Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult T-cell leukemia (ATL) is T-cell leukemic non Hodgkins' malignant lymphoma; 73 percent of 199 non Hodgkins' lymphomas were of T-cell origin, and 58 percent of these T-cell lymphomas were ATL in Nagasaki, Japan. ATL cells are mostly characteristic in the specific nuclear indentations. These cells have a commonly helper T-cell phenotype on the reaction to the Leu series monoclonal antibody, and the cells showed a suppressor function to normal B-cell differentiation by PWM. Miscellaneous infections, probably due to T-cell disfunction have been frequently experienced in ATL. Pulmonary infections, especially interstitial pneumonitis, were characteristic. Bone destraction through osteocrast proliferation was suggested to be the main cause of hypercalcemia. Many cases with familiar disposition have been found in ATL and T-ML, and 3 siblings having ATL and T-ML were presented. ATLA antibody was positive in all cases of ATL and 63 percent of T-ML. Positive rate of ATLA antibody in healthy spouses and siblings of ATL and T-ML patients was high. ATLA (antigen) on the mononuclear cells of almost all the ATL and ATLA antibody positive T-ML was positive. Peripheral blood mononuclear cells of 2 cases of mycosis fungoides were also positive for ATLA. Probably pre ATL cases with low grade leukocytosis and the presence of ATL cell like lymphocytes and positive rate of ATLA antibody and antigen of these cases were presented. By the chromosome study of 14 cases of ATL, chromosome aberrations of No. 2, 3 and 18 were frequently observed.
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PMID:[Clinical features of adult T-cell leukemia]. 660 19

An autopsy case of adult T cell leukemia associated with hypercalcemia and hyperplastic parathyroid glands is reported. A 51-year-old man complained of systemic lymphadenopathy and hepato-splenomegaly; a diagnosis of adult T cell leukemia was made based on clinico-pathological findings. The pathogenesis of hypercalcemia in adult T cell leukemia is discussed. However, cases associated with hyperplasia of the parathyroid gland are very rare. We emphasize the role of the parathyroid gland in the pathogenesis of hypercalcemia in adult T cell leukemia.
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PMID:[Autopsy case of adult T cell leukemia associated with hypertrophy of the parathyroid glands]. 660 68

Hypercalcemia is a frequent manifestation of human T-cell lymphotrophic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma (ATL). Human T-cell lymphotrophic virus type I infection is endemic in the Caribbean, Japan, Melanesia, and Africa. This article presents two cases of ATL to increase awareness of the disease by primary care physicians. The management of hypercalcemia is discussed.
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PMID:Hypercalcemia associated with adult T-cell leukemia/lymphoma (ATL). 747 48

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

Hypercalcemia accompanied with malignant tumors is generally classified into two categories, namely with or without bone metastasis. As for the latter, bone resorption-stimulating factors produced by tumor cells, such as parathyroid hormone-related protein (PTHrP), show hormone-like effects and promote a bone resorption. Many cases have been reported regarding the production of TPTHrP in adult T cell leukemia (ATL), but few have been reported with acute lymphoblastic leukemia (ALL). We report here a similar case with ALL. A 12-year-old male presented with fever, petechiae and thrombocytopenia, and was diagnosed as ALL. We started the induction therapy and confirmed complete remission. Later, he relapsed 3 times without symptoms apart from hypercalcemia at the beginning. Elevation of the serum calcium level followed by a rise of lymphoblastic cells was recognized. Bone metastasis was excluded since bone mineral density and serum mid region PTH were normal and no abnormal findings were noticed on X rays and 99mTc bone scintigraphy. However, his urinary PTHrP level was high, and his lymphoblastic cells staining immunocytochemically with the monoclonal antibodies against the C-terminal region of PTHrP showed a positively brownish color. Finally, he died of pulmonary aspergillosis. Hypercalcemia was not related to serum PTH or bone metastasis. ATL viral infection reported as a cause of PTHrP production was also excluded from several experimental data. Therefore, we concluded that lymphoblastic cells directly produced PTHrP, and that this PTHrP played an important role in the induction of hypercalcemia.
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PMID:A case of acute lymphoblastic leukemia accompanied with the production of parathyroid hormone-related protein. 756 43

Adult T-cell leukemia (ATL) is a human T-cell leukemia virus type I (HTLV-I)-infected lymphoproliferative disorder that shows a characteristic nodular infiltration into various tissues, hypercalcemia, and subsequent rapid increase of peripheral ATL cell number. ATL cells and HTLV-I-infected T-cell lines also make cluster formation rapidly after the non-stimulative culture. However, the mechanism of the acute proliferation of ATL cells remains to be understood. We report the following novel features of homotypic adhesion via leukocyte function-associated antigen-1 (LFA-1)/intracellular adhesion molecule-1 (ICAM-1) pathway that suggest a role for it in cytokine production and rapid proliferation of ATL cells: (1) ATL cells show clustering in a calcium dependent manner, even at the higher concentration; (2) ATL cells consistently and highly express ICAM-1 and an active form of LFA-1, whereas integrin expression, except for LFA-1, is rather lower compared with that of normal CD4+ T cells; (3) ATL cells make conjugate formation within 6 minutes and clustering within 48 hours, both of which are inhibited by the addition of monoclonal antibodies (MoAbs) against LFA-1 and ICAM-1; (4) spontaneous mRNA transcription and protein secretion of both interleukin-1 and parathyroid hormone-related protein are observed consistently in ATL cells, and these productions are inhibited by anti-LFA-1 and anti-ICAM-1 MoAbs but are markedly increased by cross-linking of LFA-1 and ICAM-1 by the immobilized specific MoAbs; and (5) proliferative responses of ATL cells are also inhibited by these MoAbs. We propose that ATL cells proliferate in sequential events: the homotypic and calcium-dependent adhesion through LFA-1/ICAM-1, the signal transduction through these adhesion molecules, the production of cytokines, and the proliferation.
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PMID:Calcium-dependent homotypic adhesion through leukocyte function-associated antigen-1/intracellular adhesion molecule-1 induces interleukin-1 and parathyroid hormone-related protein production on adult T-cell leukemia cells in vitro. 766 73

