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)

Distributive shock is defined as circulatory insufficiency induced by excessive dilatation of the peripheral vasculature or maldistribution of cardiac output. Septicemia, systemic inflammatory response syndrome, anaphylaxis, injuries to the central nervous system, and drug intoxication are causative factors of shock. Circulatory derangements induced by bacterial infection have been divided into hyperdynamic and hypodynamic shock. Administration of inotropic drugs, vasopressors, and/or vasodilators are primary treatments in this type of shock. Continuous infusion of norepinephrine to maintain blood pressure or administration of inoptropes such as dopamine or dobutamine are recommended to improve tissue perfusion. High-dose intravenous epinephrine is required to reestablish cardiac function, followed by continuous infusion of norepinephrine in severe anaphylactic shock. Vasoconstrictors such as norepinephrine, vasopressin, or amaminone are administered to maintain vascular tone in shock caused by nerve damage or drug overdose.
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PMID:[Distributive shock and it's therapy by cardio-vascular acting drugs]. 1057 Jul 79

The pathophysiology of circulatory and renal dysfunction in cirrhosis and the treatment of ascites and related conditions (hepatorenal syndrome and spontaneous bacterial peritonitis) have been research topics of major interest during the last two decades. However, many aspects of these problem remain unclear and will constitute major areas of investigation in the next millennium. The pathogenesis of sodium retention, the most prevalent renal function abnormality of cirrhosis, is only partially known. In approximately one third of patients with ascites, sodium retention occurs despite normal activity of the renin-aldosterone and sympathetic nervous systems and increased circulating plasma levels of natriuretic peptides and activity of the so-called natriuretic hormone. These patients present an impairment in circulatory function which, although less intense, is similar to that of patients with increased activity of the renin-aldosterone and sympathetic nervous systems, suggesting that antinatriuretic factors more sensitive to changes in circulatory function that these systems may be important in the pathogenesis of sodium retention in cirrhosis. The development of drugs that inhibit the tubular effect of antidiuretic hormone and increase renal water excretion without affecting urine solute excretion has opened a field of great interest for the management of water retention and dilutional hyponatremia in cirrhosis. Two families of drugs, the V2 vasopressin receptor antagonists and the kappa-opioid agonists, have been shown to improve free water clearance and correct dilutional hyponatremia in human and experimental cirrhosis with ascites. The first type of drugs blocks the tubular effect of antidiuretic hormone and the second inhibits antidiuretic hormone secretion by the neurohypophysis. On the other hand, two new treatments have also been proved to reverse hepatorenal syndrome in cirrhosis. The most interesting one is that based on the simultaneous administration of plasma volume expansion and vasoconstrictors. The second is transjugular intrahepatic porto-systemic shunt. The long-term administration (1-3 weeks) of analogs of vasopressin (ornipressin or terlipressin) or other vasoconstrictors together with plasma volume expansion with albumin is associated with a dramatic improvement in circulatory function and normalization of serum creatinine concentration in patients with severe hepatorenal syndrome. Of interest is the observation that in many of these patients, hepatorenal syndrome does not recur following discontinuation of the treatment, thus raising important questions about the mechanism by which hepatorenal syndrome follows a progressive course in most untreated cases. The pathogenesis of circulatory dysfunction in cirrhosis and the role of local mechanisms in the development of the splanchnic arteriolar vasodilation associated with portal hypertension will continue as important topics in clinical and basic research in Hepatology. Of special interest is the study of the mechanism by which circulatory function further deteriorates following complications such as severe bacterial infection or therapeutic interventions such as therapeutic paracentesis, and the adverse consequences of the impairment in circulatory function on renal and hepatic hemodynamics. Finally, although major advances have been made concerning the treatment and secondary prophylaxis of spontaneous bacterial peritonitis in cirrhosis, many aspects of the pathogenesis of this infection remain unclear. The mechanism of bacterial translocation and of the colonization of bacteria in the ascitic fluid are particularly important to design adequate measures for primary prophylaxis of this severe bacterial infection.
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PMID:Complications of cirrhosis. II. Renal and circulatory dysfunction. Lights and shadows in an important clinical problem. 1072 2

