11/74. bone resorption associated with uncoupling of osteoclastic and osteoblastic activities in adult T cell leukemia with hypercalcemia: case report.A 64-year-old woman with adult T cell leukemia (ATL) was admitted to our hospital with severe hypercalcemia. The serum calcium level was elevated to 14.9 mg/dl. Biochemical parameters for bone formation including serum osteocalcin (bone Gla protein, BGP) and alkaline phosphatase (ALP) were normal. The serum levels of tartrate-resistant acid phosphatase (TRAP), a parameter for bone resorption, were increased (4.6 KAU). The serum level of parathyroid hormone-related protein (PTHrP) was elevated (343 pmol/l). The cytokines with stimulatory effects on bone resorption, such as interleukin (IL)-1alpha, IL-1beta, IL-6, and tumor necrosis factor-alpha, were not detected. serum Ca levels, PTHrP levels, and TRAP levels decreased with the decrease in ATL cells after chemotherapy, while serum BGP levels and ALP levels increased. On the 29th hospital day, ATL cells began to increase again. Then serum PTHrP levels, Ca levels, and TRAP levels increased, while serum BGP levels and ALP levels decreased. A marked excessive bone resorption with suppressed bone formation (uncoupling) occurred in this patient. The ATL cells produced not only PTHrP but also IL-1alpha and IL-1beta. These results suggest that PTHrP may act as a humoral factor and IL-1 may act as a local factor in bone metabolism of ATL patients.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
12/74. philadelphia-positive T-cell acute lymphoblastic leukemia with polymyositis, migratory polyarthritis and hypercalcemia following a chronic myeloid leukemia.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.- - - - - - - - - - ranking = 2keywords = leukemia (Clic here for more details about this article) |
13/74. Soft tissue uptake of Tc99m-MDP in acute lymphoblastic leukemia.Acute lymphoblastic leukemia (ALL) is associated rarely with hypercalcemia. This may be due to elevated levels of parathyroid hormone-related peptide (PTHrP). We report a case of an 18-year-old female patient who was presented with a pathological fracture of left intertrochanteric region. Bone scintigraphy was consistent with features of hypercalcemia associated with metastatic calcification. A bone marrow biopsy led to the diagnosis of ALL. The mechanism of hypercalcemia in ALL, metastatic calcification and soft tissue uptake of bone seeking agents in this case are discussed in detail.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
14/74. Acute megakaryocytic leukemia presenting as hypercalcemia with skeletal lytic lesions.Acute megakaryocytic leukemia (AML M7) is a rare type of acute myelogenous leukemia in adults, commonly presenting with myelofibrosis. This report describes a case of a 32-yr-old male who presented with hypercalcemia and bony lytic lesions, in the absence of myelofibrosis. The diagnosis of AML M7 should be considered in a patient with pancytopenia, lytic lesions and hypercalcemia.- - - - - - - - - - ranking = 1.2keywords = leukemia (Clic here for more details about this article) |
15/74. Megakaryoblastic transformation of polycythemia vera with hypercalcemia.polycythemia vera (PV) is known to occasionally transform into acute leukemia. Administration of alkylating agents seems to be associated with an increased risk of leukemic transformation of PV. hypercalcemia is a serious complication of malignancies, but it is uncommon in acute leukemia. In the majority of malignancies with hypercalcemia, elevated parathyroid hormone-related protein (PTHrP) is thought to be the main cause of hypercalcemia. We report a rare case of megakaryoblastic transformation of PV with hypercalcemia. A 62-year-old man was diagnosed as having PV in 1983, and he had received ranimustine and busulfan. He developed acute megakaryoblastic leukemia 17 years after the initial diagnosis of PV. serum calcium was elevated, the serum level of intact parathyroid hormone (PTH) was suppressed, and the level of intact PTHrP was slightly elevated. He had no lytic bone lesions; however, uncoupling of bone turnover due to an increase in bone resorption and a decrease in bone formation was detected by using biochemical markers. Since the level of PTHrP was slightly elevated from the normal value, we speculated that PTHrP produced in the local field by leukemic cells might have been more abundant than circulating PTHrP. Pamidronate and adrenocortical hormone were effective in reducing the serum calcium level. However, the patient died shortly after the start of induction chemotherapy. The prognosis of cases of PV that has transformed into acute leukemia is generally poor because the majority of such cases are refractory to chemotherapy.- - - - - - - - - - ranking = 0.8keywords = leukemia (Clic here for more details about this article) |
