Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 30% to 35% of patients with portal hypertension bleed from gastroesophageal varices and mortality remains high reflecting the challenges of effectively dealing with the bleeding event itself and the problems of underlying liver disease. Careful resuscitation and control of risk of complications is the most essential element of medical therapy (Fig. 2). Use of newer, more effective drug combinations with vasopressin or somatostatin permit control of hemorrhage in the majority of patients with fewer drug-induced complications. Endoscopic sclerotherapy and, more recently, banding therapy provide immediate control of hemorrhage and eradication of varices and rebleeding in up to 90% of patients. Persistent, recurrent bleeding in the small number of remaining patients can be effectively managed by "portacaval shunt rescue" or orthotopic liver transplantation in selected cases with acceptable surgical morbidity and mortality. The contribution and role of the TIPS procedure is unknown but very promising; at least as a bridge procedure in patients awaiting transplantation. Until appropriate prospective, comparative trials are performed, the role of TIPS as a long-term alternative to portacaval shunt surgery or other endoscopic or surgical options remains unknown.
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PMID:Treatment of acute gastroesophageal variceal hemorrhage. 837 25

In patients with advanced liver disease, decreases in renal blood flow, glomerular filtration rate, and urinary output are frequently observed. The deterioration in renal function is usually not due to a unique cause but is the result of the concerted action of several mechanisms operating in parallel; decreased plasma protein formation and increased intrahepatic vascular resistance lead to sequestration of blood volume, favoring hypovolemia and reduction in cardiac output. At the same time enhanced formation of nitroxide leads to peripheral vasodilation; bacterial endotoxin escaping clearance by the diseased liver stimulates the expression of a long-acting nitroxide synthase. Furthermore, vasodilating intestinal mediators such as substance P escape inactivation by the liver. In the face of peripheral vasodilation the maintenance of blood pressure requires an increase in cardiac output, which is achieved by activation of sympathetic nervous tone, renal vasoconstriction, enhanced release of renin, angiotensin, aldosterone, and antidiuretic hormone, leading to renal retention of sodium and water. Renal vasoconstriction is opposed by vasodilatatory prostaglandins, and renal failure may be triggered by inhibition of prostaglandin formation. On the other hand, vasoconstrictive eicosanoids, such as thromboxane B2 and leukotriene E2, which escape hepatic inactivation, may contribute to renal vasoconstriction. Beyond these mechanisms disturbed hepatic regulation of renal function may participate in the generation of hepatorenal syndrome. The liver regulates renal function via both a hepatorenal reflex decreasing renal blood flow and a hypothetical liver-borne diuretic factor increasing renal blood flow. Both enhanced hepatorenal reflex activity and decreased formation of the liver-borne diuretic factor could participate in the pathogenesis of hepatorenal syndrome.
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PMID:New clues to the pathophysiology of hepatorenal failure. 846 32

Acute bleeding due to esophageal varices continues to be a life-threatening complication of liver disease. Despite the availability of improved therapy, mortality continues to be high. Octreotide has been shown to be at least as effective as vasopressin in the treatment of bleeding varices, with fewer and less severe systemic adverse effects. In addition, octreotide has also been consistently associated with a decreased need for transfusions. Octreotide has been used safely in patients without serious cardiovascular disease when administered as a continuous intravenous infusion of 25 micrograms/h for 24 hours with or without an initial 100-micrograms bolus dose. Since these trials have used small numbers of patients, the ability to detect small but clinically important differences has been limited. Additional controlled trials comparing octreotide with the combination of vasopressin and nitroglycerin are needed to more clearly determine the efficacy and cost-effectiveness of therapy. Furthermore, the optimal dosage, duration, and route of administration of octreotide in the treatment of bleeding esophageal varices has yet to be determined.
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PMID:Octreotide or vasopressin for bleeding esophageal varices. 903 26