In patients with community-acquired pneumonia, traditional criteria of infection based on clinical signs and symptoms, clinical scoring systems, and general inflammatory indicators (for example, leukocytosis, fever, C-reactive protein and blood cultures) are often of limited clinical value and remain an unreliable guide to etiology, optimal therapy and prognosis. Procalcitonin is superior to other commonly used markers in its specificity for bacterial infection (allowing alternative diagnoses to be excluded), as an indicator of disease severity and risk of death, and mainly as a guide to the necessity for antibiotic therapy. It can therefore be viewed as a diagnostic, prognostic, and perhaps even theragnostic test. It more closely matches the criteria for usefulness than other candidate biomarkers such as C-reactive protein, which is rather a nonspecific marker of acute phase inflammation, and proinflammatory cytokines such as plasma IL-6 levels that are highly variable, cumbersome to measure, and lack specificity for systemic infection. Elevated levels of pro-adrenomedullin, copeptin (which is produced in equimolar amounts to vasopressin), natriuretic peptides and cortisol are significantly related to mortality in community-acquired pneumonia, as are other prohormones such as pro-atrial natriuretic peptide, coagulation markers, and other combinations of inflammatory cytokine profiles. However, all biomarkers have weaknesses as well as strengths. None should be used on its own; and none is anything more than an aid in the exercise of clinical judgment based upon a synthesis of available clinical, physiologic and laboratory features in each patient.
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PMID:Clinical review: the role of biomarkers in the diagnosis and management of community-acquired pneumonia. 2023 71

A 5-year-old female Chihuahua was presented for acute collapse. Laboratory examinations showed markedly elevated levels of hepatobiliary enzymes. Empiric antibiotic therapy for bacterial infection of the liver was ineffective. The clinical signs worsened with the development of hyponatremia with hypoosmolality and elevated urine sodium levels. The dog was suspected of having acute cholangiohepatitis associated with an immune-mediated disease. Subsequently, it was diagnosed with syndrome of inappropriate antidiuretic hormone secretion (SIADH) on the basis of the specific disease criteria. Further tests showed normal function of the adrenal and thyroid glands, and MRI and cerebrospinal fluid (CSF) analysis did not show any intracranial diseases. Immunosuppressive therapy and water restriction resolved the clinical signs and improved the SIADH in this dog. This case indicates that SIADH can occur concurrently with suspected immune-mediated liver disease in dogs.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion concurrent with liver disease in a dog. 2218 69

Procalcitonin is a biomarker for estimating the likelihood of a bacterial infection. Procalcitonin-guided antibiotic therapy can reduce antibiotic overuse in respiratory tract infections. The differential diagnosis of water-electrolyte imbalances is challenging. Copeptin is co-secreted with arginine vasopressin (AVP) and is a reliable surrogate of plasma AVP. Copeptin may become a useful diagnostic tool in patients with polydipsia-polyuria syndrome and hyponatremia. Copeptin is also known to mirror different levels of stress. It appears to have an interesting potential as a new prognostic biomarker in patients with ischemic stroke. Biomarkers should not be used without the clinical context. They are meant to complement clinical judgment based upon a synthesis of available clinical and laboratory features in each patients.
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PMID:[Hormones as biomarkers for diagnosis and prognosis]. 2233 15

Hepatorenal syndrome (HRS) is a unique type of kidney failure that occurs in advanced cirrhosis. It is characterized by functional impairment of the kidneys due to vasoconstriction of the renal arteries in the setting of preserved tubular function and absence of significant histologic abnormalities. Renal vasoconstriction in HRS is due to severe vasodilation of the splanchnic arteries associated with portal hypertension, leading to a decrease in effective arterial blood volume and arterial pressure. HRS commonly develops after a trigger, usually a bacterial infection, that disrupts the arterial circulation, but it also may occur spontaneously. There are 2 forms of HRS: type 1 is characterized by an acute progressive decrease in kidney function and very short survival without treatment, whereas type 2 features stable less severe kidney failure and longer survival compared with type 1. A liver transplant is the preferred treatment for HRS. Pharmacologic treatment with vasoconstrictors to reverse splanchnic vasodilation, together with albumin, is effective in 40%-50% of patients with type 1 HRS and improves survival. The drug of choice is the vasopressin analogue terlipressin. Renal replacement therapy should not be used as first-line therapy.
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PMID:Hepatorenal syndrome: a severe, but treatable, cause of kidney failure in cirrhosis. 2248 Jul 95