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)

Patients with cirrhosis and ascites have high plasma levels of atrial (ANP) and brain (BNP) natriuretic peptides, two cardiac hormones released by the atria and ventricles, respectively. We evaluated renal hemodynamics, sodium excretion, and intrarenal sodium handling (lithium clearance method) in seven cirrhotic patients with ascites and avid sodium retention before, during, and after the infusion of synthetic human BNP, at the dose of 4 pmol/kg.min for 1 hour, which has been shown to increase renal plasma flow, glomerular filtration rate (GFR), and sodium excretion in healthy subjects without affecting systemic hemodynamics. Plasma BNP levels were 7.31 +/- 0.85 pmol/L in baseline conditions, and increased to 33.60 +/- 2.96 pmol/L at the end of the infusion (P < .01 vs. baseline). Urinary excretion of guanosine 3',5'-cyclic monophosphate (cGMP) also significantly increased during the infusion, indicating stimulation of natriuretic peptide receptors by BNP. BNP administration did not modify renal plasma flow, GFR, sodium excretion or tubular sodium reabsorption to any appreciable extent. Arterial pressure heart rate, plasma norepinephrine, and plasma renin activity (PRA) where also unchanged, whereas plasma aldosterone concentration showed a significant, 35% reduction at the end of the postinfusion period, ruling out the possibility that BNP-induced vasodilation might be responsible for failure of the peptide to induce a natriuretic response. Overactivity of antinatriuretic factors is probably the main determinant of the blunted natriuretic effect of BNP in these patients.
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PMID:Blunted natriuretic response to low-dose brain natriuretic peptide infusion in nonazotemic cirrhotic patients with ascites and avid sodium retention. 748 83

To investigate the clinical significance of endothelin (ET), natriuretic peptides, and the renin-angiotensin-aldosterone system in pediatric liver transplantation, we measured plasma levels of ET, atrial and brain natriuretic peptides (ANP, BNP), aldosterone, and plasma renin activity in 18 patients (aged 0.5-12 yr; median 1 yr) undergoing living-related liver transplantation due to congenital biliary atresia and severe liver cirrhosis. Before transplantation, the plasma ET level (28.9 +/- 2.5 [mean +/- SEM] pg/mL) was increased compared with that of healthy children (10-18 pg/mL), but decreased during the anhepatic phase (22.5 +/- 1.6 pg/mL). It increased again after reperfusion and remained at high levels in the early postoperative period (postoperative day 3, 27.8 +/- 3.0 pg/mL). Plasma levels of ANP and BNP and aldosterone and plasma renin activity were also high before surgery. Plasma ANP and BNP did not change significantly during surgery. After transplantation, plasma BNP significantly increased, and plasma ANP tended to increase. Plasma aldosterone increased markedly during the anhepatic phase, although plasma renin activity decreased. After transplantation, plasma aldosterone and plasma renin activity both decreased to within normal levels. Mean arterial blood pressure increased gradually after reperfusion and surgery (postoperative day 3, 35.7 +/- 5.2% increase). No substantial differences in these variables occurred between the younger (< or = 1.0 yr, n = 9) and older patients (> 1.0 yr, n = 9). These results suggest that ET production in the cirrhotic liver is augmented and ET, natriuretic peptides, and the renin-angiotensin-aldosterone system all play some role in the circulatory regulation during perioperative periods of pediatric liver transplantation.
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PMID:Perioperative plasma concentrations of endothelin and natriuretic peptides in children undergoing living-related liver transplantation. 856 19

Cirrhotic patients with ascites show increased plasma levels of natriuretic peptides from cardiac origin (i.e., atrial natriuretic peptide [ANP] and brain natriuretic peptide [BNP]). Urodilatin is a unique member of the natriuretic peptide family because it is exclusively synthesized in the kidney acting on a paracrine fashion in the regulation of sodium excretion. To investigate the renal production of urodilatin in cirrhosis and its relationship with other natriuretic peptides and sodium retention, urodilatin excretion and plasma levels of ANP were measured in 21 healthy subjects, 13 cirrhotic patients without ascites and 23 cirrhotic patients with ascites. Urine urodilatin was measured with a highly specific radioimmunoassay using a polyclonal antibody against human urodilatin. Patients with ascites had marked sodium retention (UNa 7 +/- 2 mEq/d) as compared to patients without ascites and healthy subjects (29 +/- 3 mEq/d and 34 +/- 5 mEq/d, respectively, P < .001). Patients with cirrhosis and ascites had urine urodilatin excretion similar to patients without ascites and healthy subjects (82 +/- 8 pmol/g, 95 +/- 10 pmol/g, and 89 +/- 9 pmol/ g of creatinine, respectively; not significant). In addition, immunoreactive urodilatin from cirrhotic patients with ascites and healthy subjects showed a similar chromatographic pattern. By contrast, plasma ANP levels were increased significantly in patients with ascites (29 +/- 3 fmol/mL) as compared with patients without ascites or healthy subjects (14 +/- 3 fmol/mL and 6 +/- 1 fmol/mL, respectively; P < .01). In conclusion, urine urodilatin excretion is normal in patients with cirrhosis even in the presence of marked sodium retention. The coexistence of increased ANP levels and normal urodilatin excretion suggests that in cirrhosis both natriuretic peptides are regulated independently.
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PMID:Urinary excretion of urodilatin in patients with cirrhosis. 893 75

