Abstract:A patient with chronic myeloid leukemia developed hypercalcemia as a presenting sign of the accelerated phase of the disease. Ultrasound of the neck showed a large hypodense mass connected to the thyroid gland, which was thought to be a parathyorid tumor and the cause of the hypercalcemia. Histology of the surgically removed mass revealed a chloroma. The patient’s course was complicated by respiratory failure and metastatic calcinosis of the lung, an unusual finding in hypercalcemia of short duration.
“…Since the first description of GS in 1811 by Burns several reports about GS or so-called chloromas have been published [10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22]. The term ‘chloroma’ is used to describe the green color created by the intracellular enzyme myeloperoxidase.…”
Section: Discussionmentioning
confidence: 99%
“…In contrast to extramedullary hematopoiesis, cells of the megakaryocytic and erythroid lines are lacking in GS. However, GS, often referred to as chloroma or extramedullary myeloblastoma, is rare [10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22]. GS are solid tumors composed of immature cells of the granulocytic lineage [23]and occur during either leukemic relapse or remission or may be the only presentation of the disease.…”
Granulocytic sarcoma (GS) occurs in patients with chronic myeloproliferative disorders as well as in patients with acute myeloid leukemia (AML). These tumorous masses can occur anywhere in the body and have to be differentiated from lymphoma, carcinoma or infectious processes. We report the results of fine-needle aspiration cytology (FNAC) in 26 patients with GS. Seventeen patients suffered from AML and 9 from chronic myeloid leukemia (CML) blast crisis. In 5 patients with AML, GS was the initial presentation of hematological malignancy, in the remaining 21 patients, FNAC confirmed relapse of AML or extramedullary blast crisis of CML. In 8 patients, GS was located in the skin, in 17 in the lymph node and in another patient in the spinal canal. This study demonstrates the clinical utility and diagnostic accuracy of FNAC in the evaluation of GS from multiple sites.
“…Since the first description of GS in 1811 by Burns several reports about GS or so-called chloromas have been published [10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22]. The term ‘chloroma’ is used to describe the green color created by the intracellular enzyme myeloperoxidase.…”
Section: Discussionmentioning
confidence: 99%
“…In contrast to extramedullary hematopoiesis, cells of the megakaryocytic and erythroid lines are lacking in GS. However, GS, often referred to as chloroma or extramedullary myeloblastoma, is rare [10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22]. GS are solid tumors composed of immature cells of the granulocytic lineage [23]and occur during either leukemic relapse or remission or may be the only presentation of the disease.…”
Granulocytic sarcoma (GS) occurs in patients with chronic myeloproliferative disorders as well as in patients with acute myeloid leukemia (AML). These tumorous masses can occur anywhere in the body and have to be differentiated from lymphoma, carcinoma or infectious processes. We report the results of fine-needle aspiration cytology (FNAC) in 26 patients with GS. Seventeen patients suffered from AML and 9 from chronic myeloid leukemia (CML) blast crisis. In 5 patients with AML, GS was the initial presentation of hematological malignancy, in the remaining 21 patients, FNAC confirmed relapse of AML or extramedullary blast crisis of CML. In 8 patients, GS was located in the skin, in 17 in the lymph node and in another patient in the spinal canal. This study demonstrates the clinical utility and diagnostic accuracy of FNAC in the evaluation of GS from multiple sites.
“…(1998) [11]56/FNRAPHydration, glucocorticoids, furosemideHU, cytarabineNRQuitt et al . (1998) [12]49/F10 yearsAPHydration, diuretic, calcitonin, steroids, surgeryHU, BUMinimal response; died 24 hours laterKwak et al . (2000) [13]57/M6 yearsBPHydration, corticosteroids, calcitoninHUCR32/M0APHydration, corticosteroids, calcitoninHUCRNadal et al .…”
BackgroundPatients with chronic myeloid leukemia typically present with high white blood cell counts revealed during annual checkups. Leukemic arthritis and hypercalcemia are rare manifestations in patients with chronic myeloid leukemia.Case presentationA 35-year-old Thai man who had been diagnosed with chronic myeloid leukemia in the chronic phase developed blast crisis while he was receiving ongoing treatment with imatinib at 400 mg/day. Initially, he presented with oligoarthritis in both knees and ankles. A bone scintigraphy showed a prominent bony uptake, with a symmetrical, increased uptake in many bone areas. Induction therapy with a 7 + 3 induction regimen was prescribed in conjunction with 600 mg of imatinib once daily before switching to 140 mg of dasatinib. He subsequently developed severe hypercalcemia (total serum calcium of 17.8 mg/dL), with generalized osteolytic lesions detected on a bone survey. His serum vitamin D level was 50.64 ng/mL, while the serum parathyroid hormone level was 9.82 pg/mL. Despite the administration of an aggressive intravenously administered hydration, intravenously administered calcitonin, and 600 mg/day of imatinib, the severe hypercalcemia was refractory. We therefore decided to prescribe 20 mg/day of intravenously administered dexamethasone; fortunately, his serum calcium level decreased dramatically to normal range within a few days.ConclusionsAlthough leukemic arthritis and severe hypercalcemia are extraordinary presentations in patients with chronic myeloid leukemia, the advanced phase of the disease might bring on these symptoms. Apart from parathyroid hormone-related protein-related hypercalcemia, vitamin D is a mechanism of humoral-mediated hypercalcemia.Electronic supplementary materialThe online version of this article (10.1186/s13256-018-1798-5) contains supplementary material, which is available to authorized users.
“…Characteristics of 30 reported CML patients with hypercalcemia are summarized as follows [16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38]. The median age of patients was 44 years with a male:female ratio of 14:16.…”
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.
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