- Email: [email protected]
Chronic Myeloid Leukemia After Treatment with 131I for Thyroid Carcinoma
CASE REPORT
Chronic Myeloid Leukemia After Treatment 131 with I for Thyroid Carcinoma Kang-Ling Wang, Liang-Yu Lin1, Po-Min Chen2,3, Hong-Da Lin1,3* Division of Endocrinology and Metabolism, Armed Forces Tao-Yuan General Hospital, 1Division of Endocrinology and Metabolism, and 2Division of Medical Oncology, Department of Medicine, Taipei Veterans General Hospital, and 3National Yang-Ming University School of Medicine, Taipei, Taiwan, R.O.C.
A 27-year-old male developed Philadelphia chromosome-positive chronic myeloid leukemia (CML) 13 years after a first dose of radioiodine (131I) therapy for papillary thyroid carcinoma. He had received a cumulative 131I dose of 670 mCi, in 8 divided doses over 8 years, up to April 1998, for ablation of 131I avid tissues over the anterior neck region. The leukemogenic potential of radioactive iodine has been pointed out by many authors, but most reported cases have been acute leukemias. A literature review disclosed only 9 cases similar to ours. At present, there is no evidence to prove whether the development of CML after thyroid carcinoma represents a treatment-induced complication, a coincidence, or an increased susceptibility to secondary malignancies due to the malignant process itself. [J Chin Med Assoc 2005;68(5):230–233] Key Words: chronic myeloid leukemia, radioiodine therapy, thyroid cancer
131
Introduction 131
Radioiodine ( I) has been the treatment of choice for toxic nodular goiter, Graves’ disease and metastatic thyroid cancer for over half a century. We have used 131 I whole body scans and serum thyroglobulin measurements to follow patients with differentiated thyroid cancer to detect local recurrences or distant 131 metastases. If I ablation therapy for thyroid remnants is performed after total thyroidectomy, the sensitivity 131 and specificity of I whole body scans and serum thyroglobulin measurements will increase. Further, 131 I treatment for differentiated thyroid carcinoma with lung and bone metastases prolongs survival and improves quality of life. However, ionizing radiation is believed to be leukemogenic, and although uncommon, 131 leukemia after exposure to I therapy for thyroid 1–5 cancer has been reported. Many cases were of acute myeloid leukemia, usually occurring after cumulative dosages of more than 800 mCi, in patients older than 50 years, and with intervals of less than 12 months
2,5
between I therapy. Only 9 cases of chronic myeloid 131 leukemia (CML) after I therapy for thyroid cancer have been reported in the English medical literature. Here, we describe an additional case of CML, which 131 was noted 13 years after the first dose of I treatment for papillary thyroid cancer.
Case Report In November 1987, a 12-year-old male underwent total thyroidectomy and cervical lymph node resection for papillary carcinoma of the right thyroid lobe with lymph node metastasis. In July 1990, October 1991, and August 1992, he received 131I radiotherapy (doses of 30, 30, and 60 mCi, respectively) for avid uptake of 131 131 I over the anterior neck region on I whole body 131 scan. Lung metastasis was suspected on the post- I therapy scan in August 1992, but a repeat scan in March 1993 found complete resolution of the pulmonary lesions. Later, because of persistent
*Correspondence to: Dr. Hong-Da Lin, Division of Endocrinology and Metabolism, Department of Internal Medicine, Taipei Veterans General Hospital, 201, Section 2, Shih-Pai Road, Taipei 112, Taiwan, R.O.C. E-mail: [email protected] Received: July 7, 2004 Accepted: October 29, 2004
•
230
•
J Chin Med Assoc • May 2005 • Vol 68 • No 5 ©2005 Elsevier. All rights reserved.
