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The half-life of 213Bi results in a low bone marrow dose in humans, allowing administration of high activities.
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The results correlated with haematological toxicity, making it a promising method for estimating bone marrow doses in 177Lu-DOTATATE treatment without the need for blood and urine sampling.
Using the corresponding bone marrow dose estimates given in Simmonds et al (1995), the possible variations in Po skeletal burden correspond to an equivalent spread in radon exposure of about 90 Bq m−3.
The contribution of the cross-dose to the red marrow dose was substantial in relation to the contribution of the self-dose (Table 1).
The amount of additional 131I-MIBG activity that could be safely added to 90Y-DOTATOC along with the required fractional reduction in 90Y activity would change modestly if different normal organ (kidney and marrow) dose limits were applied as depicted in Table 3.
mDOTA = 90Y-DOTATOC red marrow dose per megabecquerel.
Although 300 cGy for a marrow upper limit would be high for a single non-myeloablative treatment, in practice, this dose would be spread over two or three individual treatment cycles (every 8 to 10 weeks to allow for marrow recovery) leading to a marrow dose per cycle of a very reasonable 100 to 150 cGy.
Despite the uncertainties in the presented method, it showed a dose-response relationship between absorbed bone marrow dose and haematological toxicity according to Hb, WBC and PLT counts for both mean and total absorbed dose.
In essence, our methodology and concept boils down to this: By measuring these following variables for a given patient, mMIBG = 131I-MIBG red marrow dose per megabecquerel.
We summarize the studies that evaluate the PRRT efficacy in NETs in Table 3. Dose-limiting factors for PRRT are kidney and/or bone marrow dose [ 61].
Only sparse measurements of 226Ra are available, but derived red bone marrow doses for children in the two villages obtained from a simple radio-ecological model show the significance of the drinking water pathway.
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