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/lymphoma (ATLL) remains an uncommon disorder outside well-defined risk groups. We describe the case of an Iranian woman, who presented with isolated meningeal relapse of diffuse large-cell lymphoma. The malignant cells coexpressed CD4 and CD8 and HTLV-1 seropositivity was confirmed. Despite combination chemotherapy disseminated lymphoma developed. Preterminally the characteristic features of ATLL were noted; hypercalcemia, with normal parathyroid hormone-related protein and vitamin D levels, and peripheral blood leukemic involvement.
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PMID:Lymphomatous presentation of CD4+/CD8+ HTLV-1-related adult T-cell leukemia/lymphoma in an Iranian woman. 818 Jun 10

We described a case of adult T cell leukemia (ATL) not associated with human T-cell leukemia virus type I (HTLV-I), a clinical entity that was first reported by Shimoyama et al. A 79-year-old male was admitted with anorexia and fever in October, 1989. Physical examination revealed marked hepatosplenomegaly and superficial lymphadenopathies. Hematological examination revealed marked leukocytosis (136,300/microliters) with abnormal lymphoid cells showing highly lobulated nuclei. Hypercalcemia (11.2 mg/dl) and elevation of lactic dehydrogenase were also recognized. Surface marker analysis showed that the abnormal lymphoid cells in the peripheral blood were positive for CD2 and CD4 but negative for CD8. Southern blot analysis of the DNA from peripheral blood leukemic cells revealed monoclonal rearrangement of T-cell receptor beta-chain gene. The clinical and hematological findings of the patient were compatible with those of acute type ATL, however, serum anti-HTLV-I antibody was negative and HTLV-I proviral DNA was not detected in the leukemic cells by Southern blot analysis. Furthermore, the polymerase chain reaction showed no integration of the HTLV-I proviral DNA in the leukemic cells.
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PMID:[HTLV-I negative adult T cell leukemia; a case report of acute type]. 829 28

We recently reported that mice treated with 1,25-dihydroxyvitamin D3 ( 1,25-(OH)2D3) or 19-nor-1,25-(OH)2D2 experienced a severe loss of their thymocytes and decreased proliferation in response to concanavalin A mitogen. The present study investigated the effect of short-term treatment with 1,25-(OH)2D3 on the thymic architecture and thymocyte subsets. Daily treatment with 1,25-dihydroxyvitamin D3 at 20 ng per mouse for 4 days induced significant involution of thymic tissue. The atrophy was predominantly observed in the cortical component. Flow cytometric analysis of thymocyte subsets showed that the CD4 + CD8 + population was the primary target. Since the treated mice experienced profound hypercalcemia, we studied the effect of 1,25-(OH)2D3 on animals fed a vitamin D-deficient, low calcium diet or the same diet containing vitamin D for 25 days prior to treatment. The low calcium fed mice showed severe hypocalcemia and slight thinning of thymic cortex. Treatment with 1,25-(OH)2D3 moderately improved the hypocalcemia but had no further effect on the thymus of these animals. On the other hand, hypercalcemia and thymic atrophy were found in the animals fed the diet containing vitamin D. Overall, the atrophy effect on the thymus caused by 1,25-(OH)2D3 treatment was prevented by eliminating the hypercalcemia observed in + D + Ca treated animals. Thus, thymic atrophy probably resulted from hypercalcemia and not from 1,25-(OH)2D3 itself.
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PMID:Effect of 1,25-dihydroxyvitamin D3 on mouse thymus: role of extracellular calcium. 860 Sep 85

A patient with adult T-cell leukemia (ATL) characterized by a suppressor phenotype is reported. A 52-year-old mulatto male presented with symptoms and signs of hypercalcemia. His laboratory finding disclosed a peripheral blood specimen with abnormal cells characterized by a rather pleomorphic morphology and polylobated nucleous typical of ATL cells. Serum calcium and LDH were 18.2 mg/dl and 1373 IU, respectively. The phenotype of these cells was CD2+, CD4-, CD8+, CD28+ associated with the expression of activated antigens such as CD25, CD38, CD71 and CD30. Ki-67 positive were found in 20% of cells. The argyrophilic stain for nuclear organizer regions (AgNORs) was shown one cluster in 35% of abnormal cells. The serum antibodies were positive against human T-cell lymphotropic virus type I (HTLV-I) and clinical features were compatible with the diagnosis of ATL acute type. The combination therapy with cyclophosphamide, vincristine, prednisone decreased the number of leukemic cells but the clinical course was aggressive. He only responded transiently to treatment and died of multiorgan failure due to uncontrollable septicemia two weeks after admission.
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PMID:Adult T-cell leukemia (ATL) with an unusual immunophenotype and a high cellular proliferation rate. 888 68