CML after
131
I therapy for thyroid cancer
131
accumulation of I in the thyroid bed on subsequent 131 scans, he took I in doses of 100, 100, 100, and 150 mCi, respectively, in July 1993, September 1994, November 1995, and April 1998. After the last 150 mCi of ablation therapy, a follow-up scan still showed 131 increased I uptake in the thyroid bed and right 131 pulmonary hilum (Figure 1). However, no more I was given. The patient was maintained on suppressive, exogenous thyroid hormone therapy, with the level of thyroid stimulating hormone maintained at 0.1–0.4 131 +IU/mL. The total dosage of I was 670 mCi, administered in 8 doses from July 1990 to April 1998. 131 The time intervals between I doses ranged from 10– 13 months. In January 2003, when he was 27 years old, the patient presented to our oncology ward with a 2-month history of general weakness, skin eruption, and night sweats. Priapism had occurred weeks earlier. The patient was first treated at Da-Lin Tzu-Chi Hospital, where laboratory examination revealed a white blood cell count of 56,920/mm3, with 32% neutrophils, 13% bands, 11% monocytes, 10% lymphocytes, 9% basophils, 8% metamyelocytes, 5% promyelocytes, 3% blast cells, 2% myelocytes, and 2% eosinophils. Hemoglobin was 10 g/dL and platelet 3 count was 826,000/mm . Leukocyte alkaline phosphatase score was 0, and lactate dehydrogenase level was 364 U/L. Bone marrow aspiration and biopsy showed marked hypercellularity. The Philadelphia (Ph) chromosome was present, and repeated bone marrow examination and chromosome analysis in our oncology ward confirmed the diagnosis of Ph-positive CML (Figure 2). The patient had no family history of leukemia or thyroid disease, and he had not received external radiotherapy in the past. He was treated with hydroxyurea and prepared for allogeneic stem cell transplantation from his human leukocyte antigen (HLA)-identical sibling.
Discussion 131
Leukemia as a complication of I therapy is rare, but there is still concern about the possible carcinogenic effect of 131I. For example, in 1963, Haynie and 6 Beierwaltes reported transient, dose-dependent, 131 hematopoietic changes in patients receiving I for 7 thyroid cancer, and in 1986, Van Nostrand et al 131 found transient bone marrow suppression in post- I therapy patients; some of these patients still had reduced baseline blood counts 1 year after 131I therapy. The development of leukemia in patients treated
J Chin Med Assoc • May 2005 • Vol 68 • No 5
131
Figure 1. I whole body scan (9 October 1988) showing persistent remnants in the thyroid bed and possible right hilar lymph node metastasis. In the lower figure, markers are superimposed on the scan. SN = sternal notch; XP = xyphoid process; ±A= remnant thyroid tissue; A = possible right hilar lymph node metastasis.
Figure 2. Karyotype of bone marrow cells showing the translocation t(9;22)(q34;q11.2).
for thyrotoxicosis or thyroid carcinoma has also been reported. Pochin, 1 in reviewing 60,000 cases of thyrotoxicosis treated with 131I, found 17 cases of leukemia, of which 13 were acute, 1 was subacute, and 3 were chronic monocytic. The same author described 4 cases of acute leukemia in 175 patients treated with 131 I for thyroid cancer, thus giving a leukemia incidence of 2.3%, compared with an expected incidence of 0.4% in the general population.2 Saenger et al3 reported a mildly increased risk of leukemia in hyperthyroid patients treated with radioiodine (n = 22,000) versus surgery (n = 14,000) (p < 0.05); these authors also suggested an association between hyperthyroidism
231
K.L. Wang, et al
and leukemia, but of unknown mechanism. Indeed, the observed mortality from leukemia was 50% greater in hyperthyroid patients than in the US population as a whole.3 Among the reported cases of leukemia as a 131 complication of I therapy, CML has been documented much less frequently than acute leukemia. Apart from the present case, only 9 other cases of CML after 131I therapy for carcinoma of the thyroid have been reported (Table 1).4,8–14 Most CML patients have a unique genetic translocation between chromosomes 9 and 22 in myeloid cells: the abl cellular oncogene is transferred from chromosome 9 to the bcr gene of 131 chromosome 22. Ionizing radiation, including I, is known to be markedly effective in producing chromosome translocations, thus providing a probable 131 mechanism for the development of leukemia after I treatment. In the abovementioned 10 cases of CML, 2 patients had received high-voltage radiotherapy, which could have been an important factor in the development of secondary leukemia. The mean total dosage of 131I administered to the 10 CML patients was 329.6 mCi (range, 30–850 mCi), the age range was 27–76 years, 131 and the latent period between I exposure and the detection of CML ranged from 10 months to 13 years. Among the 10 cases, our patient was the youngest and had the longest latent period. Six patients were diagnosed 4–7 years after their first radiation exposure; thus, the median latency period seemed shorter than that of 11 years (range, 2–25 years) in a group of Japanese atomic 15 bomb survivors who developed CML. Japanese atomic bomb survivors have an increased estimated risk of leukemia. Nonetheless, it is unclear whether radiation exposure over time results in a lower leukemia risk than acute exposure to the same total