Progressive renal failure in cirrhosis and fulminant liver disease remains an adverse prognostic factor. Irrespective of the type of renal functional impairment which ranges form "prerenal failure" to "hepatorenal syndrome" and "acute tubular necrosis", renal hypoperfusion, as a consequence of either reduced perfusion pressure or increased renal vascular resistance, is an important pathomechanism. Awareness of the risk of renal failure and avoidance of nephrotoxic agents and of brisk reductions in effective circulating volume are important for prevention. Plasma volume expansion, on the other hand, is mandatory in trying to reverse incipient renal functional impairment. Pharmacological attempts to improve renal hemodynamics by lowering renal and increasing extrarenal vascular resistance have so far largely been disappointing. However, increasing knowledge about mediators and synthesis of specific agonists and antagonists, such as those against endothelin or antidiuretic hormone, may add promising treatment options in the near future. TIPS is another therapeutic tool of potential interest in the management of renal failure in liver disease which needs further evaluation. Renal replacement therapy, preferentially in the form of continuous procedures, may be life-saving in those patients awaiting liver transplantation or spontaneous recovery of their hepatic function.
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PMID:Renal failure in liver disease. 1005 Oct 72

In cirrhosis of the liver, according to the peripheral arterial vasodilation hypothesis, relative underfilling of the arterial tree triggers a neurohumoral response (activation of renin-angiotensin-aldosterone system, sympathetic nervous system, nonosmotic release of vasopressin) aimed at restoring circulatory integrity by promoting renal sodium and water retention. Evidence has accumulated for a major role of increased vascular production of nitric oxide as the primary cause of arterial vasodilation in cirrhosis. Ascites is a common complication in cirrhosis. Treatment of ascites consists of a low salt diet with diuretics, and paracentesis together with plasma volume expanders in diuretic-resistant patients. Progression of cirrhosis may result in hepatorenal syndrome, a state of functional renal failure that carries an ominous prognosis. Orthotopic liver transplantation has remained the only curative treatment for patients with advanced liver disease; other modalities such as transjugular intrahepatic portosystemic shunt or vasopressin analogues may serve as a bridge to transplantation. Another complication of decompensated cirrhosis is spontaneous bacterial peritonitis, the incidence of which can be reduced by primary or secondary antibiotic prophylaxis by using orally active antibiotics.
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PMID:Update on peripheral arterial vasodilation, ascites and hepatorenal syndrome in cirrhosis. 1111 Jun 23

The hepatorenal syndrome is a form of renal failure occurring in patients with advanced liver disease. The diagnosis is based both on the demonstration of low GFR and exclusion of other common causes of renal failure that may occur in patients with cirrhosis. Orthotopic liver transplantation remains the only curative treatment for this poor outcome disease; other modalities such as vasopressin analogues, transjugular intrahepatic portosystemic shunt or renal replacement therapies may serve as a bridge to transplantation. This article reviews the pathophysiology, diagnosis and current treatment of hepatorenal syndrome.
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PMID:[Update on hepatorenal syndrome]. 1188 72

The hepatorenal syndrome (HRS) is a unique form of acute renal failure with entirely normal renal histology in advanced liver disease. Its diagnosis is made by exclusion of all causes of renal failure and by all the five major criteria as set by the International Ascites Club. The presence of hepatomegaly, poor nutritional status, and oesophageal varices at endoscopy are associated with a high risk of HRS. The liver tests, the Child-Pugh score, are of no value in prediction of its occurrence. Contraction of the effective blood volume, which may lead to renal hypoperfusion with preferential renal cortical ischaemia, is proposed pathogenesis of the condition. Because understanding of the pathogenesis of HRS is incomplete, therapy is supportive only. Optimal fluid management is vital as there is almost invariably a reduction in effective arterial blood volume. Dopamine, frusemide and haemofiltration may be helpful in management of fluid overload but do not affect renal function. TIPS has been used successfully in small series of patients. The vasopressin analog also has been used with early excellent response. The treatment of HRS has been discouraging and the only proven cure for HRS is liver transplantation at this point of time.
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PMID:Hepatorenal syndrome: pathophysiology and treatment. 1224 Aug 52

