Becker D V, Sawin C T
Department of Radiology, New York Hospital-Cornell Medical Center, New York 10021, USA.
Semin Nucl Med. 1996 Jul;26(3):155-64. doi: 10.1016/s0001-2998(96)80020-1.
In 1936, Karl Compton, then president of the Massachusetts Institute of Technology (MIT) and the thyroid group of the Massachusetts General Hospital (MGH), undertook a joint study that led to the production of small amounts of short-lived radioiodine (iodine 128, half-life, 25 min). The original intent was to use it for diagnosis and treatment of thyroid disease, but in order to explore the underlying physiology, their first work was performed in rabbits and published in 1938. It clearly showed that the radioiodine was selectively and avidly taken up by the thyroid gland. It was immediately apparent to the MGH-MIT group and another team working at the Berkeley, CA cyclotron that longer-lasting iodine isotopes were needed, and soon both developed procedures for cyclotron-produced 130 (half-life, 12.5 hr) and 131I (half-life, 8 d). In 1939, the Berkeley group, using 131I, was the first to show that the normal human thyroid gland accumulated radioiodine. By 1941, the MGH-MIT team, using mainly 130I, was able to successfully treat a few patients with hyperthyroidism, and so achieved their original goal. The Berkeley group did the same a few months later, using mainly 131I. Both presented results at the same meeting of the American Society for Clinical Investigation in Atlantic City, NJ in the spring of 1942. This was in the midst of World War II and it was not easy to get much 130I or 131I, so experience was limited. Although effective, radioiodine treatment of hyperthyroidism had not been widely adopted by the end of the war in 1945, partly because radioiodine remained in short supply and partly because another medical therapy for hyperthyroidism, antithyroid drugs, had been invented. However, by 1946, fission-derived radioiodine became readily available as a by-product of the Manhattan project in Oak Ridge, TN; hundreds of patients were treated within a few years, both for hyperthyroidism and for thyroid cancer. A new treatment, based on the physiological application of a radioisotope of iodine, was then a reality.
1936年，时任麻省理工学院（MIT）院长以及麻省总医院（MGH）甲状腺研究团队负责人的卡尔·康普顿开展了一项联合研究，成功制备出少量短寿命放射性碘（碘128，半衰期为25分钟）。最初的目的是将其用于甲状腺疾病的诊断和治疗，但为了探究其潜在生理学机制，他们首先在兔子身上进行了研究，并于1938年发表了研究成果。该研究清楚地表明，放射性碘被甲状腺选择性且大量摄取。麻省总医院-麻省理工学院研究团队以及另一个在加利福尼亚州伯克利市回旋加速器实验室工作的团队很快就意识到，需要半衰期更长的碘同位素，不久后两个团队都开发出了利用回旋加速器制备碘130（半衰期为12.5小时）和碘131（半衰期为8天）的方法。1939年，伯克利团队使用碘131首次证明正常人体甲状腺会积累放射性碘。到1941年，麻省总医院-麻省理工学院团队主要使用碘130，成功治疗了几名甲状腺功能亢进患者，从而实现了他们最初的目标。几个月后伯克利团队也做到了这一点，他们主要使用碘131。双方都在1942年春天于新泽西州大西洋城举行的美国临床研究学会同一次会议上展示了研究成果。当时正值第二次世界大战期间，获取大量碘130或碘131并不容易，因此相关经验有限。尽管放射性碘治疗甲状腺功能亢进有效，但到1945年战争结束时，它仍未被广泛采用，部分原因是放射性碘供应短缺，部分原因是另一种治疗甲状腺功能亢进的药物——抗甲状腺药物已被发明。然而，到1946年，裂变产生的放射性碘作为田纳西州橡树岭曼哈顿计划的副产品变得容易获得；几年内就有数百名患者接受了治疗，治疗的疾病包括甲状腺功能亢进和甲状腺癌。基于碘放射性同位素生理应用的一种新疗法由此成为现实。