15
dosage of radiation. The Chernobyl accident led to the release of a considerable amount of various iodine radioisotopes, including 131I, into the atmosphere, and an increased incidence of thyroid cancer has been observed in children living in the heavily contaminated areas; so far, however, the incidence of other malignancies, including leukemia, does not seem to have 16 changed markedly. In 2 retrospective studies, Brincker et al4 and Edmonds and Smith5 found a significant increase in 131 the incidence of leukemia after I therapy in 194 and 248 patients, respectively, with thyroid cancer. However, 3 large cohort studies in recent years are reassuring in that no instances of CML were observed:17–19 a Swedish study in 1,955 2-year survivors who were followed-up for a mean of 17 years, and of 131 whom 834 were treated with I, detected only an increased risk of chronic lymphocytic leukemia, a malignancy that has not so far been associated with 17 radiation; an Italian study in 941 3-year survivors who were followed-up for a mean of 8 years, and of whom 730 were treated with 131I, found no cases of 18 leukemia; and a French study in 1,771 2-year survivors with thyroid cancer who were followed-up for a mean of 10 years, and of whom 1,491 were 131 19 treated with I, reported no secondary leukemias. These inconsistent results may stem from the different dosage ranges and follow-up periods employed in the various trials. In conclusion, only a small proportion of patients with thyroid cancer treated with radioiodine have developed leukemia, and it is not absolutely certain that leukemia was caused directly by 131I. However, long-term follow-up in 131I-treated patients with thyroid cancer should be emphasized, and leukocytosis in such patients should raise the suspicion of CML.
Table 1. Review of patients who developed chronic myeloid leukemia after Authors Ozarda et al (1961) 8 Brincker et al (1973)4 Bundi et al (1977) 9 Torng et al (1984) 10 Walgraeve et al (1991) 11 Advani & Hege (1992)12 Shimon et al (1995) 13 Alfiar et al (1997)14 Wang et al (present case)
232
Age (yr)/Gender 75/F 76/F 55/M 37/M 43/M Middle-aged/F 35/M 51/M 57/F 27/M
131
I dose (mCi) 347 600 850 100 30 103 56 130 410 670
131
I treatment for thyroid cancer Time interval from first 131I dose 4.7 10 11 65 5 7 4 10 6 13
yr mo yr mo yr yr yr yr yr yr
External radiation – – + – – – – – + –
J Chin Med Assoc • May 2005 • Vol 68 • No 5
CML after
131
I therapy for thyroid cancer
References 1. Pochin EE. Leukaemia following radioiodine treatment of thyrotoxicosis. Br Med J 1960;2:1545–50. 2. Pochin EE. Prospects from the treatment of thyroid carcinoma with radioiodine. Clin Radiol 1967;18:113–5. 3. Saenger EL, Thoma GE, Tompkins EA. Incidence of leukemia following treatment of hyperthyroidism. Preliminary report of the Cooperative Thyrotoxicosis Therapy Follow-Up Study. JAMA 1968;205:855–62. 4. Brincker H, Hansen HS, Anderson AP. Induction of leukaemia by 131-I treatment of thyroid carcinoma. Br J Cancer 1973; 28:232–7. 5. Edmonds CJ, Smith T. The long-term hazards of treatment of thyroid cancer with radioiodine. Br J Radiol 1986;59:45–51. 6. Haynie TP, Beierwaltes WH. Hematologic changes observed following 131I therapy for thyroid carcinoma. J Nucl Med 1963; 4:85–91. 7. Van Nostrand D, Neutze J, Atkins F. Side effects of “rational dose” iodine-131 therapy for metastatic well-differentiated thyroid carcinoma. J Nucl Med 1986;27:1519–27. 8. Ozarda A, Ergin U, Bender MA. Chronic myelogenous leukemia following I-131 therapy for metastatic thyroid carcinoma. Report of a case and some considerations on the etiologic factors. Am J Roentgenol Radium Ther Nucl Med 1961;85: 914–8. 9. Bundi RS, Scott JS, Halnan KE. Chronic myeloid leukaemia following radioiodine therapy for carcinoma thyroid. Br J Radiol 1977;50:61–4. 10. Torng JK, Chen YC, Liu CH, Chen FU. A case of chronic 131 myelogenous leukemia following I therapy for metastatic thyroid carcinoma. J Formos Med Assoc 1984;83:730–5. 11. Walgraeve D, Verhoef G, Stul M, Cassiman JJ, Mecucci C, Van
J Chin Med Assoc • May 2005 • Vol 68 • No 5
12.
