ECE2006 Poster Presentations Thyroid (174 abstracts)
1Biomedical-Surgery Science, Morphological-Biochemical Science and Pathology Departments, University of Verona, Verona, Italy; 2Regional Centre of Nuclear Medicine and Division of Health Physics, University of Pisa, Pisa, Italy.
The long-term risk of carcinogenic and genetic damage following the treatment with 131I for differentiated thyroid cancer (DTC) is quite low. The hypothyroid status (HS), at the time of 131I administration, decreases the renal clearance of 131I and increases the whole-body, blood and bone marrow irradiation, unlike the euthyroid status (ES). Chromosome aberrations (CA) in peripheral lymphocytes reflect blood cells exposure to irradiation. This study aimed at comparing CA following ablative 131I therapy in 20 patients with DTC:
Group A: 9 patients (8 f, 1 m), aged 2867 yr (median 48) treated after L-T4 withdrawal; 131I activity: 3.7 GBq×6 pt, 4.8 GBq×2, 5.5 GBq×1.
Group B: 11 patients (6 f, 5 m), aged 1975 yr (median 52) treated after rhTSH standard protocol on L-T4 (3.7 GBq×11 pt).
CA were scored in peripheral lymphocytes obtained before and on the 15th and 45th day after the treatment according to conventional cytogenetic. Lymphocytes were stained routinely (100 cells each time).
We observed unstable anomalies (dicentrics, chromosome breaks, cromatide breaks, premature centromeric divisions) and numeric anomalies (polyploidy, aneuploidy). No correlation was found between the observed frequency of CA and the dose to the bone marrow per unit of administered radioactivity. The percentage of total CA increased significantly after the treatment in both groups, but the net increase of CA and unstable anomalies on the 15th and 45th day after the treatment were not statistically significant between the two groups. The percentage of numeric anomalies, not statistically different before the treatment, became significantly lower on the 15th (P<0.005) and on the 45th (P<0.005) day after the treatment in group B.
Conclusions: This study shows that the dynamics of radiation-induced CA in vivo is influenced by the thyroid hormone status and the kinetic of 131I parameters.