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ABSTRACT: Brain natriuretic peptide is a cardiac neurohormone secreted from ventricles in response to end diastolic pressure and increased volume. It has diuretic, natriuretic and vasodilator effects. In cirrhosis, a hyperdynamic circulation occurs because of hemodynamic and hemostatic alterations. The increase in brain natriuretic peptide concentration shows parallelism with the stage of cirrhosis. The aim of this study is to investigate the relation of increased brain natriuretic peptide level with the pathophysiologic components of cirrhosis and treatment.
Ninety-five cirrhotic patients in different stages (Child-A: 33; Child-B: 25; Child-C:37) and age and sex matched 86 healthy individuals were recruited for the study. Brain natriuretic peptide concentration was measured with brain natriuretic peptide-Triage test device using fluoresan immune assay method.
Brain natriuretic peptide levels of patients with hepatic cirrhosis were significantly higher compared to control group (288.5±329.2/60.2±29.5/p=0.000, respectively). Serum brain natriuretic peptide levels were positively correlated with Child score (Child A-B-C; 201.2±266/258.7±233.6/386.5±407.7, respectively). A negative correlation was observed between brain natriuretic peptide and albumin levels (p=0.002). Brain natriuretic peptide concentration was significantly correlated with the grade of esophagus varices, and presence of ascites and collateral circulation (p=0.006; p=0.001; p=0.002; respectively). Patients receiving with beta-blocker and diuretic treatments had significantly higher brain natriuretic peptide levels.
High brain natriuretic peptide levels in patients with cirrhosis may be due to hepatocellular insufficiency or portal hypertension, but a cardiomyopathy developing insiduously should not be regarded.
The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 12/2010; 21(4):381-6. · 0.47 Impact Factor
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European Journal of Pediatrics 10/2006; 165(9):654-7. · 1.88 Impact Factor
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Murat Aladağ,
Bülent Kantarçeken,
Melih Karincaoğlu,
Ayşe Sertkaya,
Kerim Cikim,
M M Murat Harputluoğlu,
Ulvi Demirel,
Hakan Alan,
Fehmi Ateş, Bülent Yildirim,
Fatih Hilmioğlu
The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 01/2006; 16(4):242-3. · 0.47 Impact Factor
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ABSTRACT: It has been previously proposed that electrocardiographic abnormalities may be associated with acute pancreatitis. However, there is a lack of data on the QT interval and dispersion value in patients with acute pancreatitis, and no data are also available concerning QT interval and QT dispersion in acute biliary pancreatitis (ABP).
: We aimed to investigate the QT parameters in patients with ABP, to compare them with those of healthy controls, and to analyze the relationship between QT parameters and Ranson score.
The present study included 32 patients with acute biliary pancreatitis and 35 healthy controls. The severity of the pancreatitis was determined by Atlanta criteria: fewer than 3 Ranson criteria or fewer than 8 APACHE II (the Acute Physiology and Chronic Health Evaluation) points indicated the mild disease (group 1); 3 or more Ranson criteria or 8 or more APACHE II points or organ failure or systemic complications or local complications indicated the severe disease (group 2). On admission, all patients underwent a standard 12-lead electrocardiogram, and corrected maximum QTc interval (QTcmax), corrected minimum QT interval (QTcmin), and corrected QTc dispersion (QTcd) values of the subjects were measured according to the Bazett formula in this study.
QTcmax and QTcd were significantly longer in patients with ABP than in healthy controls (442 +/- 38 milliseconds versus 413 +/- 34 milliseconds, P < 0.05; and 67 +/- 21 milliseconds versus 42 +/- 18 milliseconds, P < 0.001, respectively). Similarly, QTcmax and QTcd were significantly longer in group 2 than in group 1 (440 +/- 38 milliseconds versus 450 +/- 34 milliseconds, P < 0.01; and 66 +/- 9 milliseconds versus 71 +/- 11 milliseconds, P < 0.01, respectively). Correlation analysis showed that there is a significant positive relationship between Ranson scores of patients and QTcmax and QTcd (P < 0.01 and P < 0.001, respectively).
The effect of acute biliary pancreatitis on QT intervals and dispersion appears to be dependent not only on the disease but also on its severity, and these parameters may give additional prognostic information in ABP patients, even in the initial evaluation.
Pancreas 11/2005; 31(3):238-41. · 2.39 Impact Factor
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ABSTRACT: Esophageal varices and serum-ascites albumin gradient (SAAG) are two major findings of portal hypertension. Recently, correlation between these two findings in patients with cirrhosis due to alcohol has been attracted attention. We aimed at evaluating whether a correlation exists between these parameters in the patients with non-alcoholic cirrhosis.
Albumin levels in the serum and ascites and esophageal varices were studied and the correlation between these parameters was assessed in 45 patients with non-alcoholic cirrhosis detected between January 2002 and June 2003.
Thirty-two of the patients were male and 13 female. The average age of the patients was 56.3+/-12.5 years (range 22-85 years). The causative agents were found to be hepatitis B virus in 35 patients and hepatitis C virus in six patients; no etiology could be determined in the remaining four patients. Serum level of albumin was determined as 2.53+/-0.53 g/dl, ascites level of albumin as 0.42+/-0.31 g/dl and SAAG as 2.1+/-0.51. Endoscopic esophageal examination revealed first-degree esophageal varices in 15 patients, second-degree esophageal varices in 18 patients and third-degree esophageal varices in eight patients; no esophageal varices could be found in four patients. There was no correlation between the degree of the esophageal varices and serum levels of albumin (p=0.7) and SAAG (p=0.2); but a weak correlation was found between the degree of the esophageal varices and ascites levels of albumin (p=0.03, r=0.30). Furthermore, the patients were classified by their SAAG values, and their varices were then assessed. Two of four patients with SAAG values between 1.1 and 1.49 had esophageal varices, as did 13 of 15 patients with SAAG values between 1.5 and 1.99, and all of the patients with SAAG values greater than 2.0.
All SAAG values were greater than 1.1 in our non-alcoholic cirrhosis cases. The correlation that has been found to exist between SAAG and esophageal varices could not be found in our patients with non-alcoholic cirrhosis. It is remarkable that most of the patients with non-alcoholic cirrhosis presenting with ascites and all of the patients with an SAAG value greater than 2.0 had esophageal varices.
The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 01/2004; 14(4):219-22. · 0.47 Impact Factor
