Kratochwil and colleagues (1) demonstrate in their very elegant study that selective intraarterial (i.a.) application of 68Ga-DOTATOC into the feeding artery of liver metastases from neuroendocrine tumors leads to a significantly higher SUV compared with intravenous (i.v.) application. An advantage of their study is the absence of therapeutic interventions as a confounding factor. This is a limitation in other studies comparing different therapeutic approaches as it commonly restricts recruitment of suitably large, homogeneous patient groups.

However, we do not believe that these data can be extrapolated to suggest a higher tumor uptake or a greater therapeutic efficacy of 90Y- or 177Lu-DOTATOC following i.a. application.

Following our previously reported experience with i.a. application of 131I-MIBG (2), we have so far treated 5 patients with 90Y-DOTATOC intravenously, followed by i.a. treatment 6 months later. We could not observe a consistently higher tumor uptake following i.a. application. Intraarterial-to-intravenous uptake ratios varied widely in our patients, from 0.45 to 2.74.

We are aware that ours is a very small group of patients, but due to the markedly different receptor affinities of 68Ga-DOTATOC and 90Y-DOTATOC we do not expect a significantly greater tumor uptake following i.a. application of 90Y-DOTATOC.

Heppeler and colleagues (3) showed that SSR2 receptor affinity of 67Ga-DOTATOC was 4 to 5 times higher than that of 90Y- and 111In-DOTATOC, respectively. In their study, 67Ga-DOTATOC showed a significantly higher tumor and lower renal uptake than the other 2 compounds. These data lead us to conclude that, in contrast to 68Ga-DOTATOC, a significantly higher tumor uptake after i.a. application cannot be expected for 90Y-DOTATOC.

No potential conflicts of interest were disclosed.

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