PDF(Pubmed)
Abstract：
UNASSIGNED: Lithium inhibits iodine and thyroid hormone release from thyroid cells, possibly increasing radioiodine retention and anti-hyperthyroid efficacy when given adjunctively to radioiodine therapy (RAI) of Graves’ disease (GD). However, the literature contains limited dosimetric data regarding the influence of concomitant lithium in this setting.
UNASSIGNED: We retrospectively compared dosimetric variables in patients undergoing RAI with/without adjunctive lithium (n = 52 each). We assessed two low-dose, short-duration oral lithium carbonate regimens, 450 mg/d (n = 22) or 900 mg/d (n = 30), for a mean of 4.7 ± 1.4 d starting upon RAI administration. Patients underwent diagnostic testing to measure thyroidal radioiodine uptake (RAIU) 24 h ± 2 h after ingesting up to 5 MBq radioiodine, receiving individualized RAI activities 24 h later. Using ≥3 RAIU daily measurements starting 24 h post-RAI, researchers were able to determine the effective radioiodine half-life and absorbed dose to the thyroid; we also calculated the absorbed dose per administered activity concentration within that organ. Rates of GD cure, defined as reaching euthyroidism or hypothyroidism post-RAI, were evaluated in patients with ~6 months or longer post-RAI follow-up.
UNASSIGNED: The lithium dosage subgroups had similar dosimetric values and thus are considered together. Lithium patients and controls had similar average “diagnostic” RAIU (51.1% ± 15.7% vs. 50.6% ± 13.8%, p = 0.820), but the former had significantly higher RAIU post-RAI (56.3% ± 13.5% vs. 49.1% ± 13.5%, p = 0.002), reflecting significantly greater change in the former (+16.2% ± 30.4% vs. -1.8% ± 16.1%, p = 0.001). Radioiodine effective half-life was non-significantly longer in lithium patients (5.43 ± 1.50 d vs. 5.08 ± 1.16 d, p = 0.192). The mean RAI administered activity was 27% less in lithium patients (677 ± 294 MBq vs. 930 ± 433 MBq, p = 0.001), but GD cure rates were similar (83% [39/47] vs. 82% [33/40], p = 0.954), possibly due to the significantly higher thyroid dose in the lithium patients, especially in thyroid gland with a volume ≤ 20 mL (1.04 ± 0.44 Gy/MBq vs. 0.76 ± 0.30 Gy/MBq, p = 0.020). Day 3 serum lithium concentrations were low (450 mg/d: 0.26 ± 0.12 mmol/L, 900 mg/d: 0.50 ± 0.18 mmol/L); no lithium toxicity was noted.
UNASSIGNED: Lithium augmentation may increase the RAIU and thyroid absorbed dose, permitting potentially decreased RAI activities without sacrificing efficacy. Our observations should be confirmed in a prospective, randomized trial.
UNASSIGNED: We retrospectively compared dosimetric variables in patients undergoing RAI with/without adjunctive lithium (n = 52 each). We assessed two low-dose, short-duration oral lithium carbonate regimens, 450 mg/d (n = 22) or 900 mg/d (n = 30), for a mean of 4.7 ± 1.4 d starting upon RAI administration. Patients underwent diagnostic testing to measure thyroidal radioiodine uptake (RAIU) 24 h ± 2 h after ingesting up to 5 MBq radioiodine, receiving individualized RAI activities 24 h later. Using ≥3 RAIU daily measurements starting 24 h post-RAI, researchers were able to determine the effective radioiodine half-life and absorbed dose to the thyroid; we also calculated the absorbed dose per administered activity concentration within that organ. Rates of GD cure, defined as reaching euthyroidism or hypothyroidism post-RAI, were evaluated in patients with ~6 months or longer post-RAI follow-up.
UNASSIGNED: The lithium dosage subgroups had similar dosimetric values and thus are considered together. Lithium patients and controls had similar average “diagnostic” RAIU (51.1% ± 15.7% vs. 50.6% ± 13.8%, p = 0.820), but the former had significantly higher RAIU post-RAI (56.3% ± 13.5% vs. 49.1% ± 13.5%, p = 0.002), reflecting significantly greater change in the former (+16.2% ± 30.4% vs. -1.8% ± 16.1%, p = 0.001). Radioiodine effective half-life was non-significantly longer in lithium patients (5.43 ± 1.50 d vs. 5.08 ± 1.16 d, p = 0.192). The mean RAI administered activity was 27% less in lithium patients (677 ± 294 MBq vs. 930 ± 433 MBq, p = 0.001), but GD cure rates were similar (83% [39/47] vs. 82% [33/40], p = 0.954), possibly due to the significantly higher thyroid dose in the lithium patients, especially in thyroid gland with a volume ≤ 20 mL (1.04 ± 0.44 Gy/MBq vs. 0.76 ± 0.30 Gy/MBq, p = 0.020). Day 3 serum lithium concentrations were low (450 mg/d: 0.26 ± 0.12 mmol/L, 900 mg/d: 0.50 ± 0.18 mmol/L); no lithium toxicity was noted.