13.
14.
15. 16.
17.
18.
19.
den Berghe H, Boogaerts M. Chronic myelogenous leukemia after treatment with 131I for thyroid carcinoma. Report of a case and review of the literature. Cancer Genet Cytogenet 1991; 55:217–24. Advani SH, Hege UP. Leukemia after 131I treatment of thyroid cancer — comments on the article ‘Second cancer following chemotherapy and radiotherapy — and epidemiological perspective’ by J. Kaldor. Acta Oncol 1992; 31:65. Shimon I, Kneller A, Olchovsky D. Chronic myeloid leukaemia following 131I treatment for thyroid carcinoma: a report of two cases and review of the literature. Clin Endocrinol 1995;43: 651–4. Alfiar F, Amato D, Lipton JH. Chronic myeloid leukemia in a woman with papillary carcinoma of the thyroid treated with radioactive iodine. Leuk Lymphoma 1997;27:365–7. Molony WC. Radiogenic leukemia revisited. Blood 1987;70: 905–8. Ivanov VK, Tsyb AF, Nilova EV, Efendiev VF, Gorsky AI, Pitkevich VA, Leshakov SY, et al. Cancer risks in the Kaluga oblast of the Russian Federation 10 years after the Chernobyl accident. Radiat Environ Biophys 1997;36:161–7. Hall P, Boice JD, Berg G, Bjelkengren G, Ericsson UB, Hallquist A, Lidberg M, et al. Leukaemia incidence after iodine-131 exposure. Lancet 1992;340:1–4. Dortorini ME, Lomuscio G, Mazzucchelli L, Vignati A, Colombo L. Assessment of female fertility and carcinogenesis after iodine-131 therapy for differentiated thyroid carcinoma. J Nucl Med 1995;36:21–7. Vatharie F, Schlumberger M, Delisle MJ, Francese C, Challenton C, Genardiere E, Meunier F, et al. Leukaemias and cancers following iodine-131 administration for thyroid cancer. Br J Cancer 1997;75:734–9.
233
Chronic Myeloid Leukemia After Treatment 131 with I for Thyroid Carcinoma Kang-Ling Wang, Liang-Yu Lin1, Po-Min Chen2,3, Hong-Da Lin1,3* Division of Endocrinology and Metabolism, Armed Forces Tao-Yuan General Hospital, 1Division of Endocrinology and Metabolism, and 2Division of Medical Oncology, Department of Medicine, Taipei Veterans General Hospital, and 3National Yang-Ming University School of Medicine, Taipei, Taiwan, R.O.C.
A 27-year-old male developed Philadelphia chromosome-positive chronic myeloid leukemia (CML) 13 years after a first dose of radioiodine (131I) therapy for papillary thyroid carcinoma. He had received a cumulative 131I dose of 670 mCi, in 8 divided doses over 8 years, up to April 1998, for ablation of 131I avid tissues over the anterior neck region. The leukemogenic potential of radioactive iodine has been pointed out by many authors, but most reported cases have been acute leukemias. A literature review disclosed only 9 cases similar to ours. At present, there is no evidence to prove whether the development of CML after thyroid carcinoma represents a treatment-induced complication, a coincidence, or an increased susceptibility to secondary malignancies due to the malignant process itself. [J Chin Med Assoc 2005;68(5):230–233] Key Words: chronic myeloid leukemia, radioiodine therapy, thyroid cancer
131
Introduction 131
Radioiodine ( I) has been the treatment of choice for toxic nodular goiter, Graves’ disease and metastatic thyroid cancer for over half a century. We have used 131 I whole body scans and serum thyroglobulin measurements to follow patients with differentiated thyroid cancer to detect local recurrences or distant 131 metastases. If I ablation therapy for thyroid remnants is performed after total thyroidectomy, the sensitivity 131 and specificity of I whole body scans and serum thyroglobulin measurements will increase. Further, 131 I treatment for differentiated thyroid carcinoma with lung and bone metastases prolongs survival and improves quality of life. However, ionizing radiation is believed to be leukemogenic, and although uncommon, 131 leukemia after exposure to I therapy for thyroid 1–5 cancer has been reported. Many cases were of acute myeloid leukemia, usually occurring after cumulative dosages of more than 800 mCi, in patients older than 50 years, and with intervals of less than 12 months
2,5
between I therapy. Only 9 cases of chronic myeloid 131 leukemia (CML) after I therapy for thyroid cancer have been reported in the English medical literature. Here, we describe an additional case of CML, which 131 was noted 13 years after the first dose of I treatment for papillary thyroid cancer.
