Bacterial translocation attenuates the systemic hemodynamic improvement produced by terlipressin in patients with cirrhosis


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Bacterial Translocation Attenuates the Systemic Hemodynamic Improvement Produced by Terlipressin in Patients with Cirrhosis

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).

Figure 1.

Correlation between plasma endotoxin levels (in endotoxin units [EU]) and systemic vascular resistance changes (DSVR) after terlipressin infusion.

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

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.