Extensive Bone Marrow Necrosis and Symptomatic Hypercalcemia in B Cell Blastic Transformation of Chronic Myeloid Leukemia: Report of a Case and Review of the Literature

Abstract

Extensive bone marrow necrosis and symptomatic hypercalcemia have been described independently as rare complications of chronic myeloid leukemia. Here we report a 66-year-old man who developed B cell blastic transformation 10 years after diagnosis of CML in the chronic phase. Extensive bone marrow necrosis and symptomatic hypercalcemia concurrently developed after transformation, with development of disseminated intravascular coagulation and multifocal osteolysis. Most necrotic cells were readily identifiable as blasts. Mediators related to hypercalcemia, including prostaglandin E2, transforming growth factor-α and transforming growth factor-β, were significantly elevated in the serum. As far as we know, this is the first case report of chronic myeloid leukemia concurrently developing bone marrow necrosis and hypercalcemia; this association was not reported in other types of leukemia or bone marrow malignancies.

Leukemic arthritis and severe hypercalcemia in a man with chronic myeloid leukemia: a case report and review of the literature

“…(2002) [25]35/F2 yearsBPPRED, pamidronateCyclophosphamide, DOX, VCRCR in 1 week; died 1 month laterMiyoshi et al . (2005) [14]68/F4 yearsBPPRED, diuretic, incadronate, elcatoninEnocitabine, DAU, VCRCR; died 8 months laterNoguchi and Oshimi (2007) [26]66/M10 yearsBPHydration, PRED, bisphosphonate, elcatoninVCRCR in 3 weeks; died 8 weeks after admissionValizadeh et al . (2013) [18]70/MNRBPParathyroidectomyImatinibNRToro-Tobón et al .…”

Chronic Myeloid Leukemia Associated Hypercalcemia: A Case Report and Literature Review

“…Our extensive literature search found over 30 reported cases, most of which were last reviewed in 2007 [8]. Among the published results, the median participant age at presentation was 44 years.…”

“…It can be produced and released not only from tumor cells but from normal tissue and act on PTH receptors [2,6,9]. This polypeptide, in a similar fashion to PTH, is implicated in hypercalcemia by stimulating bone resorption and increasing renal calcium reabsorption, and releasing calcium into serum [8,9,12,13]. Although not commonly elevated in hematological malignancies [9], previous studies have demonstrated elevated mRNA for PTHrP in cultured leukemic cells, as well as increased plasma levels in patients with T-cell leukemia and B-cell lymphoma [7,8,14].…”

“…In several cases, PTHrP has been reported to be elevated as an isolated etiologic agent or together with other possible causes of CML-associated hypercalcemia [7,8,14,15]. Unfortunately, measurements of PTHrP levels have only been reported in recent case reports [16].…”

Monocytic Crisis of Chronic Myeloid Leukemia in the Era of Tyrosine Kinase Inhibitor

“…Bone marrow necrosis in CML has been reported in at least 14 patients, most of whom were in the blastic phase. 28 The necrosis results from cellular hypoxia due to ischemia of marrow microcirculation as a consequence of inflammatory damage or mechanical obstruction. 29 Bone marrow necrosis has also been associated with the use of imatinib mesylate.…”