Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes insipidus (DI) is a rare complication of leukaemia. An association between monosomy 7 and DI in leukaemias has been proposed. We present a case of Ph1-positive CML who developed polyuria at the time of lymphoid blast transformation associated with loss of chromosome 7. Biochemical results were not diagnostic of DI and a therapeutic trial of DDAVP was unsuccessful. Post-mortem showed a peripituitary and renal leukaemic infiltrate and although DI is a possibility, the cause of his polyuria remains unresolved.
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PMID:A patient with monosomy 7 and polyuria. 163 85

A boy, aged 14 1/2 years, presented with Burkitt leukemia. His renal status was normal before treatment. Chemotherapy (SFOP LMB 86 protocol) was begun Oct. 9, 1986. After the first 2 courses of chemotherapy, the patient had Gram negative sepsis treated with cefotaxime, netilmycine, Vancomycin and ornidazole. During sepsis, nephrotic syndrome developed (albumin 25 g/l, non selective proteinuria 15 g/24 h), with moderately high blood pressure, functional renal failure (creatinine 141 mumols/l, U/P urea = 20), polyuria and tubular damage. Kidney ultrasonography was normal. Needle biopsy showed minimal glomerular lesions, acute tubular lesions, and no deposits in immunofluorescence. The nephrotic syndrome disappeared within 3 weeks, with treatment of leukemia. He is at present in complete remission with a follow-up of 25 months.
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PMID:[Nephrotic syndrome and B leukemia]. 262 44

An 18-year-old male patient who had suffered from polyuria, nocturia and easy fatigability since childhood is described. A germ cell tumor in the suprahypophyseal region was diagnosed at the age of 13 years, and was treated by cranial irradiation. Growth retardation and other signs of hypophyseal deficiency successively occurred, and human growth hormone was administered for two years and five months from the age of 16 years until acute lymphoblastic leukemia developed. Adriamycin, vincristine and prednisolone therapy induced complete remission, but the patient died of disseminated intravascular coagulation two months later. The relationship between the occurrence of leukemia and administration of growth hormone is discussed.
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PMID:Occurrence of acute lymphoblastic leukemia in a boy treated with growth hormone for growth retardation after irradiation to the brain tumor. 283 38

A 37-year-old man was admitted because of general malaise, slight fever, pain in the knee joint and lower extremities, polydypsia, polyuria and skin lesion in September, 1985. The white blood cell count was 16,920/cmm with 41% of abnormal lymphoid cells with convoluted nuclei, which were compatible with adult T-cell leukemia (ATL). The serum calcium level was 15.1 mg/dl, serum LDH 307 IU/l, and the titer of anti-ATLA antibody in serum x 160. The cell surface phenotype of abnormal lymphocyte was OKT-3+, OKT-4+ and OKT-8-. Therefore the diagnosis of acute ATL was made. He was treated with cisplatin because VEPA therapy was not effective. About five months after the start of chemotherapy, he entered remission with almost complete disappearance of abnormal lymphocyte. The remission continued over twenty-nine months with maintenance therapy by cisplatin alone. The clinical course of this patient suggests that cisplatin could be applied to a case of ATL which is refractory to the conventional treatment.
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PMID:[A case of acute adult T-cell leukemia with long-term remission by cisplatin therapy]. 317 45

A female patient, aged 44, with diabetes insipidus as a complication of acute myelomonocytic leukaemia (AMML) is described. She presented with bleeding, anaemia, polyuria and polydypsia. She was treated with intranasal vasopressin for diabetes insipidus and responded well to treatment. Chemotherapy was administered for the leukaemia and a full remission was achieved. The patient relapsed a few days before final admission to hospital and died of septicaemia 7 months after initial diagnosis. A short review of the literature related to this subject is also presented.
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PMID:Diabetes insipidus as a complication of acute myelomonocytic leukaemia. 657 53

A patient being treated for leukemia received lithium carbonate and ticarcillin for sepsis, and polyuria and severe hypernatremia developed. Although useful in neutropenic patients, the simultaneous use of these drugs may result in life-threatening hypernatremia.
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PMID:Hypernatremia during lithium and ticarcillin therapy. 678 44