Adult T-cell leukemia (ATL) associated with HTLV-1 infection is characterized by the development of hypercalcemia in over two thirds of patients. Dysregulation of cellular gene transcription by viral proteins is an emerging paradigm for molecular pathogenesis of disease. A recent example is the parathyroid hormone-related protein (PTHrP) gene, which has been implicated in the hypercalcemia of ATL, and is transactivated by the HTLV-1 tax and HTLV-11 tax proteins. PTHrP is expressed at high levels in leukemia cells derived from ATL patients, as well as in asymptomatic HTLV-1 positive carriers. This article reviews the interaction of the HTLV-1 transcriptional regulator tax with the PTHrP promoter. Tax mediates its effects on PTHrP via cellular transcription factors AP-2 and AP-1, and transactivation via an AP-2 motif represents a novel interaction of tax with a cellular transcription factor.
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PMID:Hypercalcemia, parathyroid hormone-related protein expression and human T-cell leukemia virus infection. 781 98

A 38-year-old woman was admitted to our hospital with symptoms and signs of hypocalcemia in 1977 and a diagnosis of primary hypoparathyroidism was made with a positive Ellsworth Howard test. She was then lost to follow up until 1992 when she returned this time with symptoms and signs of hypercalcemia. An inguinal lymph node was biopsied showing non-Hodgkin's lymphoma, diffuse pleomorphic type and monoclonal integration of proviral human T-cell lymphotropic virus-1 DNA was detected in lymph node cells indicating ATLL. Serum parathyroid hormone-related peptide (PTHrP) was slightly elevated and the tumor cells were positively stained with anti-PTHrP serum. Combination chemotherapy with vincristine, adriamycin, cyclophosphamide and prednisolone was given to the patient with disappearance of the lymphadenopathy and subsequent normalization of PTHrP levels. Interestingly, the signs and symptoms of hypocalcemia reappeared after the treatment requiring replacement therapy with calcium and vitamin D.
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PMID:A patient with primary hypoparathyroidism developing hypercalcemia associated with adult T-cell leukemia/lymphoma. 781 15

Simian T-cell leukemia virus type 1 (STLV-1), a type C retrovirus associated with leukemia/lymphoma in Old World monkeys, is closely related to human T-cell leukemia virus type 1, the etiologic agent of adult T-cell leukemia/lymphoma in humans. In a colony of 3200 baboons, the prevalence of antibodies to STLV-1 is more than 40%. Seropositivity is more frequent in female baboons than in males and increases with age. Of 27 STLV-1 antibody-positive baboons with non-Hodgkin's lymphoma, 20 were females and 7 were males, ranging in age from 3 to 21 years (mean, 13 years). Non-Hodgkin's lymphoma was not found in STLV-1 antibody-negative baboons. Clinical signs and laboratory findings were variable but generally included lethargy, low body weights, anemia, dyspnea, lymphadenopathy, hepatosplenomegaly, pneumonia, nodular skin lesions, and leukemia with or without multilobulated lymphocytes in peripheral blood. Radiography revealed pulmonary infiltrates consistent with pneumonia in 17 of the baboons. Serum chemical values were normal except for hypercalcemia in one baboon. Lymphocytosis was found in 18 of the baboons, with leukemia diagnosed in 11. At necropsy, variable enlargement of lymph nodes and other lymphopoietic tissue was usually found. Pale tan to white space-occupying foci typical of proliferative lymphoid tissue were often found in various organs, including lungs, spleens, livers, skin, and hearts. The lungs in 14 baboons had thickened pleuras, congestion,edema, and large tan to brown areas of consolidation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneously generated non-Hodgkin's lymphoma in twenty-seven simian T-cell leukemia virus type 1 antibody-positive baboons (Papio species). 790 50

We describe the clinical and laboratory features of nine patients born in Chile with HTLV-I-positive adult T-cell leukemia/lymphoma (ATLL). All were adults (median age 51 years) of Caucasian origin without evidence of Indian or foreign extraction and none had been out of the country. The main disease features were organomegaly, cutaneous lesions, hypercalcemia and leukemia with atypical polylobed lymphocytes displaying a CD2+, CD3+, CD4+, CD8-, CD7- T-cell phenotype. Eight patients presented with acute type ATLL and one had a chronic form lasting for 16 months prior to the development of the acute phase. Lymph node histology (three cases) was consistent with a T-cell non-Hodgkin's lymphoma (large and small cells). Antibodies to HTLV-I were detected by ELISA and particle agglutination in the serum from eight of nine patients. DNA analysis showed HTLV-I proviral DNA in all seven cases investigated, including the single serologically negative patient. In five cases, HTLV-I was monoclonally integrated and in one case oligoclonal. In the seventh case viral DNA clonal status was ambiguous. Response to therapy was poor and median survival was 3 months (range 2-20 months). This study provides further evidence that HTLV-I is endemic in Chile, a non-tropical country where the two main diseases associated with HTLV-I, ATLL and TSP, are found.
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PMID:HTLV-I positive adult T-cell leukaemia/lymphoma (ATLL) in Chile. 793 73


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