16/74. Glomerular calcification in hypercalcemic nephropathy.Hypercalcemic nephropathy has been classified as a tubulointerstitial renal disease. The presence of glomerular pathologic findings attributable to hypercalcemia has been observed in only a few patients and therefore has been considered an unusual finding. In the current study, calcium deposition within glomeruli was investigated in 2 patients with extreme elevations in serum calcium levels and hypercalcemic nephropathy. The study material consisted of a renal biopsy specimen from a 31-year-old woman (patient 1) who had T-cell lymphoma/leukemia and a serum calcium level of 20.2 mg/dL (5.0 mmol/L) and autopsy kidney specimens from a 19-year-old woman (patient 2) who was being evaluated for primary hyperparathyroidism and a calcium level of 18.4 mg/dL (4.6 mmol/L). The renal biopsy specimen for patient 1 exhibited calcium deposits present in the glomerular capillary basement membranes, where they were associated with segmental sclerosing lesions (21% of glomeruli). Nine percent of the cortical tubules contained calcifications. In patient 2, calcium was found in the mesangial areas in 95% of glomeruli, filling the Bowman space in 7% of glomeruli, or associated with capillary basement membranes and segmental sclerosing lesions (12% of glomeruli). Fifteen percent of cortical tubules, 4% of outer medullary tubules, and 40% of inner medullary tubules were calcified. In neither case was there immunofluorescence or electron microscopic evidence of primary glomerular disease. Thus, glomerular calcification may exceed that occurring in the cortical and outer medullary tubules and may play a significant role in the loss of renal function in hypercalcemic nephropathy. Glomerular calcinosis may also be recognized as an additional cause of segmental glomerulosclerosis and nephrotic range proteinuria in patients with extremely high levels of serum calcium.- - - - - - - - - - ranking = 0.2keywords = leukemia (Clic here for more details about this article) |
17/74. Novel B-cell acute lymphoblastic leukemia sister cell lines BALM 19-23 and BALM-26 with interclonal proliferative and phenotypic heterogeneity from a patient with hypercalcemia.A series of human acute lymphoblastic leukemia (ALL) cell lines, BALM-19, -20, -21, -22, -23 (BALM 19-23) and BALM-26 were established from a patient with B-cell characteristics of ALL L2 type. All cell lines were derived from bone marrow specimens, BALM 19-23 from a sample taken at diagnosisand BALM-26 from one at relapse. Like the original leukemia cells, the established lines present various B-cell characteristics, being positive for cell surface immunoglobulin (Ig) chains but also for nuclear terminal deoxynucleotidyl transferase; hence the cell lines should be assigned to B-cell category B-IV. As a unique feature, the cell lines expressed the CD33 myeloid antigen in addition to the common B-cell markers. Heterogeneous antigen expression among the different cell lines was found regarding CD35, CD39, CD45RA, CD78 and CD95. The malignant nature of the cell lines was documented by negativity for the Epstein-Barr virus and by the occurrence of clonal non-random structural chromosome abnormalities. The patient's serum showed hypercalcemia, prompting further investigation of the established cell lines which expressed parathyroid hormone related peptide (PTHrP) mRNA as examined by reverse transcriptase polymerase chain reaction. The established B-cell ALL sister cell lines, BALM 19-23 and BALM-26, could provide useful material for clarifying the pathogenesis of this type of B-cell malignancy. The scientific significance of this panel of cell lines lies in the availability of a series of clonally derived but phenotypically different sister cell lines established at different phases of the disease.- - - - - - - - - - ranking = 1.2keywords = leukemia (Clic here for more details about this article) |