UNASSIGNED: Lithium augmentation may increase the RAIU and thyroid absorbed dose, permitting potentially decreased RAI activities without sacrificing efficacy. Our observations should be confirmed in a prospective, randomized trial.
摘要：
■锂抑制碘和甲状腺激素从甲状腺细胞释放，当在Graves病（GD）的放射性碘治疗（RAI）的辅助治疗时，可能会增加放射性碘的保留和抗甲状腺功能亢进的功效。然而,文献中关于伴随锂在这种情况下的影响的剂量数据有限。
■我们回顾性比较了有/没有辅助锂的RAI患者的剂量学变量（每个n=52）。我们评估了两种低剂量，短期口服碳酸锂方案，450mg/d（n=22）或900mg/d（n=30），从RAI给药后开始，平均4.7±1.4d。患者在摄入高达5MBq的放射性碘后24小时±2小时接受诊断测试以测量甲状腺放射性碘摄取（RAIU），24小时后接受个性化RAI活动。使用≥3RAIU每日测量值，从RAI后24小时开始，研究人员能够确定甲状腺的有效放射性碘半衰期和吸收剂量;我们还计算了该器官内每个给药活动浓度的吸收剂量.GD固化率,定义为RAI后达到甲状腺功能正常或甲状腺功能减退，在RAI后随访6个月或更长时间的患者中进行评估。
■锂剂量亚组具有相似的剂量测定值,因此一起考虑。锂患者和对照组的平均“诊断”RAIU相似（51.1％±15.7％与50.6%±13.8%,p=0.820)，但前者在RAI后的RAIU明显更高(56.3%±13.5%vs.49.1%±13.5%,p=0.002),反映前者的变化明显更大(+16.2%±30.4%与-1.8%±16.1%,p=0.001)。锂患者的放射性碘有效半衰期无明显延长（5.43±1.50dvs.5.08±1.16d，p=0.192）。锂患者的平均RAI给药活性降低了27％（677±294MBq与930±433MBq，p=0.001),但GD治愈率相似(83%[39/47]与82%[33/40]，p=0.954),可能是由于锂患者的甲状腺剂量明显较高，尤其是体积≤20mL的甲状腺（1.04±0.44Gy/MBq与0.76±0.30Gy/MBq,p=0.020)。第3天血清锂浓度较低（450mg/d：0.26±0.12mmol/L，900mg/d：0.50±0.18mmol/L）；未发现锂毒性。
■锂增强可能会增加RAIU和甲状腺吸收剂量，允许潜在降低RAI活性而不牺牲功效。我们的观察结果应该得到证实，随机试验。
■我们回顾性比较了有/没有辅助锂的RAI患者的剂量学变量（每个n=52）。我们评估了两种低剂量，短期口服碳酸锂方案，450mg/d（n=22）或900mg/d（n=30），从RAI给药后开始，平均4.7±1.4d。患者在摄入高达5MBq的放射性碘后24小时±2小时接受诊断测试以测量甲状腺放射性碘摄取（RAIU），24小时后接受个性化RAI活动。使用≥3RAIU每日测量值，从RAI后24小时开始，研究人员能够确定甲状腺的有效放射性碘半衰期和吸收剂量;我们还计算了该器官内每个给药活动浓度的吸收剂量.GD固化率,定义为RAI后达到甲状腺功能正常或甲状腺功能减退，在RAI后随访6个月或更长时间的患者中进行评估。
■锂剂量亚组具有相似的剂量测定值,因此一起考虑。锂患者和对照组的平均“诊断”RAIU相似（51.1％±15.7％与50.6%±13.8%,p=0.820)，但前者在RAI后的RAIU明显更高(56.3%±13.5%vs.49.1%±13.5%,p=0.002),反映前者的变化明显更大(+16.2%±30.4%与-1.8%±16.1%,p=0.001)。锂患者的放射性碘有效半衰期无明显延长（5.43±1.50dvs.5.08±1.16d，p=0.192）。锂患者的平均RAI给药活性降低了27％（677±294MBq与930±433MBq，p=0.001),但GD治愈率相似(83%[39/47]与82%[33/40]，p=0.954),可能是由于锂患者的甲状腺剂量明显较高，尤其是体积≤20mL的甲状腺（1.04±0.44Gy/MBq与0.76±0.30Gy/MBq,p=0.020)。第3天血清锂浓度较低（450mg/d：0.26±0.12mmol/L，900mg/d：0.50±0.18mmol/L）；未发现锂毒性。
■锂增强可能会增加RAIU和甲状腺吸收剂量，允许潜在降低RAI活性而不牺牲功效。我们的观察结果应该得到证实，随机试验。
