LAUSR

allowing specific analysis of the interstages kinetic of FRL function in parallel with volume. This robust methodology allowed us to draw the clear conclusion that evaluating the FRL volume alone is not appropriate and that HBS should be systematically performed. Regarding the second point underlined by de Santibañes’ team, we indeed ‘‘confirm using HBS that the excluded liver segments . . . works as an auxiliary liver until its removal’’. . . knowing that the verb ‘‘confirm’’ (ie, ‘‘to give approval to’’) means that similar observations were indeed made before. On the contrary, rather than confirming this established phenomenon, we aimed to warn surgeons about the drop of total liver function and the delayed functional gain in the FRL, which was on average 2-fold lower than its volumetric gain. This message of caution was important to give to surgeons likely to perform ALPPS. This may indeed explain why ‘‘the one-week interval dogma has been penalized in several series with high complication rates and mortality, despite all patients were operated with a theoretically sufficient FRL,’’ as indicated by de Santibanes et al. Third, we did not contrast our results with those of Tanaka et al, as we felt that both the objectives and methodologies of each study deeply differed. First, Tanaka et al used 99mTc-galactosyl human serum albumin HBS, and not mebrofenin HBS. Second, the authors aimed to compare ALPPS 1 week after the stage 1 with classical 2-stage hepatectomy 3 weeks after the stage 1, whereas we focused on ALPPS before and after the stage 1. Third, HBS results for the FRL were once more expressed as a percentage of total liver function and the ratio of FRL hypertrophy calculated according to a formula different from ours. These different designs rendered the 2 studies not comparable in terms of volumetric versus functional changes. Nevertheless, it is interesting to note that the authors similarly concluded that the functional volume of the FRL 1 week after the ALPPS stage 1 tended to be smaller than that in the classical group 3 weeks after the stage 1. De Santibañes’ team reported that no patient with an FRL representing at least 30% of the total functioning liver by HBS before the stage 2 developed liver failure once the diseased hemi-liver was removed, regardless of the FRL kinetic growth rate. Nevertheless, such calculation of the FRL as a proportion of the total liver is questionable, regarding the drop of function in the total liver reported in our study: if the drop is marked, the FRL will easily reach the cutoff of 30%, which will be no more discriminatory. This may be especially true in patients with a low functional reserve, such as the deceased elderly in our series. Accordingly, after continuing their experience, de Santibanes et al recognized that 3 of 17 patients developed liver failure by ‘‘50– 50’’ criteria despite being above the 30% cut-off. Thus, it may be more relevant to consider the FRL function by itself (exactly as for the volume, when we first proposed to consider the FRL volume as a ratio to body weight, deliberately omitting the total liver volume). Overall, we fully agree with de Santibanes et al that HBS ‘‘should become part of standard patient care in ALPPS.’’