The long-predicted endocrine function of the heart has been proven by the discovery of atrial natriuretic peptide (atrial natriuretic factor, A-type natriuretic peptide; ANP) 20 years ago. This subsequently led to the description of a whole family of structurally similar but genetically distinct peptides, the natriuretic peptide family, which contributes to cardiovascular homeostasis. These looped peptides promote natriuresis and diuresis, act as vasodilators, and exert antimitogenic effects on cardiovascular tissues. Two members, ANP and brain natriuretic peptide (B-type natriuretic peptide; BNP) are secreted by the heart mainly in response to myocardial stretch induced by volume load. The natriuretic peptides are synthesized as preprohormones. The C-terminal endocrinological active peptides (ANP, BNP) and their N-terminal prohormone fragments are found in plasma. The natriuretic peptide system is activated to its highest degree in ventricular dysfunction. However, natriuretic peptides are increased in all patients with edematous disorders which lead to an increase in atrial tension or central blood volume, such as renal failure or ascitic liver cirrhosis. It could be demonstrated that in chronic heart failure patients and during the subacute phase of myocardial infarction, of all tested neurohormones, the cardiac natriuretic peptides were best markers to identify heart failure and the most powerful predictors of morbidity and mortality. Natriuretic peptides are independent markers for risk assessment. In comparative studies BNP was superior to ANP and its N-terminal prohormone fragments in myocardial infarction as well as in chronic heart failure patients. Less data on N-terminal proBNP (NT-proBNP) is available, but BNP and NT-proBNP appear to be equivalent markers. For primary care physicians natriuretic peptide measurement is useful to decide which patient with suspected heart failure warrants further investigation, particularly when assessment of left ventricular function is not readily available. Natriuretic peptides have an excellent negative predictive value, particularly in high risk patients. An increase in BNP is serious enough to warrant follow-up examinations. For the cardiologists the natriuretic peptides are helpful for guidance of therapy and monitoring disease course in heart failure patients and for risk stratification in heart failure and myocardial infarction.
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PMID:The impact of cardiac natriuretic peptide determination on the diagnosis and management of heart failure. 1152 2

Utility of the dosage of brain natriuretic factor (BNP) in the diagnosis and treatment of heart failure. Congestive heart failure (HF) is the main reason for hospitalisation of elderly patients. HF affects nearly 15% of patients aged 75 years or older. Prognosis after the diagnosis of HF is comparable to that of cancers with 50% survival after 4 years for mild HF and 50% after one year in more severe cases. Systolic HF defined by a left ventricular ejection fraction (LVEF) < 40% is asymptomatic in half the patients. In patients with symptomatic HF, LVEF is normal in almost 50% of the cases suggesting a diastolic HF. BNP is secreted after distension of left ventricule mainly in patients with systolic or diastolic HF, in proportion to the severity of the disease. A serum level of BNP > 100 pg/ml has a sensitivity of 90 percent and a specificity of 76 percent for the diagnosis of HF. Serum BNP is also increased in kidney insufficiency and in cirrhosis. BNP increase has a prognostic value to predict mortality after cardiac failure or myocardial infarction. Except for digoxin, all the drugs used to treat HF decrease serum levels of BNP. In dyspneic patients, serum levels of BNP < 50 pg/ml can exclude HF with a good probability. However BNP determination is not useful to diagnose HF in a general population.
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PMID:[Use of brain natriuretic peptide (BNP) in the diagnosis and treatment of heart failure]. 1509 95

