P3252 Serum levels of different tumoral markers in patients with congestive heart failure

2003 ◽  
Vol 24 (5) ◽  
pp. 613
Author(s):  
P FAGGIANO
2015 ◽  
Vol 75 (3) ◽  
Author(s):  
T. Zaga ◽  
D. Makris ◽  
I. Tsilioni ◽  
T. Kiropoulos ◽  
S. Oikonomidi ◽  
...  

Background and Aim. Hyaluronic acid (HA) is a component of extracellular matrix and may play a role in the pleural inflammation which is implicated in parapneumonic effusions.The aim of the current study was to investigate HA levels in serum and pleura in patients with parapneumonic effusions. Methods. We prospectively studied pleural and serum levels of HA in 58 patients with pleural effusions due to infection (complicated and uncomplicated parapneumonic effusions), malignant effusions and transudative effusions due to congestive heart failure. In addition to HA, TNF-α and IL-1β levels were determined in pleural fluid and serum by ELISA. Results. The median±SD HA levels (pg/ml) in pleural fluid of patients with complicated effusions (39.058±11.208) were significantly increased (p<0.005), compared to those with uncomplicated parapneumonic effusions (11.230±1.969), malignant effusions (10.837±4.803) or congestive heart failure (5.392±3.133). There was no correlation between pleural fluid and serum HA values. Pleural fluid TNF-α levels (146±127 pg/mL) and IL-1β levels (133.4±156 pg/mL) were significantly higher in patients with complicated parapneumonic effusions compared to patients with other types of effusion (p<0.05). No significant association between HA and TNF-α or IL-1β was found. Conclusions. HA may play a significant role in the inflammatory process which characterises exudative infectious pleuritis. Further investigation might reveal whether HA is a useful marker in the management of parapneumonic effusions.


1997 ◽  
Vol 79 (12) ◽  
pp. 1698-1701 ◽  
Author(s):  
Masaki Okuyama ◽  
Seiji Yamaguchi ◽  
Naoki Nozaki ◽  
Minako Yamaoka ◽  
Masanori Shirakabe ◽  
...  

2013 ◽  
Vol 62 (18) ◽  
pp. C105
Author(s):  
Huseyin Altug Cakmak ◽  
Hasan Ali Barman ◽  
Ender Coskunpinar ◽  
Yasemin Musteri Oltulu ◽  
Baris Ikitimur ◽  
...  

2014 ◽  
Vol 60 (06/2014) ◽  
Author(s):  
Marcus Franz ◽  
Alexander Berndt ◽  
Friedhelm Kuethe ◽  
Michael Fritzenwanger ◽  
Hans-Reiner Figulla ◽  
...  

2017 ◽  
Vol 10 (1) ◽  
pp. 24
Author(s):  
Dyah Siswanti E ◽  
Fatmawati Fatmawati ◽  
M. Ikhsanul Fikri

Worsening renal function in patient with congestive heart failure affect the length of hospital stay. The purpose of thisstudy was to describe the creatinine serum levels and the length of hospital stay in patient with congestive heartfailure treated in Arifin Achmad hospital Riau Province January 2012 – December 2014. This study was done withcross sectional approach. This study found the most common creatinine serum levels found were <1.5 mg/dl (73.2%)with an average of 1.30 mg/dl and the range was 0.10 – 6.63 mg/dl. The value of left ventricular ejection fraction withan average of 44.9% and the range was 12% - 79%. Length of hospital stay in patients were >5 days commonly withan average of 7.29 days and the range was 1 – 29 days. The result of this study showed that the possibility ofcreatinine serum levels is not the only one predictor to determine the length of hospital stay in patient with congestiveheart failure.


2019 ◽  
Vol 20 (11) ◽  
pp. 2610
Author(s):  
Margarita Kunin ◽  
Vered Carmon ◽  
Pazit Beckerman ◽  
Dganit Dinour

