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)

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

Patients with cancer are especially vulnerable to the development of hyper- and hypocalcemia. These disorders may be the basic clinical manifestation of cancer or may result from vigorous cancer treatment. During cytotoxic treatment of a child with leukemia we describe the longitudinal course of ionized calcium in a complex syndrome of hypocalcemia and hypoparathyroidism. The results suggest that the development of severe hypocalcemia can be explained on the basis of hypoparathyroidism in relation to hyperphosphatemia, hypomagnesemia, and acute renal failure. The low ionized calcium was unsuccessfully treated with several doses of calcium levulinate but successfully treated with 1 alpha-hydroxycholecalciferol.
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PMID:Complex biochemical syndrome of hypocalcemia and hypoparathyroidism during cytotoxic treatment of an infant with leukemia. 345 55

A case of Burkitt's lymphoma cell leukemia with recurrent hypophosphatemia that coincided with tumor growth, and hyperphosphatemia during tumor lysis is presented. Redistribution of body phosphorus with increased uptake by the rapidly replicating tumor cells is suggested. Tumor genesis syndrome seems to us to be a proper term to include metabolic abnormalities that result directly from tumor growth.
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PMID:Tumor genesis syndrome. Hypophosphatemia accompanying Burkitt's lymphoma cell leukemia. 372 4

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

Tumor lysis syndrome (TLS) is a rare serious acute complication of cancer therapy, reported mainly following chemotherapy in patients with large tumor load and chemosensitive disease. These are mainly patients with non-Hodgkin's lymphoma, leukemia and rarely in solid tumors. It is less frequently described after radiotherapy for lymphoid and hematological malignancies. TLS following radiotherapy for solid tumors is a very rare complication. In this report/review we describe a seventy-three-year-old male patient with progressive metastatic carcinoma of the breast to the lungs, liver and bone. He was referred for radiotherapy because of generalized bony pains. The patient was planned for sequential hemi-body irradiation starting with the more symptomatic upper half body. After premedication, he was given 8.5 Gy to the mid point at the maximum chest separation with anterior lung attenuator limiting uncorrected lung dose to 6.15 Gy. A further 3.5 Gy electron boost to the fungating breast tumor was given to the 100%. Forty-eight hours after irradiation he developed hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia and renal failure. These clinical and biochemical changes are typical of tumor lysis syndrome (TLS). Despite hydration, and treating the hyperuricemia, the patient developed coma and died eight days after irradiation. The prophylaxis and management of TLS and in high-risk patients are described to avoid this frequently fatal complication.
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PMID:Tumor lysis syndrome following hemi-body irradiation for metastatic breast cancer. 1110 26

Acute tumor lysis syndrome (TLS) is a catastrophic complication of the treatment of certain neoplastic disorders. It most commonly occurs in association with hematologic malignancies and manifests a few hours to a few days after initiation of specific chemotherapy. Acute spontaneous TLS has been described in leukemia and lymphoma and in some patients with solid tumors prior to institution of therapy. The findings that may be seen in acute TLS include hyperphosphatemia, hypocalcemia, hyperuricemia, hyperkalemia, and acute oliguric or anuric renal failure due to uric acid precipitation within the tubules (acute uric acid nephropathy) and to calcium phosphate deposition in the renal parenchyma and vessels. We report here a case of acute spontaneous TLS (high grade B-cell lymphoma of the right colon) in which serum uric acid concentration attained exceptionally high levels (36.7 mg/dL). The patient underwent acute oliguric renal failure soon after right colectomy. He was treated by means of a large infusion of saline. The renal function recovered in such a rapid way that no dialysis treatment was required. In conclusion the present case report has two peculiarities: that of being one of the rare examples of spontaneous TLS, and that of showing an exceptionally severe hyperuricemia, probably the highest ever reported in the literature. The administration of a large volume of saline was able to ensure a complete recovery of renal function. Therefore, hydration with saline remains the keystone in the prevention and treatment of acute TLS.
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PMID:[An exceptionally severe hyperuricemia in acute renal failure caused by spontaneous tumor lysis syndrome (TLS)]. 1463 69

