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Query: UMLS:C0023473 (chronic myeloid leukemia)
18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic granulocytic leukaemia may undergo metamorphosis characterized by diffuse granulocytic sarcomas resulting in lytic bone lesions and hypercalcaemia. A patient with this rare complication is reported.
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PMID:Metamorphosis of chronic granulocytic leukaemia, lytic bone lesions and hypercalcaemia. A case report. 625 Feb 38

Within a recent one-year period, 3 patients in the accelerated phase of chronic myelogenous leukemia were admitted to our medical center with severe hypercalcemia. Simultaneous determinations of ionized calcium and parathyroid hormone levels in 2 of the patients confirmed the hypercalcemia and revealed suppression of parathyroid hormone. We conclude that hypercalcemia in the accelerated phase of chronic myelogeneous leukemia may be more common than previously described and is not mediated by parathyroid hormone. An elevated parathyroid hormone level accompanying hypercalcemia in these patients should suggest the additional diagnosis of primary hyperparathyroidism. Mithramycin was necessary for control in 2 of our cases as well as in others reported in the medical literature and should be an early therapeutic consideration whenever saline diuresis is inadequate.
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PMID:Hypercalcemia in the accelerated phase of chronic myelogenous leukemia. 645 95

A patient with blastic crisis of chronic myelogenous leukemia (CML) is presented. The acute phase was localized in the lymph nodes and bones, causing severe osteolytic lesions and hypercalcemia. The blast cells were undifferentiated in light microscopy and by histochemical stains. As viewed under electron microscopy, a considerable proportion of the blast cells were of myeloid origin, while immunologic markers and cytogenetics indicated a lymphoid origin. It seems plausible that the patient had a mixed myeloid-lymphoid blast crisis, but that the lymphoid blasts were responsible for the severe osteolytic lesions and the hypercalcemia.
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PMID:Hypercalcemia and diffuse osteolytic lesions in the acute phase of chronic myelogenous leukemia. A possible relation between lymphoid transformation and hypercalcemia. 657 58

We established a novel T cell line, designated TK-6, from a patient with T cell lineage blast crisis of chronic myelogenous leukemia (CML) complicated by hypercalcemia. A surface marker study showed T cell phenotype, cluster designation (CD)4, CD5 and CD7. Light and electron microscopic examination revealed myeloperoxidase (MPO)-negative, however, ultrastructural examination under certain specific conditions demonstrated that some cells were MPO-positive. The TK-6 cell karyotype carried a t(9;22)(q34;q11) and additional chromosome aberrations, including a deletion of the long arm of chromosome 6 and the abnormality of chromosome 7. Southern blot analysis showed rearrangement of the T cell receptor beta-chain (TCR beta) gene and the major breakpoint cluster region (bcr) gene. Northern blot analysis detected the expression of the parathyroid hormone-related protein (PTHrP) gene, however, the proviral genome of human T cell leukemia virus type I (HTLV-I) was negative. This cell line will provide a valuable resource for the analysis of the relationship between T cell lineage crisis and myeloid differentiation and for the analysis of humoral hypercalcemia of malignancy (HHM) or leukemia.
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PMID:Establishment and characterization of a novel cell line, TK-6, derived from T cell blast crisis of chronic myelogenous leukemia, with the secretion of parathyroid hormone-related protein. 747 85

We describe a case of hypercalcemia without lytic bone lesions complicating myeloid blast crisis of chronic myeloid leukemia (CML). Serum levels of parathyroid hormone-related protein (PTHrP) were elevated during the initial hypercalcemic period and became undetectable during chemotherapy-induced chronic phase, only to become elevated again during subsequent recurrent blastic periods repeatedly associated with hypercalcemia. Previously reported cases of hypercalcemia complicating CML are reviewed. It is suggested that PTHrP was responsible for the hypercalcemia in this case and may be an important mediator of hypercalcemia in CML.
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PMID:Hypercalcemia in the blastic phase of chronic myeloid leukemia associated with elevated parathyroid hormone-related protein. 841 32

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 parathyroid 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.
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PMID:Accelerated phase of chronic myeloid leukemia presenting with hypercalcemia and a mediastinal mass. 964 3

