Lithium as a potential adjuvant to ¹³¹I therapy of metastatic, well differentiated thyroid carcinoma

As lithium inhibits the release of iodine from the thyroid but does not change iodine uptake, it may potentiate ¹³¹I therapy of thyroid cancer. The effects of lithium on the accumulation and retention of ¹³¹I in metastatic lesions and thyroid remnants were evaluated in 15 patients with differentiated thyroid carcinoma. Two ¹³¹I turnover studies were performed while the patients were hypothyroid. One was performed while the patient received lithium; the second served as a control study. From a series of γ- camera images, it was found that lithium increased ¹³¹I retention in 24 of 31 metastatic lesions and in 6 of 7 thyroid remnants. A comparison of ¹³¹I retention during lithium with that during the control period showed that the mean increase in the biological or retention half-life was 50% in tumors and 90% in remnants. This increase occurred in at least 1 lesion in each patient and was proportionally greater in lesions with poor ¹³¹I retention. When the control biological half life was less than 3 days, lithium prolonged the effective half-life, which combines both biological turnover and isotope decay, in responding metastases by more than 50%. More ¹³¹I also accumulated during lithium therapy, probably as a consequence of its effect on iodine release. The increase in the accumulated ¹³¹I and the lengthening of the effective half-life combined to increase the estimated ¹³¹I radiation dose in metastatic tumor by 2.29 ± 0.58 (mean ± SEM) times. These studies suggest that lithium may be a useful adjuvant for ¹³¹I therapy of thyroid cancer, augmenting both the accumulation and retention of ¹³¹I in lesions.