Potential conflict of interest: Nothing to report.
Regarding “liver stiffness is influenced by a standardized meal in patients with chronic hepatitis C virus at different stages of fibrotic evolution”
Article first published online: 8 NOV 2013
© 2013 by the American Association for the Study of Liver Diseases
Volume 59, Issue 1, pages 350–351, January 2014
How to Cite
Berzigotti, A., Abraldes, J. G. and Bosch, J. (2014), Regarding “liver stiffness is influenced by a standardized meal in patients with chronic hepatitis C virus at different stages of fibrotic evolution”. Hepatology, 59: 350–351. doi: 10.1002/hep.26501
- Issue published online: 20 DEC 2013
- Article first published online: 8 NOV 2013
- Accepted manuscript online: 23 MAY 2013 03:33PM EST
- Manuscript Accepted: 25 MAR 2013
- Manuscript Received: 18 MAR 2013
To the Editor:
We congratulate Arena et al. for their interesting article regarding the confounding effect of a meal on the accuracy of liver stiffness (LS) measurements for the prediction of fibrosis stage in patients with chronic hepatitis C virus (HCV) hepatitis. In that study the most prominent postprandial increase in LS was observed in patients with cirrhosis. Hemodynamic parameters were not measured, but it is suggested that the postprandial changes in LS are likely consequent to the adaptation of the hepatic microcirculation to increased portal blood flow (PBF) and to the postprandial increase in portal pressure.
We recently published a study involving 19 patients with cirrhosis and portal hypertension in whom LS and hepatic hemodynamics were measured by Doppler-ultrasonography at baseline and 30 minutes after the ingestion of a standardized meal similar to that used by Arena et al. In a subgroup of 10 patients, the baseline and postprandial hepatic venous pressure gradient (HVPG) were also measured. In agreement to what was described by Arena et al., showing that most patients irrespective of the stage of fibrosis had a peak increase of LS 30 minutes after the meal, in our series postprandial hyperemia (confirmed by a marked increase in PBF, +33 ± 31%, P < 0.0001 versus baseline) was accompanied by a marked increase in LS (+27 ± 33%; P < 0.0001).
However, we observed that postprandial changes in LS did not correlate with the changes in PBF. Similarly, in patients in whom HVPG was measured, LS changes did not mirror the HVPG increase after the standardized meal. In contrast, postprandial changes in LS were directly correlated with changes in hepatic artery blood flow (r = 0.658; P = 0.002), so that in patients showing the expected postprandial decrease in hepatic artery blood flow (reflecting the “buffer response” to increased PBF after a meal) the LS increase was significantly attenuated as compared with patients lacking this adaptive mechanism (+12 ± 21% versus +62 ± 29%, P < 0.0001). Altogether, our results suggest that the postprandial increase in LS in cirrhosis cannot be explained by the increase in PBF and portal pressure, while it seems at least in part dependent on changes in the arterial component of hepatic blood flow. Since extensive formation of collaterals in advanced portal hypertension leads to increased dependence of the hepatic blood flow on its arterial component, and since hepatic artery buffer response is reduced in cirrhosis, a greater postprandial increase in LS should be anticipated in overt cirrhosis.
Annalisa Berzigotti, M.D.
Juan G. Abraldes, M.D.
Jaume Bosch, M.D.
Hepatic Hemodynamic Laboratory, Liver Unit, IDIBAPS and CIBERehd, Hospital Clinic, Barcelona, Spain