Monsieurs M A, Thierens H M, van de Wiele C V, Vral A M, Meirlaen I A, de Winter H A, de Sadeleer C J, de Ridder L I, Kaufman J M, Dierckx R A
Department of Biomedical Physics and Radiation Protection, University of Gent, Belgium.
Nucl Med Commun. 1999 Oct;20(10):911-7. doi: 10.1097/00006231-199910000-00008.
A multicentre study was undertaken to assess the cytogenetic damage to peripheral blood lymphocytes in 31 patients treated with 131I for thyrotoxicosis using the cytokinesis-blocked micronucleus assay. The results were compared to those for eight thyroid carcinoma patients using the same method. For each patient, blood samples were taken immediately before and 1 week after iodine administration. The first blood sample was divided into three fractions and each fraction was subsequently irradiated in vitro with 0, 0.5 and 1 Gy 60Co gamma rays, respectively. After blood culture for 70 h, cells were harvested, stained with Romanowsky-Giemsa and the micronuclei scored in 1000 binucleated cells. For both patient groups, a linear-quadratic dose-response curve was fitted through the data set of the first blood sample by a least squares analysis. The mean increase in micronuclei after 131I therapy (second blood sample) was fitted to this curve and the mean equivalent total body dose (ETBD) calculated. Surprisingly, in view of the large difference in administered activity between thyroid carcinoma patients and thyrotoxicosis patients, the increase in micronuclei after therapy (mean +/- S.D.: 32 +/- 30 and 32 +/- 23, respectively) and the equivalent total body dose (0.34 and 0.32 Gy, respectively) were not significantly different (P > 0.1). The small number of micronuclei induced by 131I therapy (32 +/- 29), compared with external beam radiotherapy for Hodgkin's disease (640 +/- 381) or cervix carcinoma (298 +/- 76) [1], gave a cancer mortality estimate of less than 1%. This also explains why late detrimental effects in patients after 131I treatment have not been reported in the literature.
开展了一项多中心研究，采用胞质分裂阻滞微核试验评估31例因甲状腺毒症接受¹³¹I治疗的患者外周血淋巴细胞的细胞遗传学损伤。将结果与8例采用相同方法的甲状腺癌患者的结果进行比较。对于每位患者，在碘给药前和给药后1周立即采集血样。第一份血样分为三份，每份随后分别在体外接受0、0.5和1 Gy的⁶⁰Coγ射线照射。血培养70小时后，收获细胞，用罗曼诺夫斯基-吉姆萨染色，并在1000个双核细胞中对微核进行计数。对于两组患者，通过最小二乘法分析将第一份血样的数据拟合为线性二次剂量反应曲线。将¹³¹I治疗后（第二份血样）微核的平均增加量拟合到该曲线上，并计算平均等效全身剂量（ETBD）。令人惊讶的是，鉴于甲状腺癌患者和甲状腺毒症患者给药活度的巨大差异，治疗后微核的增加量（平均值±标准差：分别为32±30和32±23）和等效全身剂量（分别为0.34和0.32 Gy）并无显著差异（P>0.1）。与霍奇金病（640±381）或宫颈癌（298±76）的外照射放疗相比，¹³¹I治疗诱导的微核数量较少（32±29）[1]，癌症死亡率估计低于1%。这也解释了为什么文献中未报道¹³¹I治疗后患者的晚期有害影响。