A 42-year-old man was diagnosed with acute adult T-cell leukemia/lymphoma (ATL/L). Abnormal peripheral blood cells (45% of white blood cells) (Fig. 1a), hypercalcemia, and systemic lymphadenopathy were observed. Flow cytometric analysis (FCM) using peripheral mononuclear cells (PMNC) revealed that the immunophenotype of tumor cells was CD4+ CD8- CD25+ CD45RA- CD45RO+. Nevertheless, he developed a spontaneous remission 6 months later. At remission, the number of CD4-, CD25-, and CD45RO-positive cells decreased, while CD8- and CD45RA-positive cells increased to normal levels as previously reported by Suzuki et al. [1]. He was then referred to the outpatient clinic where he was periodically evaluated and received no therapy. Because of a serious sense of fullness he was re-admitted 30 months after diagnosis. Physical examination revealed ascites and small lymphadenopathy in the right axilla. Atypical lymphoid cells were not observed on microscopic examination of the blood smear. FCM using PMNC revealed that CD4+ CD25+ cells (3%) were within the normal range. Serum calcium was also within the normal range. Abdominal ultrasound examination showed massive ascites. Paracentesis demonstrated that the ascitic fluid had a high white blood cell count (3.15 x 10(9)/l) with a marked increase in abnormal large cells (Fig. 1b). FCM using mononuclear cells in the fluid revealed that 87.3% of the cells were double-positive for CD4 and CD25. Southern blot analysis of the cells confirmed monoclonal integration of human T-lymphotropic virus type 1 (HTLV-1) proviral DNA. The integrated genome was considered to be identical with that detected at initial presentation (Fig. 2). A diagnosis of relapsed ATL/L, with the same clone as was detected at initial diagnosis, was made. Although he was treated with cytotoxic drugs, he did not respond and he died of renal failure 1 month after relapse. Autopsy revealed nodular invasive lesions at the rectovesical pouch, omentum, diaphragm, and pericardium with peritoneal dissemination.
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PMID:Unusual relapse of adult T-cell leukemia/lymphoma after spontaneous remission. 959 77

Adult T-cell leukemia/lymphoma(ATL) was first discovered and reported in Japan, where it has a high incidence in the southwestern region of the country. The retrovirus human T-cell leukemia virus type I(HTLV-I) is considered to be related to its etiology. ATL shows divers clinical features. It can be divided into four types of smoldering, chronic, acute, and lymphoma. ATL cells originate from the CD4-positive subset of peripheral T cells showing a characteristic notch in the nucleus and a tendency for lobulation. A definit diagnosis of ATL is made by documenting the presence of HTLV-I proviral DNA in the DNA of leukemic or lymphoma cells. Crinico-Pathological aspects of ATL are more complexed than other types of lymphoma because of the verity of the disease type, state of immunodeficiency, hypercalcemia, cytokine activation, and so on.
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PMID:[Clinico-pathological aspects of adult T-cell leukemia/lymphoma(ATL)]. 1074 Nov 41

We describe the case of a patient with acquired immunodeficiency syndrome (AIDS) who had a CD4 cell count of 60/microL, bilateral hilar adenopathy, and hypercalcemia. Transbronchial biopsy showed T-cell anaplastic large cell lymphoma. Serology was negative for human T-cell leukemia virus-I (HTLV-I). This appears to be the first case of T-cell anaplastic large cell lymphoma occurring in an AIDS patient with hypercalcemia who was seronegative for HTLV-I.
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PMID:Hypercalcemia and T-cell lymphoma with acquired immunodeficiency syndrome: occurrence without human T-cell leukemia virus-I. 1100 50

Sarcoidosis is a multisystem granulomatous disease of unknown origin. No single biological marker allows definitive diagnosis of sarcoidosis or may accurately predict the disease prognosis. However, some biological markers are helpful tools as diagnostic aids and disease activity markers. At the blood level, lymphopenia with CD4 depletion, elevated levels of serum-angiotensin converting enzyme, lyzozyme, beta 2 microglobulin and disturbed calcium metabolism resulting in hypercalcemia and hypercalciuria can help guide diagnosis. Lymphocytic alveolitis with a high CD4/CD8 ratio in bronchoalveolar lavage fluid is highly suggestive of the disease. A wide range of new biological markers are proposed but their pronostic significance is still controversial. In clinical practice, biological markers may help in monitoring treated patients with sarcoidisis.
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PMID:[Biological manifestations of sarcoidosis]. 1124 Apr 24

T-cell leukemia/lymphoma (T-c LL) associated with prior infection with HTLV-I is rarely described in children. We present herein, the clinical, morphological, and virologic features of T-c LL, which occurred in eight pediatric cases with similar features of ATLL described in adults. There were three girls and five boys with age ranging from 2 to 18 years. Lymphoadenopathy, hepatosplenomegaly and marked skin lesions were presented in all cases. Five patients had hypercalcemia. The diagnostic criteria of T-c LL were based on both morphological and immunophenotypical analyses characterized by T-cell markers positively. Seven cases were cCD3+, CD4/CD25+, whereas CD1a and TdT were negative in all cases tested. HTLV-I antibodies were detected in all cases. HTLV-I provirus integration of at least one provirus was seen in all cases tested by molecular analysis. Mother-to-child transmission of HTLV-I was demonstrated in six cases. Interestingly, a homozygous deletion in p16 gene locus was observed in all four cases studied, while exons 7 and 8 of p53 were deleted in one child. The deletion of the p16(INK4A)/p14(ARF) or mutation of p53, key regulatory protein of cell cycle checkpoint in G1/S progression, found in five of the eight pediatric patients suggests that in these cases genetic lesions associated with HTLV-I infection may predispose for an early onset of leukemia.
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PMID:Genetic mutation and early onset of T-cell leukemia in pediatric patients infected at birth with HTLV-I. 1175 65

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


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