Cirrhotic cardiomyopathy is a condition recently known in liver cirrhosis consisting of systolic dysfunction to stress factors, diastolic dysfunction and electrophysiological abnormalities in the absence of cardiac disease. The prevalence of cirrhotic cardiomyopathy remains unknown until now. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers (brain natriuretic factor--BNP, proBNP, TnI). Pathogenic mechanisms underlying cirrhotic cardiomyopathy development include abnormal signaling betaadrenergic, cardiomyocites membrane fluidity changes, interstitial fibrosis, myocardial hypertrophy, altered transmembrane ion channels as intervention with negative inotropic effect of different substances whose concentration is increased in cirrhosis. Major stresses on the cardiovasculary system such as liver transplantations, infections, insertion of transjugular portosystemic stent-shunt (TIPSS) have been demonstrated to put in evidence the presence of cirrhotic cardiomyopathy. Heart failure is a significant cause of mortality after liver transplantation but the improvement of liver function determines cardiac abnormalities reversal. Current management recommendations include empirical, nonspecific and mainly supportive measures, no specific treatment can be recommended, and cardiac failure should be treated as in non-cirrhotic patients with sodium restriction, diuretics, and oxygen therapy when necessary. The exact prognosis remains unclear. The extent of cirrhotic cardiomyopathy generally correlates to the degree of liver insufficiency. Reversibility is possible (either pharmacological or after liver transplantation), but further studies are needed.
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PMID:[Cardiomyopathy in liver cirrhosis--an undiagnosed entity?]. 2070 Sep 61

Plasma preoperative values of natriuretic B peptide (pro-BNP) were correlated with ascites in men experiencing hepatic cirrhosis due to different etiologies on the active waiting list for liver transplantation. The study was performed in 54 male recipients of a liver transplant. Written informed consent was obtained from the patients or their relatives, and the study protocol was approved by our local Clinical Research (Ethics) Committee. Male patients were classified into two groups: group 1 included patients with alcoholic hepatic cirrhosis (n = 30) distributed as 19 men with no ascites, four with nonrefractory ascites, and seven with refractory ascites; group 2 included cases of viral hepatitis cirrhosis (n = 24) distributed as 13 men with no ascites, nine with non-refractory ascites, and two with refractory ascites. A group of six healthy male volunteers was used to establish normal (basal) values of pro-BNP and left auricular diameter (LAD). Pro-BNP values were determined in plasma samples by an electrochemiluminiscence immunoassay. Pro-BNP plasma levels in patients with alcoholic cirrhosis were threefold greater among patients with no ascites or no refractory ascites compared with healthy men, whereas pro-BNP values were fivefold enhanced among alcoholic patients with refractory ascites. The viral hepatitis cirrhosis group showed pro-BNP plasma values 1.5-fold enhanced in men with no ascites, whereas pro-BNP reached fivefold with either nonrefractory or refractory ascites. The enhanced pro-BNP plasma levels indicated advanced hepatic degradation, seemingly related to the presence of refractory ascites associated with cirrhosis.
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PMID:Preoperative natriuretic peptide-B values and ascites in male liver transplant recipients. 2148 79

Natriuretic neuropeptides (ANP, BNP, CNP) are produced primarily in the cardiac atria under normal conditions. The main stimulus for ANP and BNP peptide synthesis and secretion is cardiac wall stress. Cardiac ventricular myocytes constitute the major source of BNP-related peptides. Ventricular NT-proBNP production is upregulated in cardiac failure and locally in the area surrounding a myocardial infarct. NT-proBNP is cleared passively by organs with high rate of blood flow (muscle, liver, kidney). It has a longer half life than BNP and higher plasma concentration. BNP and NTproBNP tend to be higher in women and lower in obese individuals. They are also higher in elderly, in left ventricular tachycardia, right ventricular overload, myocardial ischemia, hypoxaemia, renal dysfunction, liver cirrhosis, sepsis and infection. NT-proBNP is useful both in the diagnosis and prognosis of heart failure and is considered to be a gold standard biomarker in heart failure similar to BNP. A cut-off point 300 pg/ml has 99% sensitivity, 60%specificity and NPV 98%for exclusion of acute heart failure. NT proBNP has also a strong prognostic value of death in acute and chronic heart failure and also predicts short and long term mortality in patient with suspected or confirmed unstable CVD. Natriuretic peptides are also prognostic markers for the RV (Right Ventricular) Dysfunction. Their release is due to myocardial stretch from right ventricular pressure overload.Finally, there are data supporting that NT-proBNP might be useful to put a time frame on atrial fibrillation of unknown onset.
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PMID:NTproBNP: an important biomarker in cardiac diseases. 2347 72

The hepatorenal syndrome (HRS) is defined as a potentially reversible kidney failure in patients with cirrhosis and ascites. An association of HRS and cirrhotic cardiomyopathy has been reported recently, but there are no result studies about the use of positive inotropes as part of the acute phase treatment. We report the case of a patient diagnosed with HRS, with high levels of NT pro-BNP, but with normal ejection fraction of the left ventricle, which showed abnormalities in systolic function through speckle tracking in echocardiography, reversible after the infusion of dobutamine. The patient showed clinical and laboratory improvement of his renal function after the infusion of dobutamine. Clinical studies are needed on HRS therapeutic approach taking into account the myocardial dysfunction as a major contributing factor to renal dysfunction.
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PMID:Hepatorenal syndrome with cirrhotic cardiomyopathy: case report and literature review. 2587 40