|LETTER TO THE EDITOR
|Year : 2022 | Volume
| Issue : 3 | Page : 436-437
Chronic myeloid leukemia following radioiodine treatment for papillary carcinoma of thyroid
Gopila Gupta, Mukul Aggarwal, Richa Juneja, Tulika Seth
Department of Haematology, All India Institute of Medical Sciences, New Delhi, India
|Date of Submission||01-Sep-2020|
|Date of Decision||08-Oct-2020|
|Date of Acceptance||10-Feb-2021|
|Date of Web Publication||12-Oct-2022|
Department of Haematology, All India Institute of Medical Sciences, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gupta G, Aggarwal M, Juneja R, Seth T. Chronic myeloid leukemia following radioiodine treatment for papillary carcinoma of thyroid. Indian J Cancer 2022;59:436-7
A 27-year-old male patient was diagnosed with papillary carcinoma thyroid in December 2015 and underwent total thyroidectomy with lymph node resection. Five months postsurgery, imaging with I-131 showed tracer uptake in the neck and lungs. He was started on I-131 therapy and received 425 mCi (millicurie) cumulative dose. Hemogram done after I-131 was normal [hemoglobin (Hb) 12.1 g/dL, white blood count (WBC)5,200/mm3, neutrophils–65%, lymphocytes 33%, monocytes–2% and platelets–310,000/μL. Three years later he presented with a lump in the left hypochondrium with dragging pain and early satiety. This was not associated with weight loss, easy fatiguability, fever, bleeding or lymphadenopathy. On examination, the spleen was palpable 20 cm below left costal margin. Rest of the general physical and systemic examination was within normal limits. Hemogram showed Hb 11.1 g/dL, WBC 230,000/mm3, and platelets 500,000/μL. Peripheral smear was suggestive of leukocytosis with left shift with neutrophils–55%, blasts–1%, metamyelocytes–7%, myelocytes–25%, eosinophils–2%, and basophils–1%. Bone marrow was hypercellular with increased myeloid and megakaryocytic precursors [Figure 1]. Conventional karyotyping showed Philadelphia chromosome in all 20 metaphases [46 XY, t (9, 22) (q34, q11)]. Real-time polymerase chain reaction (RT-PCR) for Breakpoint cluster region gene- Abelson proto- oncogene (BCR-ABL) was positive for p210 transcript. A diagnosis of Chronic myeloid leukemia (CML) in chronic phase was confirmed with a Sokal score of 1.6 (intermediate risk). Patient was started on imatinib 400 mg once daily. At 1-month clinical symptoms subsided, spleen regressed to normal and hemogram normalized. Patient achieved optimal response with early molecular response at 3 months and major molecular response at 12 and 18 months.
|Figure 1: Bone marrow aspirate is particulate and hypercellular. Marked granulocytic hyperplasia is noted with a left shift. Eosinophilic myeloid precursors are increased. Megakaryocytes are increased with the presence of dwarf forms. Erythroid precursors are markedly reduced. Blasts, basophils and eosinophils constitute 3%, 5% and 2%, respectively (Jenner and Giemsa stain, 400×)|
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I-131 can cause sublethal bone marrow damage resulting in malignant transformation. Majority of secondary hematological malignancies (SHM) after radioactive iodine (RAI) include lymphomas, myelodysplastic syndrome, and acute leukemias., Rarely CML has also been reported., In a 40-year (1973-2014) retrospective data from SEER (surveillance, epidemiology, and end results) registries, 0.5% patients with thyroid malignancies developed SHM after a median follow-up of 6.6 years.
CML is a rare SHM after thyroid malignancy that can occur both after surgery as well as RAI. In the SEER database 70% cases had undergone surgery as well as RAI, while 30% had surgery only. The mean total dosage of I-131 administered in various case reports ranged from 30-850 mCi and the latent period between I-131 exposure and the detection of CML ranged from 10 months to 13 years. In our case report patient had surgery and received 425 mCi dose of I-131 and developed CML 18 months after radioiodine exposure. No correlation has been found between the dose of I-131 and the duration of development of CML from the time of exposure to RAI.
The prognosis of CML developing post-RAI is similar to de novo CML. Our patient also has classical findings on karyotyping and has an optimal response to Imatinib.
Although there is no clear association between RAI and development of SHM, these disorders are being increasingly diagnosed during follow-up. The mechanism of its causation remains poorly understood. Patient receiving RAI should be actively monitored for SHM during follow-up period with a detailed physical examination and hemogram.
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