An association between primary mediastinal germ cell tumors and hematologic malignancies has been recognized since 1985. We present a patient with a suprasellar germ cell tumor and an associated leukemia. A 20-year-old black female presented in December 1987 with a 6-month history of headaches and weight loss, confusion, polyuria, and polydipsia. Evaluation revealed hypernatremia, normal neurologic examination except poor recall, and an enhancing inhomogeneous suprasellar mass on cranial computed tomography. Biopsy of the mass diagnosed a dysgerminoma, which was treated with craniospinal radiation. In February 1988, the patient developed pancytopenia, which resolved with discontinuation of cimetidine and phenytoin. She did well until June 1988 when she presented with skin lesions over the trunk and extremities. Skin biopsy revealed a leukemic infiltration. She was admitted with a WBC 1,500/microliter (without blasts), Hb 11.6 g/dl, PLT 210,000 microliter. Bone marrow biopsy revealed hypercellularity with 50% blasts, demonstrating mixed-lineage acute myeloblastic leukemia (myelomonocytic-M4; megakaryoblastic-M7). The patient was induced with a standard Ara-C/daunorubicin regimen. Two weeks postinduction, she became septic and expired. An autopsy demonstrated leukemic involvement of the spleen, liver, bone marrow, and skin, without residual dysgerminoma. This represents the first reported case of suprasellar dysgerminoma associated with a mixed-lineage leukemia not related to chemotherapy.
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PMID:Mixed-lineage acute myeloid leukemia associated with a suprasellar dysgerminoma. 784 66

Hyperglycemia may occur as a complication in patients with leukemia during induction therapy with L-asparaginase and steroids. The reported incidence is about 10%. The present report concerns three patients with acute lymphoblastic leukemia (ALL), complicated by hyperglycemia. Their ages were 10, 12, and 9 years, respectively. Past histories were normal, with no diabetes mellitus or other endocrine disorders in their families. Case 1 was an obese boy who developed pancreatitis and diabetic ketoacidosis (DKA) in his remission induction therapy which had included both L-asparaginase and steroids. Cases 2 and 3 both presented with polyuria and elevated postprandial blood sugar. For all patients, insulin was administered to control their blood sugars; the maximal daily dosage of insulin dispensed was 2.1 U/kg, 0.5 U/kg, and 0.7 U/kg, respectively. Increased plasma insulin and C-peptide levels suggestive of insulin resistance were observed in Case 3. The outcome of hyperglycemia in these three patients was good. The symptoms of this complication may vary from mild glucose intolerance to severe, or even fatal, DKA. Thus, periodic determinations of urine glucose and postprandial blood sugar are important for early recognition to prevent further life-threatening consequences.
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PMID:Hyperglycemia induced by chemotherapeutic agents used in acute lymphoblastic leukemia: report of three cases. 828 94

We describe a patient who, at the onset of acute myelomonocytic leukemia, presented with marked polyuria, polydipsia and laboratory findings consistent with diabetes insipidus (DI). He was treated with vasopressin (DDAVP) with a good response and concurrently induced with daunorubicin and conventional doses of cytosine arabinoside. CR was achieved. The vasopressin requirement decreased progressively, but the patient remained DDAVP-dependent after consolidation treatment. He underwent allogeneic BMT, conditioned with busulfan and cyclophosphamide. By day 15 after BMT vasopressin was no longer required and at a follow-up of 9 months the patient has no evidence of DI. In the absence of specific findings, we think it possible that he had leukemic microinfiltration of the hypothalamic-pituitary area. The drugs used for conditioning may have eradicated CNS disease.
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PMID:Recovery from diabetes insipidus associated with AML after a BMT conditioning regimen including busulfan. 843 67

A 52-year-old woman presented with polyuria and polydipsia. A diagnosis of central diabetes insipidus (DI) was made, which turned out to be the first sign of acute myeloid leukemia (AML). Cytogenetic analysis revealed a balanced translocation between chromosome 3 and 12 t(3;12)(q26;p12). The patient was treated with standard induction chemotherapy and vasopressin. Before consolidation chemotherapy could be administered, deep venous thrombosis was diagnosed and leukemia relapsed. Rescue chemotherapy was started. This is the first report of an association between AML with t(3;12) and DI. Its possible pathogenesis is discussed with a review of the literature.
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PMID:Central diabetes insipidus preceding acute myeloid leukemia with t(3;12)(q26;p12). 1071 Sep 39


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