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Table of Contents
Year : 2013  |  Volume : 17  |  Issue : 5  |  Page : 942-943

Primary hyperparathyroidism in a case of chronic myelogenous leukemia

1 Department of Hematology/Medical Oncology, Urmia University of Medical Sciences, Urmia, Iran
2 Department of Endocrinology and Metabolism, Urmia University of Medical Sciences, Urmia, Iran
3 Department of Internal Medicine, Urmia University of Medical Sciences, Urmia, Iran

Date of Web Publication29-Aug-2013

Correspondence Address:
Nasim Valizadeh
Department of Hematology/Medical Oncology, Urmia University of Medical Sciences, Urmia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2230-8210.117201

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How to cite this article:
Valizadeh N, Herfehdoust F, Valizadeh N, Vossoghian S. Primary hyperparathyroidism in a case of chronic myelogenous leukemia. Indian J Endocr Metab 2013;17:942-3

How to cite this URL:
Valizadeh N, Herfehdoust F, Valizadeh N, Vossoghian S. Primary hyperparathyroidism in a case of chronic myelogenous leukemia. Indian J Endocr Metab [serial online] 2013 [cited 2021 May 8];17:942-3. Available from: https://www.ijem.in/text.asp?2013/17/5/942/117201


Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasm that is characterized with uncontrolled proliferation of granulocytes. CML has tree clinical phase: A chronic phase, an accelerated phase and blastic crisis. [1]

Hypercalcemia was reported in patients with CML in accelerated phase and blastic crisis [2],[3],[4],[5] due to secretion of parathyroid hormone (PTH) related peptide.

Here, we present the first case of CML and coexistence primary hyperparathyroidism due to a parathyroid adenoma. A 70-year-old male was admitted with hyperleukocytosis and splenomegaly. He had history of renal stones and litothripsy. Laboratory findings are included: White blood cells (WBCs) = 201,600/μl polymorphonuclear neutrophil (PMN) = 65%, L = 5%, Basophils = 5%, Eosinophils = 1.5%, Blast = 5-10%, Mixed = 15-20%) Hemoglobin (Hb) = 13.2 g/dl, and platelets (PLTs) = 511,000/μl.

Peripheral blood smear showed nucleated red blood cells (RBCs), Basophilia, eosinophilia, shift to the left in myeloid series and 5-10% of myeloid series were myeloblasts.

Bone marrow aspiration and biopsy were hypercellular marrow (95% cellularity), shift to the left in myeloid serried, 5% basophilia, 5% eosinophilia, 5-10% myeloblasts, M/E ratio more than 25 and increased in number of megakaryocytes suggestive of CML in chronic phase. Cytogenetic study was positive for Philadelphia chromosome. Imatinib was administered and he achieved a hematologic remission. Serum calcium level was high and serum phosphorus level was low. PTH level was markedly elevated in repeated assays. Results of laboratory findings on admission and in follow-up visits are showed in [Table 1] and [Table 2].
Table 1: Laboratory findings at presentation

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Table 2: Laboratory findings in our follow up visit

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Sestamibi scan showed a parathyroid adenoma in the lower part of left thyroid lobe. Color Doppler sonography of parathyroid glands showed a 20 nm × 16 mm tumor in left lower parathyroid gland with severe hyperemia suggestive for parathyroid adenoma. Bone mass densitometry revealed T score −2.7 in spine and −0.7 for femur. Since, he had osteoporosis in bone mass densitometry of lumbar vertebrae and history of renal stones thus, he underwent parathyroidectomy and the diagnosis of parathyroid adenoma was confirmed after surgery.

Hasselbalch et al. reported two cases of CML that was complicated with hypercalcemia in the accelerated phase of their disease. After excluding of primary hyperparathyroidism by serum PTH assay, they concluded that in CML patients a non-parathyroidal hormone, which has partial bioactivity of PTH causes bone resorption and hypercalcemia. [6] However, our patient presented with hypercalcemia in the chronic phase, elevated PTH level and hypophosphatemia thus, the diagnosis of primary hyperparathyroidism was made. He underwent parathyroidectomy because of osteoporosis in lumbar spine and nephrolithiasis. We found a new association between CML and primary heprparathyroidism in this patient. Finding a new association between CML and parathyroid adenoma direct our minds for the possible involvement of the same oncogenes, signaling pathways and/or epigenetic, and environmental factors in the pathogenesis of parathyroid adenoma and CML or other malignancies.

   References Top

1.Faderl S, Talpaz M, Estrov Z, O'Brien S, Kurzrock R, Kantarjian HM. The biology of chronic myeloid leukemia. N Engl J Med 1999;341:164-72.  Back to cited text no. 1
2.Quitt M, Kelner J, Sova J, Froom P, Aghai E. Accelerated phase of chronic myeloid leukemia presenting with hypercalcemia and a mediastinal mass. Acta Haematol 1998;99:231-3.  Back to cited text no. 2
3.Nadal E, Cervantes F, Rosiñol L, Talarn C, Montserrat E. Hypercalcemia as the presenting feature of t-cell lymphoid blast crisis of ph-positive chronic myeloid leukemia. Leuk Lymphoma 2001;41:203-6.  Back to cited text no. 3
4.Seymour JF, Grill V, Martin TJ, Lee N, Firkin F. Hypercalcemia in the blastic phase of chronic myeloid leukemia associated with elevated parathyroid hormone-related protein. Leukemia 1993;7:1672-5.  Back to cited text no. 4
5.Kwak HS, Sohn MH, Lim ST, Kwak JY, Yim CY. Technetium-99m MDP bone scintigraphic findings of hypercalcemia in accelerated phase of chronic myelogenous leukemia. J Korean Med Sci 2000;15:598-600.  Back to cited text no. 5
6.Hasselbalch H, Birgens HS, Geisler C, Hansen NE. Hypercalcaemia in the accelerated phase of chronic myelogenous leukaemia: No relationship to the phenotype of the blast cells. Scand J Haematol 1985;35:333-8.  Back to cited text no. 6


  [Table 1], [Table 2]

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