Potential conflict of interest: Nothing to report.
Bacterial translocation attenuates the systemic hemodynamic improvement produced by terlipressin in patients with cirrhosis†
Article first published online: 25 JUL 2011
Copyright © 2011 American Association for the Study of Liver Diseases
Volume 54, Issue 2, pages 743–744, August 2011
How to Cite
Kalambokis, G. N., Mouzaki, A., Rodi, M., Pappas, K. and Tsianos, E. V. (2011), Bacterial translocation attenuates the systemic hemodynamic improvement produced by terlipressin in patients with cirrhosis. Hepatology, 54: 743–744. doi: 10.1002/hep.24424
- Issue published online: 25 JUL 2011
- Article first published online: 25 JUL 2011
- Accepted manuscript online: 12 MAY 2011 01:59PM EST
To the Editor:
We read with interest the article by Bellot et al., who found an association between bacterial translocation (BT) and systemic hemodynamic derangement in patients with cirrhosis.1 BT worsens splanchnic arterial vasodilation in cirrhosis by stimulating nitric oxide (NO) production in the splanchnic vasculature, either directly or through the cytokine cascade.2 Indeed, intestinal decontamination reduces BT2 and serum NO levels,3 and improves systemic hemodynamics3 in patients with cirrhosis. However, increased NO synthesis could also adversely affect systemic hemodynamics by decreasing mesenterial arterial reactivity to endogenous4 or exogenous vasoconstrictors, such as terlipressin.5
We present preliminary data on the impact of BT on systemic hemodynamic effects of terlipressin in 17 patients with decompensated cirrhosis (male, n = 13; mean age = 52 ± 3 years; Child-Pugh score = 10.1 ± 0.5). Plasma endotoxin levels were detected by the Limulus amebocyte lysate chromogenic endpoint assay (Hycult biotech, Uden, the Netherlands) at baseline. Mean arterial pressure, cardiac output by Doppler ultrasound, and systemic vascular resistance (SVR) as the ratio mean arterial pressure/cardiac output were evaluated at baseline and 30 minutes after bolus intravenous administration of terlipressin (1 mg). SVR increased significantly after terlipressin (1768 ± 101 versus 1404 ± 91 dyn/second/cm−5; P < 0.001). Endotoxin levels were correlated inversely and significantly with baseline SVR values (r = −0.587; P = 0.01) and SVR changes after terlipressin (Fig. 1).
Endotoxin is detectable in all patients6 whereas bacterial DNA is detectable in only 58% of patients with decompensated cirrhosis1 and was preferred as a marker of BT in our study. Furthermore, bacterial DNA was not correlated with systemic hemodynamics in the study by Bellot et al.1 The present results support the link between BT and systemic circulatory dysfunction in cirrhosis, suggesting that intestinal decontamination could enhance the hemodynamic effects of terlipressin and contribute to a decrease in rebleeding events in patients with variceal bleeding taking antibiotic prophylaxis.7
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- 2Gut microflora in the pathogenesis of the complications of cirrhosis. Best Pract Res Clin Gastroenterol 2004; 18: 353-372..
- 3Increased lipopolysaccharide binding protein in cirrhotic patients with marked immune and hemodynamic derangement. Hepatology 2003; 37: 208-217., , , , , , et al.
- 4Aortic hyporeactivity to norepinephrine induced by lipopolysaccharide in cirrhotic rats: beneficial effects of a non-steroidal anti-inflammatory drug coupled with a nitric oxide donor. J Gastroenterol Hepatol 2001; 16: 70-78., , , , , , et al.
- 5Effect of terlipressin on in vitro vascular hyporeactivity of portal hypertensive rats. J Hepatol 1996; 24: 739-746., .
- 6Is bacterial DNA a better marker of bacterial translocation than endotoxin in decompensated cirrhosis? Hepatology 2011; doi:10.1002/hep.24303, , , , .
- 7Antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding. Cochrane Database Syst Rev 2010;( 9): CD002907., , , , .
Georgios N. Kalambokis M.D.*, Athanasia Mouzaki M.D., Ph.D., Maria Rodi M.D., Konstantinos Pappas M.D., Epameinondas V. Tsianos M.D., Ph.D.*, * First Division of Internal Medicine and Hepato-Gastroenterology Unit, Ioannina, Greece, Department of Cardiology, Medical School of Ioannina, Ioannina, Greece, Division of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece.