Primary hyperparathyroidism in a case of chronic myelogenous leukemia.

Sir,

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[2345] 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 [Tables 1 and 2].

Table 1

Laboratory findings at presentation

Table 2

Laboratory findings in our follow up visit

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.