scheme, were retrospectively studied. In 25 (66 %) of 38 treatment episodes complete response was achieved (Kaplan-Meier survival method). Predictive for positive response to treatment were duration of treatment and cumulative terlipressin dosis (p < 0.01, 95 % CI 0.31 - 0.59 and p < 0.01, 95 % CI 0.93 - 0.98, respectively) as well as a low level of serum creatinine and MELD score at inclusion (p = 0.01, 95 % CI 0.3 - 9.85 and p < 0.01, 95 % CI 0.87 - 0.98 respectively) and HRS type II (p = 0.04, 95 % CI 1.04 - 9.93). The median duration of therapy was 6 days +/- 4.9 (SD) vs. 8 days +/- 6.3 in the nonresponder group. The median dose of terlipressin in the responder group was 3.9 mg +/- 1.3 per day vs. 3.4 mg +/- 1.4 in the nonresponder group (p = n. s.). The probability that complete response was obtained at day 17 of treatment was 84 % (95 % CI 0.64 - 0.96), whereas at day 7 it was just 52 % (95 % CI 0.36 - 0.7). In conclusion, these data confirm that terlipressin plus albumin is effective in two-thirds of patients with HRS. Prolongation of treatment beyond 7 days up to 20 days is capable of increasing the response rates. Whether outcome can be predicted depending on parameters like type of HRS and base-level of serum creatinine needs to be confirmed in further studies, especially with regard on the previously revised criteria of HRS.
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PMID:Terlipressin in 30 patients with hepatorenal syndrome: results of a retrospective study. 1915 88

Hepatorenal syndrome (HRS) is a reversible form of functional renal failure that occurs with advanced hepatic cirrhosis and liver failure. Despite mounting research in HRS, its etiology and medical therapy has not been resolved. HRS encompasses 2 distinct types. Type 1 is characterized by the rapid development of renal failure that occurs within 2 wk and involves a doubling of initial serum creatinine. Type 2 has a more insidious onset and is often associated with ascites. Animal studies have shown that both forms, in particular type 1 HRS, are often precipitated by bacterial infections and circulatory changes. The prognosis for HRS remains very poor. Type 1 and 2 both have an expected survival time of 2 wk and 6 mo, respectively. Progression of liver cirrhosis and the resultant portal hypertension leads to the pooling of blood in the splanchnic vascular bed. The ensuing hyperdynamic circulation causes an ineffective circulatory volume which subsequently activates neurohormonal systems. Primarily the sympathetic nervous system and the renin angiotensin system are activated, which, in the early stages of HRS, maintain adequate circulation. Both advanced cirrhosis and prolonged activation of neurohormonal mechanisms result in fatal complications. Locally produced nitric oxide may have the potential to induce a deleterious vasodilatory effect on the splanchnic circulation. Currently medical therapy is aimed at reducing splanchnic vasodilation to resolve the ineffective circulation and maintain good renal perfusion pressure. Terlipressin, a vasopressin analogue, has shown potential benefit in the treatment of HRS. It prolongs both survival time and has the ability to reverse HRS in the majority of patients. In this review we aim to focus on the pathogenesis of HRS and its treatment with terlipressin vs other drugs.
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PMID:Terlipressin and hepatorenal syndrome: what is important for nephrologists and hepatologists. 2104 48

Ascites that does not respond or recurs after high-dose diuresis and sodium restriction should be considered refractory ascites. As cirrhosis advances, the escaping fluid overwhelms the lymphatic return. Decrease in renal plasma flow leads to increased sodium reabsorption at the proximal tubule leading to decreased responsiveness to loop diuretics and mineralocorticoid antagonists, which work distally. These complex hemodynamic alterations lead to refractory ascites. In refractory ascites, high-dose diuresis (400 mg of spironolactone and 160 mg of furosemide) and sodium restriction (<90 mmol/d) result in inadequate weight loss and sub optimal sodium excretion (<78 mmol/d). Further use of diuretics is limited by complications such as encephalopathy, azotemia, renal insufficiency, hyponatremia, and hyperkalemia. Therapy for refractory ascites is limited. The available therapies are repeated large volume paracentesis (LVP), transjugular intrahepatic portosystemic shunts, peritoneovenous shunts, investigational medical therapies, and liver transplantation. LVP with concomitant volume expanders is the initial treatment of choice. Transjugular intrahepatic portosystemic seems to be superior to LVP in reducing the need for repeated paracentesis and improves the quality of life. Several treatments that act at different steps in the pathogenesis of ascites are investigational, and some show promising results. Splanchnic and peripheral vasoconstrictors (Octreotide, Midodrine, and Terlipressin) increase effective arterial volume and decrease activation of the renin-angiotensin system with resultant increase in renal sodium excretion. Clonidine when given with spironolactone has been shown to cause rapid mobilization of ascites by significantly decreasing the sympathetic activity and renin-aldosterone levels. Natural aquaretics and synthetic V2 receptor antagonists (satavaptan) are being evaluated for mobilization of ascites by increasing the excretion of solute-free water. Liver transplantation remains the only definitive therapy for refractory ascites. Because refractory ascites is a poor prognostic sign, liver transplantation should be considered and incorporated early in the treatment plan.
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PMID:Management of refractory ascites. 2119 46


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