Toro-Tobón David, Agosto Sarimar, Ahmadi Sara, Koops Maureen, Bruder Jan M
Department of Medicine, CES University, Medellin, Colombia.
Division of Endocrinology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Am J Case Rep. 2017 Feb 27;18:203-207. 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.
慢性髓性白血病(CML)相关的高钙血症是一个不祥的征兆。尽管罕见,但已有数例报道,并且已独立提出多种病理生理机制。我们报告一例患者病例,并对CML相关高钙血症的临床表现及机制进行文献综述。病例报告:一名58岁男性,六年前被诊断为CML,因急性意识模糊、定向障碍、多尿和烦渴一周就诊于急诊科。体格检查发现心动过速、精神状态改变和脱水。血液分析显示白细胞增多、血小板增多和明显的高钙血症(18.6mg/dL)。他的胸部CT扫描显示弥漫性溶骨性病变和骨质破坏,提示弥漫性骨髓受累。该患者被诊断为处于CML急变期的高钙血症。通过补液、降钙素和唑来膦酸治疗,其症状得到控制,血清钙水平恢复正常。出院后,患者接受姑息治疗和唑来膦酸治疗,未再出现高钙血症发作。然而,八个月后,患者死亡。结论:文献证据表明,CML相关高钙血症的临床表现高度可变,通常发生在加速期或急变期,且与生存率低相关。可能涉及多种机制,且这些机制并非相互排斥。更好地理解CML相关高钙血症的病理生理机制,可能会改善对这些患者的临床和实验室评估,并为制定更好的管理策略以及可能的靶向治疗奠定基础,从而积极改善预后。