Case Report In November 1987, a 12-year-old male underwent total thyroidectomy and cervical lymph node resection for papillary carcinoma of the right thyroid lobe with lymph node metastasis. In July 1990, October 1991, and August 1992, he received 131I radiotherapy (doses of 30, 30, and 60 mCi, respectively) for avid uptake of 131 131 I over the anterior neck region on I whole body 131 scan. Lung metastasis was suspected on the post- I therapy scan in August 1992, but a repeat scan in March 1993 found complete resolution of the pulmonary lesions. Later, because of persistent
*Correspondence to: Dr. Hong-Da Lin, Division of Endocrinology and Metabolism, Department of Internal Medicine, Taipei Veterans General Hospital, 201, Section 2, Shih-Pai Road, Taipei 112, Taiwan, R.O.C. E-mail: [email protected] Received: July 7, 2004 Accepted: October 29, 2004
•
230
•
J Chin Med Assoc • May 2005 • Vol 68 • No 5 ©2005 Elsevier. All rights reserved.
CML after
131
I therapy for thyroid cancer
131
accumulation of I in the thyroid bed on subsequent 131 scans, he took I in doses of 100, 100, 100, and 150 mCi, respectively, in July 1993, September 1994, November 1995, and April 1998. After the last 150 mCi of ablation therapy, a follow-up scan still showed 131 increased I uptake in the thyroid bed and right 131 pulmonary hilum (Figure 1). However, no more I was given. The patient was maintained on suppressive, exogenous thyroid hormone therapy, with the level of thyroid stimulating hormone maintained at 0.1–0.4 131 +IU/mL. The total dosage of I was 670 mCi, administered in 8 doses from July 1990 to April 1998. 131 The time intervals between I doses ranged from 10– 13 months. In January 2003, when he was 27 years old, the patient presented to our oncology ward with a 2-month history of general weakness, skin eruption, and night sweats. Priapism had occurred weeks earlier. The patient was first treated at Da-Lin Tzu-Chi Hospital, where laboratory examination revealed a white blood cell count of 56,920/mm3, with 32% neutrophils, 13% bands, 11% monocytes, 10% lymphocytes, 9% basophils, 8% metamyelocytes, 5% promyelocytes, 3% blast cells, 2% myelocytes, and 2% eosinophils. Hemoglobin was 10 g/dL and platelet 3 count was 826,000/mm . Leukocyte alkaline phosphatase score was 0, and lactate dehydrogenase level was 364 U/L. Bone marrow aspiration and biopsy showed marked hypercellularity. The Philadelphia (Ph) chromosome was present, and repeated bone marrow examination and chromosome analysis in our oncology ward confirmed the diagnosis of Ph-positive CML (Figure 2). The patient had no family history of leukemia or thyroid disease, and he had not received external radiotherapy in the past. He was treated with hydroxyurea and prepared for allogeneic stem cell transplantation from his human leukocyte antigen (HLA)-identical sibling.
Discussion 131
Leukemia as a complication of I therapy is rare, but there is still concern about the possible carcinogenic effect of 131I. For example, in 1963, Haynie and 6 Beierwaltes reported transient, dose-dependent, 131 hematopoietic changes in patients receiving I for 7 thyroid cancer, and in 1986, Van Nostrand et al 131 found transient bone marrow suppression in post- I therapy patients; some of these patients still had reduced baseline blood counts 1 year after 131I therapy. The development of leukemia in patients treated
J Chin Med Assoc • May 2005 • Vol 68 • No 5
131
Figure 1. I whole body scan (9 October 1988) showing persistent remnants in the thyroid bed and possible right hilar lymph node metastasis. In the lower figure, markers are superimposed on the scan. SN = sternal notch; XP = xyphoid process; ±A= remnant thyroid tissue; A = possible right hilar lymph node metastasis.