18/74. Treatment of acute lymphoblastic leukemia-induced extreme hypercalcemia with pamidronate and calcitonin.OBJECTIVE: To describe extreme hypercalcemia as the presenting feature of acute lymphoblastic leukemia in an 8-yr-old girl and the combined use of pamidronate and calcitonin for its treatment. DESIGN: Case report. SETTING: Pediatric intensive care unit. PATIENT: An 8-yr-old girl with 20.0 mg/dL serum calcium (reference range, 8.8-10.4 mg/dL) and 2.66 mmol/L ionized calcium (reference range, 1.13-1.32 mmol/L). INTERVENTION: Intravenous pamidronate and subcutaneous calcitonin. MEASUREMENTS AND MAIN RESULTS: Our patient presented with nausea, vomiting, lethargy, weight loss, fatigue, and weakness but, remarkably, did not exhibit electrocardiographic changes. Initial treatment with hydration at 8 mL x kg(-1) x hr(-1) and furosemide was ineffective. A single dose of 1 mg/kg intravenous pamidronate given over 24 hrs complemented by three doses of 5 units/kg subcutaneous calcitonin over 36 hrs lowered serum calcium to a normal range within 3 days. Side effects noted were hypocalcemia, hypomagnesemia, and hypophosphatemia. They were most pronounced 7-9 days after treatment, stabilized with supplementation, and returned to acceptable ranges by 1 month without need for ongoing electrolyte supplements. A renal computed tomographic scan did not show nephrocalcinosis. The patient remained free from recurrence of hypercalcemia 6 wks after initiating chemotherapy for acute lymphoblastic leukemia. CONCLUSIONS: Extreme hypercalcemia can be a presenting feature of acute lymphoblastic leukemia, but it may not result in life-threatening organ dysfunction. Combined treatment with pamidronate and calcitonin should be considered for treating hypercalcemia that does not respond to conventional therapy with hydration and furosemide.- - - - - - - - - - ranking = 1.4keywords = leukemia (Clic here for more details about this article) |
19/74. CD19 negative precursor B acute lymphoblastic leukemia presenting with hypercalcemia.A 9-month-old infant presented with hypercalcemia and lytic bone lesions. Suspicion for malignancy led to a bone marrow examination, which showed replacement of the marrow by a small round blue cell infiltrate. Flow cytometric analysis of these cells showed an unusual immunophenotype in that these cells were dim CD45, HLA-DR, and CD10 positive, but CD19, CD20, CD79a, and CD34 negative. Southern blotting showed clonal rearrangement of immunoglobulin heavy chain (IgH) which confirmed a diagnosis of precursor B acute lymphoblastic leukemia (ALL). He received supportive treatment with hydration and pamidronate, but had recurrent episodes of hypercalcemia. Once the correct diagnosis of ALL was established, the patient was treated with an infantile ALL chemotherapeutic regimen and the hypercalcemia resolved. This case highlights the usefulness of immunoglobulin gene rearrangement studies in atypical cases of ALL.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
20/74. Severe hypercalcemia in a child with acute nonlymphocytic leukemia: the role of parathyroid hormone-related protein and proinflammatory cytokines.Among the hematological malignancies, hypercalcemia has often been reported in lymphoid malignancies such as multiple myeloma and adult T cell leukemia/lymphoma, but it has only rarely been described in acute nonlymphocytic leukemia. We describe here a 14-month-old girl with acute monocytic leukemia complicated by severe hypercalcemia (4.6 mmol/l) at presentation. A bone survey showed generalized bone resorption, but no localized osteolytic lesions. A search for the etiology of the hypercalcemia revealed that the serum levels of parathyroid hormone-related protein (PTHrP) and also proinflammatory cytokines with stimulatory effects on osteolytic bone resorption - TNF-alpha, IL-6 and M-CSF - were elevated. The patient achieved complete remission with induction chemotherapy, and the levels of PTHrP and the cytokines became normalized. In this case, PTHrP and cytokines might have acted cooperatively to exacerbate bone resorption, resulting in severe hypercalcemia.- - - - - - - - - - ranking = 1.4keywords = leukemia (Clic here for more details about this article) |
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