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)

Thirteen leukemic patients with disease refractory to conventional chemotherapy were treated with 1.0 to 7.5 g/m2 of Cytosine Arabinoside (Ara-C) over 29 drug cycles. Drug infusions were spaced at 12-hour intervals; a maximum of four doses was administered over 36 hours. After single dose tolerance had been established, three or four dose cycles were given at 2- to 30-day intervals. There were three partial remissions (PR) and one complete remission (CR) in a treatment group of four patients with AML, five with ALL, two with lymphoma converted to leukemic phase, one CML in blast crisis, and one promyelocytic leukemia. Five of the patients were septic and considered terminally ill at the time of treatment. All other patients had evidence of drug responsiveness. The nadir of the white count occurred from 3 to 12 days after treatment, with subsequent recovery of the peripheral granulocyte count between days 12 and 28. Toxicity included nausea and vomiting (GI symptoms) in twelve patients, central nervous system (CNS) disturbances in eight patients, one episode of inappropriate antidiuretic hormone syndromes (SIADH), one of hyperuricemia, and fever in eleven patients. There was no evidence of hepatic or renal dysfunction. These high doses of Ara-C appear useful for treatment of patients with refractory leukemia. Hospitalization is brief and toxicity acceptable.
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PMID:High dose cytosine arabinoside (HDARAC) in refractory acute leukemia. 49 9

The tubules appear to be the primary sites of injury in renal failure and urate nephropathy associated with leukemia. Tubular injury is not always associated with precipitation and phagocytosis of crystals, except in the collecting tubules where cellular changes are invariably caused by intraluminal crystallization of urates. The electron microscopical observations in this communication may apply to the urate nephropathy associated with hyperuricemia of various causes.
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PMID:Leukemic urate nephropathy. 105 83

A clinicopathological study of leukemic kidney was carried out by observing the changes of the kidney in 104 autopsied cases of leukemia. The main changes of the leukemic kidney were increase of renal weight, calcinosis of renal tubules, interstitial leukemic cell infiltration, intravascular stasis and renal bleeding. Calcinosis intravascular stasis, renal bleeding as well as hyperuricemia may lead to abnormal urinary findings. The presence and severity of interstitial infiltration have no obvious relation with the level of blood urea nitrogen, creatinine and muric acid as well as the abnormal change of the urine. However, the presence of intravascular stasis by leukemic cells are correlated with the disturbance of renal function.
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PMID:[A clinicopathological study of leukemic kidney]. 139 26

In this article, the acid-base disturbances encountered in hematologic diseases are discussed. Occurrence of lactic acidosis (LA) without obvious clinical tissue hypoxia has been reported in patients with leukemia and lymphoma. Most of the patients with LA had liver involvement and clinical evidence of impaired hepatic function, suggesting that both increased production and decreased lactate metabolism are necessary for the development of LA in leukemia and lymphoma. Acute tumor lysis syndrome consists of hyperuricemia, hyperpotassemia, and hyperphosphatemia with hypocalcemia following neoplastic cell lysis, particularly in lymphoproliferative disorders. In patients with multiple myeloma (MM), proximal renal tubular acidosis (Fanconi syndrome) associated with Bence Jones proteinuria has been reported. In addition, MM is one of the first conditions recognized to be associated with lower anion gap.
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PMID:[Acid-base disturbances in hematologic diseases]. 143 14

The acute tumor-lysis syndrome is a potentially fatal complication which characteristically arises during initial chemotherapy of malignant hematological diseases with large tumor burdens. The syndrome is characterized by hyperphosphatemia, hypocalcemia, hyperuricemia and often acute renal failure. Prior to chemotherapy the patient should be treated for 12-24 hour with intensified diuresis to ensure optimal renal function. The treatment of the fully developed syndrome is hemodialysis. Three cases of TLS which developed during initial chemotherapy of patients with acute lymnphoblastic leukemia and non-Hodgkin lymphoma are presented.
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PMID:[Metabolic disorders in the treatment of malignant hematologic diseases--the acute tumor lysis syndrome]. 194 22

Hyperuricemia is an unusual presenting feature of acute lymphoblastic leukemia (ALL) and is generally associated with a large leukemic cell burden. We describe three children with T-cell ALL who presented with acute renal failure and very high serum uric acid concentrations, despite a relatively small leukemic cell burden. Two of the three patients had normal complete blood counts without circulating blasts or other physical evidence of leukemia. An isolated renal relapse in one case was associated with hyperuricemia, increased renal excretion of uric acid, and renal dysfunction. An unusually high rate of purine catabolism of the lymphoblasts may cause hyperuricemia in these cases. Unexplained hyperuricemia should prompt a search for occult malignancy.
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PMID:Renal dysfunction and hyperuricemia at presentation and relapse of acute lymphoblastic leukemia. 235 88

A patient with a disseminated small cell tumor presented with hyperuricemia, gingival hypertrophy, lymphadenopathy, and bone marrow replacement with tumor cells. Initial histologic examination and clinical presentation were consistent with presumed marker silent lymphoma/leukemia. Despite initial treatment with and response to lymphoma/leukemia therapy the patient relapsed in the testis, bone marrow, pancreas, and skin whereupon subsequent and retrospective immunocytochemical, ultrastructural, cytogenetic, and molecular analysis led to the diagnosis of primitive neuroectodermal tumor (PNET). Despite extensive investigation and autopsy no primary site of tumor could be found demonstrating that PNET should be considered in the differential diagnosis of disseminated small cell tumors without an apparent primary.
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PMID:Disseminated primitive neuroectodermal tumor: diagnosis using immunocytochemistry, electron microscopy, and molecular probes. 254 89

Renal failure in patients with lymphoma or leukemia may be brought about by different causes, including ureteral obstruction, hypercalcemia, hyperuricemia, amyloidosis, immunologically mediated nephrosis and paraproteinemic nephropathy. Lymphomatous or leukemic infiltration of the kidneys is a frequent finding at autopsy but is rarely seen as a cause of renal failure. In this report three patients with lymphomatous infiltration of the kidneys causing renal failure are described. Clinical and laboratory criteria for establishment of diagnosis in such cases are suggested. Using these diagnostic criteria, a renal biopsy may not be necessary.
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PMID:[Renal insufficiency due to lymphomatous infiltration of the kidney: report of 3 cases and review of the literature]. 281 88

A program in chemotherapy is described in which antimetabolites to constituents of nucleic acids were used as probes of enzymes and metabolic pathways. These studies led to a number of insights into nucleic acid biosynthesis and related biochemical fields. They also provided exploitable information that was developed into drugs for the treatment of leukemia, the prevention of rejection of organ transplants, and a new therapy for hyperuricemia and gout. Studies on infectious diseases provided insights into the modeling of inhibitor-enzyme complexes and led to new and effective antimicrobial and antiviral agents. Basic research and relative absences of specific targeting are shown to have greatly facilitated the progress of the program.
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PMID:A biochemical approach to chemotherapy. 689 Aug 94

We report on a 14-year-old boy with acute lymphoblastic leukemia (lymphoma-leukemia) who had two episodes of acute tumor lysis syndrome during induction of remission with oral prednisolone alone and oral prednisolone, intravenous vincristine, and doxorubicin, respectively. Subsequently he had severe hyperphosphatemia (29.3 and 14.1 mg/dl; 9.46 and 4.55 mmol/L), hypocalcemia, hyperuricemia, hyperkalemia, and azotemia. Multiple stones and tumor cells infiltration were demonstrated in both kidney. He responded favorably to hemodialysis.
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PMID:Severe hyperphosphatemia following acute tumor lysis syndrome. 796 98


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