Figure 2. Karyotype of bone marrow cells showing the translocation t(9;22)(q34;q11.2).
for thyrotoxicosis or thyroid carcinoma has also been reported. Pochin, 1 in reviewing 60,000 cases of thyrotoxicosis treated with 131I, found 17 cases of leukemia, of which 13 were acute, 1 was subacute, and 3 were chronic monocytic. The same author described 4 cases of acute leukemia in 175 patients treated with 131 I for thyroid cancer, thus giving a leukemia incidence of 2.3%, compared with an expected incidence of 0.4% in the general population.2 Saenger et al3 reported a mildly increased risk of leukemia in hyperthyroid patients treated with radioiodine (n = 22,000) versus surgery (n = 14,000) (p < 0.05); these authors also suggested an association between hyperthyroidism
231
K.L. Wang, et al
and leukemia, but of unknown mechanism. Indeed, the observed mortality from leukemia was 50% greater in hyperthyroid patients than in the US population as a whole.3 Among the reported cases of leukemia as a 131 complication of I therapy, CML has been documented much less frequently than acute leukemia. Apart from the present case, only 9 other cases of CML after 131I therapy for carcinoma of the thyroid have been reported (Table 1).4,8–14 Most CML patients have a unique genetic translocation between chromosomes 9 and 22 in myeloid cells: the abl cellular oncogene is transferred from chromosome 9 to the bcr gene of 131 chromosome 22. Ionizing radiation, including I, is known to be markedly effective in producing chromosome translocations, thus providing a probable 131 mechanism for the development of leukemia after I treatment. In the abovementioned 10 cases of CML, 2 patients had received high-voltage radiotherapy, which could have been an important factor in the development of secondary leukemia. The mean total dosage of 131I administered to the 10 CML patients was 329.6 mCi (range, 30–850 mCi), the age range was 27–76 years, 131 and the latent period between I exposure and the detection of CML ranged from 10 months to 13 years. Among the 10 cases, our patient was the youngest and had the longest latent period. Six patients were diagnosed 4–7 years after their first radiation exposure; thus, the median latency period seemed shorter than that of 11 years (range, 2–25 years) in a group of Japanese atomic 15 bomb survivors who developed CML. Japanese atomic bomb survivors have an increased estimated risk of leukemia. Nonetheless, it is unclear whether radiation exposure over time results in a lower leukemia risk than acute exposure to the same total
15
dosage of radiation. The Chernobyl accident led to the release of a considerable amount of various iodine radioisotopes, including 131I, into the atmosphere, and an increased incidence of thyroid cancer has been observed in children living in the heavily contaminated areas; so far, however, the incidence of other malignancies, including leukemia, does not seem to have 16 changed markedly. In 2 retrospective studies, Brincker et al4 and Edmonds and Smith5 found a significant increase in 131 the incidence of leukemia after I therapy in 194 and 248 patients, respectively, with thyroid cancer. However, 3 large cohort studies in recent years are reassuring in that no instances of CML were observed:17–19 a Swedish study in 1,955 2-year survivors who were followed-up for a mean of 17 years, and of 131 whom 834 were treated with I, detected only an increased risk of chronic lymphocytic leukemia, a malignancy that has not so far been associated with 17 radiation; an Italian study in 941 3-year survivors who were followed-up for a mean of 8 years, and of whom 730 were treated with 131I, found no cases of 18 leukemia; and a French study in 1,771 2-year survivors with thyroid cancer who were followed-up for a mean of 10 years, and of whom 1,491 were 131 19 treated with I, reported no secondary leukemias. These inconsistent results may stem from the different dosage ranges and follow-up periods employed in the various trials. In conclusion, only a small proportion of patients with thyroid cancer treated with radioiodine have developed leukemia, and it is not absolutely certain that leukemia was caused directly by 131I. However, long-term follow-up in 131I-treated patients with thyroid cancer should be emphasized, and leukocytosis in such patients should raise the suspicion of CML.