Hypercalcemia in accelerated phase of chronic myelogenous leukemia (CML) is very rare. Its pathogenesis is considered humoral hypercalcemia of malignancies mediated by parathyroid hormone-related protein (PTHrP). In severe hypercalcemia, calcifications in kidneys, skin, vessels, heart, and stomach may occur. Our two cases were admitted because of severe hypercalcemia in accelerated phase of CML. On Tc-99m methylene diphosphonate (MDP) bone scintigraphies, a marked tracer accumulation was seen in the lung, heart, stomach and kidney. We report increased tracer accumulation of multiple organs on Tc-99m MDP bone scintigraphy in two rare hypercalcemic patients with CML.
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PMID:Technetium-99m MDP bone scintigraphic findings of hypercalcemia in accelerated phase of chronic myelogenous leukemia. 1106 1

Hypercalcemia is a rare complication of chronic myeloid leukemia (CML), usually seen in the accelerated or blastic phases of the disease and associated with a poor prognosis. T-cell lymphoid phenotype is also an infrequent finding in the blast crisis (BC) of CML. A CML patient who had hypercalcemia as the presenting feature of a T-cell BC is reported. She was a 78 year-old woman who, at four months of CML diagnosis, developed weakness, bone pain, and mental confusion, with hypercalcemia being subsequently found. Although the peripheral blood and bone marrow were consistent with the chronic phase of CML, mediastinal enlargement, a soft tissue mass adjacent to the iliac bone, and multiple osteolytic lesions were seen. Serum levels of parathyroid hormone (PTH) and PTH-related peptide were normal, whereas the search for a second neoplasm was negative. The hypercalcemia initially responded to conventional treatment, but it reappeared two weeks later. Coincidentally, a high proportion of blast cells of T-cell origin at the cortical thymocyte stage were observed in the patient's peripheral blood and bone marrow, and she died shortly afterwards.
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PMID:Hypercalcemia as the presenting feature of t-cell lymphoid blast crisis of ph-positive chronic myeloid leukemia. 1134 75

Transformation of chronic myeloid leukemia (CML) often results in acute myeloblastic or, less frequently, in precursor B-cell acute lymphoblastic leukemia (ALL). T-cell blast crisis is rare. Hypercalcemia has also been described as a rare complication of CML, but this usually occurs as a terminal event. Here we report a case of a 35-year-old woman who developed a CD4(+)/CD8(+) T-cell ALL 2 years after the diagnosis of a typical Ph(+) CML. Polymyositis and polyarthritis preceded by 4 months, and symptomatic hypercalcemia occurred just before blastic transformation, probably representing paraneoplastic manifestations of the disease.
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PMID:Philadelphia-positive T-cell acute lymphoblastic leukemia with polymyositis, migratory polyarthritis and hypercalcemia following a chronic myeloid leukemia. 1190 47

A 45-year-old man with chronic myelogenous leukemia (CML) in the accelerated phase was admitted to our hospital because of lower back pain and hypercalcemia. On admission, he was confused and found to have massive splenomegaly. The hypercalcemia and splenomegaly improved significantly after administration of incadronate, hydroxyurea, vincristine and prednisolone. Splenomegaly recurred after cessation of the chemotherapy, and examination of the peripheral blood showed 31% blasts, positive for both CD13 and CD33, on which basis myeloid blastic transformation was diagnosed. Vindesine, cytarabine and prednisolone were administered, and the splenomegaly improved again. On admission, when the patient's serum calcium level was 16.0 mg/dl, his serum parathyroid hormone-related protein (PTHrP) level was elevated to 118.3 pmol/l. Furthermore, RT-PCR analysis revealed that the patient's CML cells expressed PTHrP mRNA, and a high level of PTHrP was detected in the supernatant of cultured mononuclear cells derived from the patient's peripheral blood. These findings indicated that the hypercalcemia was due to production of PTHrP by the leukemic cells. Several cases of PTHrP. mediated hypercalcemia associated with CML have been reported previously, and are reviewed here.
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PMID:[Hypercalcemia mediated by parathyroid hormone-related protein in the blastic phase of chronic myelogenous leukemia]. 1192 71


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