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

• Published in: The American journal of case reports 2017-02, Vol.18, p.203-207
• Main Authors: Toro-Tobón, David, Agosto, Sarimar, Ahmadi, Sara, Koops, Maureen, Bruder, Jan M
• Format: Article
• Language: English
• Subjects: Blast Crisis - blood; Blast Crisis - pathology; Bone Density Conservation Agents - therapeutic use; Calcitonin - therapeutic use; Diphosphonates - therapeutic use; Disease Progression; Drug Therapy, Combination; Fatal Outcome; Humans; Hypercalcemia - diagnosis; Hypercalcemia - drug therapy; Hypercalcemia - etiology; Imidazoles - therapeutic use; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - complications; Male; Middle Aged; Zoledronic Acid
• ISSN: 1941-5923; 1941-5923
• DOI: 10.12659/AJCR.902467

BACKGROUND Hypercalcemia associated with chronic myeloid leukemia (CML) is an ominous sign. Although rare, several cases have been reported and multiple pathophysiologic mechanisms have been independently proposed. We present a patient case and a literature review of the clinical presentation and mechanisms of CML-associated hypercalcemia. CASE REPORT A 58-year-old male with a past medical history of CML diagnosed six years earlier, presented to the emergency department with one week of acute confusion, disorientation, polyuria, and polydipsia. On physical examination, we observed tachycardia, altered mental status, and dehydration. Blood analysis revealed leukocytosis, thrombocytosis, and marked hypercalcemia (18.6 mg/dL). His chest CT scan showed diffuse lytic lesions and bone destruction concerning for diffuse bone marrow involvement. The patient was diagnosed with hypercalcemia in the context of a CML blast phase. Treatment with hydration, calcitonin, and zoledronic acid lead to control of his symptoms and normalization of his serum calcium levels. After discharged, the patient was maintained on palliative treatment and zoledronic acid management without new episodes of hypercalcemia. However, eight months later, the patient died. CONCLUSIONS Evidence from the literature demonstrates a highly variable clinical presentation of CML-associated hypercalcemia, commonly occurring during an accelerated or a blast phase, and associated with poor survival. Multiple mechanisms could be involved and are not exclusive of each other. Better understanding of the pathophysiologic mechanisms involved in CML-associated hypercalcemia could lead to improvement in clinical and laboratory evaluation of these patients and be the foundation for the development of better management strategies and possibly target-directed therapy to positively improve prognosis.