Table 1. Review of patients who developed chronic myeloid leukemia after Authors Ozarda et al (1961) 8 Brincker et al (1973)4 Bundi et al (1977) 9 Torng et al (1984) 10 Walgraeve et al (1991) 11 Advani & Hege (1992)12 Shimon et al (1995) 13 Alfiar et al (1997)14 Wang et al (present case)
232
Age (yr)/Gender 75/F 76/F 55/M 37/M 43/M Middle-aged/F 35/M 51/M 57/F 27/M
131
I dose (mCi) 347 600 850 100 30 103 56 130 410 670
131
I treatment for thyroid cancer Time interval from first 131I dose 4.7 10 11 65 5 7 4 10 6 13
yr mo yr mo yr yr yr yr yr yr
External radiation – – + – – – – – + –
J Chin Med Assoc • May 2005 • Vol 68 • No 5
CML after
131
I therapy for thyroid cancer
References 1. Pochin EE. Leukaemia following radioiodine treatment of thyrotoxicosis. Br Med J 1960;2:1545–50. 2. Pochin EE. Prospects from the treatment of thyroid carcinoma with radioiodine. Clin Radiol 1967;18:113–5. 3. Saenger EL, Thoma GE, Tompkins EA. Incidence of leukemia following treatment of hyperthyroidism. Preliminary report of the Cooperative Thyrotoxicosis Therapy Follow-Up Study. JAMA 1968;205:855–62. 4. Brincker H, Hansen HS, Anderson AP. Induction of leukaemia by 131-I treatment of thyroid carcinoma. Br J Cancer 1973; 28:232–7. 5. Edmonds CJ, Smith T. The long-term hazards of treatment of thyroid cancer with radioiodine. Br J Radiol 1986;59:45–51. 6. Haynie TP, Beierwaltes WH. Hematologic changes observed following 131I therapy for thyroid carcinoma. J Nucl Med 1963; 4:85–91. 7. Van Nostrand D, Neutze J, Atkins F. Side effects of “rational dose” iodine-131 therapy for metastatic well-differentiated thyroid carcinoma. J Nucl Med 1986;27:1519–27. 8. Ozarda A, Ergin U, Bender MA. Chronic myelogenous leukemia following I-131 therapy for metastatic thyroid carcinoma. Report of a case and some considerations on the etiologic factors. Am J Roentgenol Radium Ther Nucl Med 1961;85: 914–8. 9. Bundi RS, Scott JS, Halnan KE. Chronic myeloid leukaemia following radioiodine therapy for carcinoma thyroid. Br J Radiol 1977;50:61–4. 10. Torng JK, Chen YC, Liu CH, Chen FU. A case of chronic 131 myelogenous leukemia following I therapy for metastatic thyroid carcinoma. J Formos Med Assoc 1984;83:730–5. 11. Walgraeve D, Verhoef G, Stul M, Cassiman JJ, Mecucci C, Van
J Chin Med Assoc • May 2005 • Vol 68 • No 5
12.
13.
14.
15. 16.
17.
18.
19.
den Berghe H, Boogaerts M. Chronic myelogenous leukemia after treatment with 131I for thyroid carcinoma. Report of a case and review of the literature. Cancer Genet Cytogenet 1991; 55:217–24. Advani SH, Hege UP. Leukemia after 131I treatment of thyroid cancer — comments on the article ‘Second cancer following chemotherapy and radiotherapy — and epidemiological perspective’ by J. Kaldor. Acta Oncol 1992; 31:65. Shimon I, Kneller A, Olchovsky D. Chronic myeloid leukaemia following 131I treatment for thyroid carcinoma: a report of two cases and review of the literature. Clin Endocrinol 1995;43: 651–4. Alfiar F, Amato D, Lipton JH. Chronic myeloid leukemia in a woman with papillary carcinoma of the thyroid treated with radioactive iodine. Leuk Lymphoma 1997;27:365–7. Molony WC. Radiogenic leukemia revisited. Blood 1987;70: 905–8. Ivanov VK, Tsyb AF, Nilova EV, Efendiev VF, Gorsky AI, Pitkevich VA, Leshakov SY, et al. Cancer risks in the Kaluga oblast of the Russian Federation 10 years after the Chernobyl accident. Radiat Environ Biophys 1997;36:161–7. Hall P, Boice JD, Berg G, Bjelkengren G, Ericsson UB, Hallquist A, Lidberg M, et al. Leukaemia incidence after iodine-131 exposure. Lancet 1992;340:1–4. Dortorini ME, Lomuscio G, Mazzucchelli L, Vignati A, Colombo L. Assessment of female fertility and carcinogenesis after iodine-131 therapy for differentiated thyroid carcinoma. J Nucl Med 1995;36:21–7. Vatharie F, Schlumberger M, Delisle MJ, Francese C, Challenton C, Genardiere E, Meunier F, et al. Leukaemias and cancers following iodine-131 administration for thyroid cancer. Br J Cancer 1997;75:734–9.
233