Authors present the case of 15-year-old girl with diagnosed pre T-acute lymphoblastic leukaemia with hyperleukocytosis--at admission 213 x 10(9)/l. At clinical evaluation a major peripheral and abdominal lymphadenopathy, mediastinal mass, hepatosplenomegaly were revealed. After administration of prednisone for two times--11.4 mg/m2/24 h--the features of tumour lysis syndrome rapidly increased. Hyperphosphatemia, hyperkalemia and hyperuricemia resulted in acute renal failure. Renal replacement therapy was introduced with simultaneous application of cytoreduction phase therapy and induction of remission according to New York protocol. Total number of performed hemodialysis sessions was 12. Obtained haematological remission in 8th week of treatment is still present. Renal function remains normal. Remission supportive treatment has been continued according to above-mentioned protocol.
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PMID:[Tumor lysis syndrome in the course of acute lymphoblastic leukemia as the consequence of prednisone monotherapy]. 1464 89

The objective of this study was to determine the frequency of electrolyte perturbations and their relationship with leukemic status before and after chemotherapy in patients with acute lymphocytic leukemia. Blood biochemistry, liver and renal function tests, and renal sonograms were examined at diagnosis and during induction therapy in 334 patients. Renal and electrolyte disturbances were then studied in 116 patients between 3 and 110 months after cessation of the St. Jude chemotherapy treatment protocol. Glomerular filtration rate, electrolyte, protein, and beta-2-microglobulin levels were determined in fresh urine samples, and serum electrolyte levels were examined in blood samples. Renal sonographic examinations and scintigraphic examinations were performed with DMSA and MAG-3. Renal leukemic involvement was detected by sonographic examination in 32 patients who had also presented with hyperphosphatemia or hyperuricemia. Patients with electrolyte disorders at diagnosis were less likely to have tumor lysis syndrome during induction chemotherapy. This may be explained by correction of their electrolyte disorders at the time of diagnosis, which may protect them from tumor lysis syndrome. Hypocalcemia and hyponatremia at the time of diagnosis were found to be significant initial risk factors for renal scan abnormalities and microproteinuria, respectively, during the late therapy period (P < 0.05). Electrolyte abnormalities and renal changes were commonly observed before and after therapy for leukemia. Patients presenting with hypocalcemia and hyponatremia should be examined for microproteinuria and should undergo renal scanning during the late therapy period.
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PMID:Electrolyte abnormalities at diagnosis of acute lymphocytic leukemia may be a clue for renal damage in long-term period. 1583 91

Tumor lysis syndrome is a life-threatening complication of chemotherapy for patients with leukemia and large tumors with a high proliferative index, such as Burkitt's lymphoma. The syndrome is characterized by hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. The standard of care for hyperuricemia consists of hydration with or without alkalinization and administration of allopurinol. When treated in this manner, patients often experience persistent hyperuricemia that lasts several days after the start of antineoplastic therapy; sometimes they develop uric acid nephropathy as a consequence. Rasburicase, a recombinant urate oxidase enzyme, quickly removes large amounts of uric acid from plasma. The drug is approved by the United States Food and Drug Administration for management of elevated plasma uric acid levels in pediatric patients with leukemia, lymphoma, or solid tumor malignancies who are receiving chemotherapy. We undertook a retrospective review of adult patients treated with a single dose of rasburicase 6 mg for hyperuricemia associated with malignancy. Ten patients received one 6-mg dose of rasburicase, and one patient received two 6-mg doses as an adjuvant therapy to normalize uric acid levels. In most of the patients, a single 6-mg dose of rasburicase was effective in correcting uric acid levels in the typical time between diagnosis and start of antineoplastic therapy.
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PMID:Reduced-dose rasburicase in the treatment of adults with hyperuricemia associated with malignancy. 1646 28


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