DEFINITION OF HYPOURICEMIA: Hypouricemia (serum uric acid less than 120 micro mol/l) is a biological abnormality often discovered accidentally and with a low prevalence depending on its permanent or transitory nature ranging from 0.15 to 3.38%. NEW PHYSIOLOGICAL CONCEPTS OF ITS PATHOGENESIS: Recently, our knowledge of the physiopathological mechanisms of hypouricemia has been emphasized by the identification of three systems of renal and extra-renal uric acid transport: a Cl/urate (URAT1) transporter, a multispecific organic anion transporter (OAT) and a urate transporter/channel. ETIOLOGY AND COMPLICATIONS OF HYPOURICEMIA: Through questioning, drugs and toxics (allopurinol.) are generally rapidly recognized as responsible for half of the hypouricemia encountered. It can be concomitant to a known disease: severe liver disease, neoplasia, diabetes, AIDS, syndrome of inappropriate antidiuretic hormone secretion. Hypouricemia can also be isolated and justifies the measurement of uric acid clearance, the normality or reduction of which orients towards a deficiency in xanthine-oxydase, the increase in which suggests an abnormality in uric acid transport in the proximal tubule (Fanconi syndrome, primary hereditary anomaly of tubular uric acid transport). Hypouricemia does not appear to expose the patient to any danger, but the onset of nephrolithiasis or acute renal failure secondary to the combination of severe hypouricemia and oxidant stress is always possible.
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PMID:[Hypouricemia, an old subject and new concepts]. 1523 14

Hepatorenal syndrome (HRS) is a serious complication of advanced liver disease. Historically, the development of HRS was considered a pre-terminal event due to a lack of efficacious therapy. Although liver transplantation remains the optimum therapy for HRS, many patients may be unsuitable for liver grafting. In addition, organ shortage may necessitate the institution of alternative pharmacological therapies to bridge patients to transplantation or to maintain renal function. This article reviews the definitions of Types-1 and -2 HRS, and addresses strategies for the prevention of the syndrome. It will also discuss management approaches to the cirrhotic patient with renal failure, specifically, assessment of novel vasoconstrictor therapies, such as vasopressin analogues, alpha-adrenoreceptor agonists, and the use of transjugular intra-hepatic shunts either alone or in combination with other therapeutic agents.
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PMID:Current management of the hepatorenal syndrome. 1609 65

Hepatorenal syndrome (HRS) is defined as functional renal failure that develops in patients with advanced liver disease. HRS may be either slowly or rapidly progressive (type I and II HRS, respectively). Untreated HRS carries a high mortality. Liver transplantation is the best available treatment for HRS. However, all patients with HRS are not suitable candidates for transplantation. Moreover, an organ is often not available in a timely manner in those who are candidates for transplantation. Treatment with vasoconstrictors (terlipressin, octreotide, and midodrine) and plasma expansion with albumin is beneficial and serves as a bridge to transplantation in such cases. The vasopressin analog, terlipressin, produces a sustained reversal of HRS in about 57% to 78% of the patients. The benefits of terlipressin are seen mainly in those who are also receiving albumin simultaneously. In those who improve, recurrence of HRS is reported to be relatively uncommon in the short and intermediate term. In the United States, terlipressin is not available, and octreotide and midodrine are often used for the medical management of HRS. Unfortunately, there are only limited uncontrolled data to support the use of these drugs for HRS. In those who respond to octreotide and midodrine, the subsequent placement of a transjugular intrahepatic portasystemic shunt (TIPS) has been shown to produce a sustained improvement in renal function. TIPS alone also improves renal functions in selected patients with HRS. The exact role of TIPS in HRS needs further evaluation, as patients with HRS are particularly at risk for complications such as encephalopathy and liver failure. Molecular adsorbent recirculating system (MARS) is an albumin-based dialysis system that has a promising role in the treatment of HRS and liver failure. MARS is a very expensive form of treatment, and further clinical trials are needed to establish its utility. Development of HRS can be prevented by adding albumin to the antibiotic regimen to treat spontaneous bacterial peritonitis and through pentoxifylline administration to the patients with acute alcoholic hepatitis.
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PMID:Hepatorenal syndrome. 1631 61


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