Background: Cardiac collagen remodeling is important in the progression of heart failure. Estimation of cardiac collagen turnover by serum levels of serological markers is used for monitoring cardiac tissue repair and fibrosis. Peritoneal dialysis (PD) is used for the long-term management of refractory congestive heart failure (CHF). In this study, we investigated the effect of PD treatment on circulating fibrosis markers levels in patients with refractory CHF and fluid overload. Methods: Twenty-five patients with refractory CHF treated with PD were prospectively enrolled in the study. Circulating fibrosis markers procollagen type III C-peptide (PIIINP), matrix metalloproteinase 2 (MMP-2), and tissue inhibitor of metalloproteinases I (TIMP-1) levels were checked at baseline and after three and six months of treatment. Results: The clinical benefit of PD manifested by improved NYHA functional class and reduced hospitalization rate. Serum brain natriuretic peptide (BNP) levels decreased significantly during the treatment. Serum MMP-2 and TIMP-1 decreased significantly on PD. Circulating PIIINP showed two patterns of change, either decreased or increased following PD treatment. Patients in whom circulating PIIINP decreased had significantly lower baseline serum albumin, lower baseline mean arterial blood pressure, higher serum CRP, and a less significant improvement in hospitalization rate compared to the patients in whom circulating PIIINP increased. Patients in whom all three markers decreased demonstrated a trend to longer survival compared to patients whose markers increased or did not change. Conclusion: In refractory CHF patients PD treatment was associated with a reduction in circulating fibrosis markers.


2014 ◽  
Vol 111 (04) ◽  
pp. 725-735 ◽  
Author(s):  
Steven Hildemann ◽  
Christian Schulz ◽  
Daniela Fraccarollo ◽  
Corinna Schöpp ◽  
Ulrike Flierl ◽  
...  

SummaryEndothelial dysfunction and enhanced platelet reactivity in congestive heart failure (CHF) contribute to poor prognosis. CHF patients display an impaired responsiveness to clopidogrel. Fractalkine activates platelets and elevated plasma levels of this chemokine are a feature of CHF. We here addressed the interrelation of fractalkine, platelet reactivity and clopidogrel efficacy in humans and rats with CHF. Fractalkine serum levels determined by ELISA were increased in CHF patients (CHF: 1548 ± 650 pg/ml; Control: 968 ± 575 pg/ml, p<0.01) and following CHF induction in rats (CHF: 1509 ± 753 pg/ ml; Sham: 1181 ± 275 pg/ml, p<0.05). Expression of fractalkine and its receptor CX3CR1 was enhanced in aortas of CHF rats as determined by immunofluorescence microscopy and molecular analysis. Fractalkine significantly aggravated endothelial dysfunction and augmented P-selectin expression on platelets from CHF rats. Platelet surface expression of CX3CR1 was increased in CHF rats, who displayed an impaired response to clopidogrel (platelet reactivity to ADP: CHF 30 ± 22%; Sham: 8 ± 5%, p<0.05). Similarly in humans with CHF, elevated fractalkine levels were accompanied by reduced clopidogrel responsiveness. Patients with high on-clopidogrel treatment platelet P2Y12 reactivity displayed higher fractalkine levels (1525 ± 487 pg/ml) than those with sufficient clopidogrel response (684 ± 315 pg/ml, p<0.01). In conclusion, in CHF fractalkine was increased on the endothelium and in blood serum, and platelet surface- expression of CX3CR1 was enhanced. Fractalkine diminished endothelial function beyond the impairment already observed in CHF and was associated with a reduced responsiveness to the platelet inhibitor clopidogrel. These findings may indicate a novel pathophysiological mechanism contributing to impaired clopidogrel responsiveness in CHF.


2002 ◽  
Vol 283 (3) ◽  
pp. C802-C810 ◽  
Author(s):  
Giorgio Vescovo ◽  
Barbara Ravara ◽  
Valerio Gobbo ◽  
Marco Sandri ◽  
Annalisa Angelini ◽  
...  

Skeletal muscle in congestive heart failure is responsible for increased fatigability and decreased exercise capacity. A specific myopathy with increased expression of fast-type myosins, myocyte atrophy, secondary to myocyte apoptosis triggered by high levels of circulating tumor necrosis factor-α (TNF-α) has been described. In an animal model of heart failure, the monocrotaline-treated rat, we have observed an increase of apoptotic skeletal muscle nuclei. Proapoptotic agents, caspase-3 and -9, were increased, as well as serum levels of TNF-α and its second messenger sphingosine. Treatment of rats withl-carnitine, known for its protective effect on muscle metabolism injuries, was found to inhibit caspases and to decrease the levels of TNF-α and sphingosine, as well as the number of apoptotic myonuclei. Staurosporine was used in in vitro experiments to induce apoptosis in skeletal muscle cells in culture. Whenl-carnitine was applied to skeletal muscle cells, before staurosporine treatment, we observed a reduction in apoptosis. These findings show that l-carnitine can prevent apoptosis of skeletal muscles cells and has a role in the treatment of congestive heart failure-associated myopathy.


Sign in / Sign up

Export Citation Format

Share Document