allopurinol and Hypocalcemia

Tumour lysis syndrome (TLS) is a life-threatening emergency characterised by a massive cytolysis with the release of intracellular electrolytes, nucleic acids, and metabolites into the circulation. TLS comprises laboratory derangements (hyperuricaemia, hyperkalaemia, hyperphosphataemia, and hypocalcaemia) responsible for acute kidney injury. In patients with hematologic malignancies after cytotoxic therapy or spontaneously and also in advanced solid tumours. Assessment of disease specific risk level for TLS in patients receiving anti-tumoural therapy is essential for early diagnosis. Prophylaxis is the mainstay of management of TLS. It is important to routinely initiate a risk-adapted prophylactic strategy to correct metabolic alterations and preserve renal function. High and intermediate risk patients and patients with established TLS should be managed with multidisciplinary medical care in a hospital unit to receive monitoring and medical care. Renal replacement therapy should be considered in patients with refractory TLS.

Topics: Acute Kidney Injury; Allopurinol; Combined Modality Therapy; Fluid Therapy; Humans; Hyperkalemia; Hyperphosphatemia; Hyperuricemia; Hypocalcemia; Prognosis; Renal Replacement Therapy; Risk Factors; Severity of Illness Index; Tumor Lysis Syndrome; Urate Oxidase

Tumor lysis syndrome (TLS) is an oncologic emergency triggered by the rapid release of intracellular material from lysing malignant cells. Most common in rapidly growing hematologic malignancies, TLS has been reported in virtually every cancer type. Central to its pathogenesis is the rapid accumulation of uric acid derived from the breakdown of nucleic acids, which leads to kidney failure by various mechanisms. Kidney failure then limits the clearance of potassium, phosphorus, and uric acid leading to hyperkalemia, hyperphosphatemia, and secondary hypocalcemia, which can be fatal. Prevention of TLS may be more effective than treatment, and identification of at-risk individuals in whom to target preventative efforts remains a key research area. Herein, we discuss the pathophysiology, epidemiology, and treatment of TLS with an emphasis on the kidney manifestations of the disease.

Topics: Acute Kidney Injury; Allopurinol; Bicarbonates; Buffers; Calcium; Diuretics; Enzyme Inhibitors; Febuxostat; Fluid Therapy; Humans; Hyperkalemia; Hyperphosphatemia; Hyperuricemia; Hypocalcemia; Renal Dialysis; Thiazoles; Tumor Lysis Syndrome; Urate Oxidase

The tumor lysis syndrome (TLS) is a life-threatening complication caused by the massive release of nucleic acids, potassium and phosphate into the blood. This complication is the result of tumor cell lysis, which may occur due to treatment of drug sensitive and is characterized by rapid capacity of proliferation, that is often hematological origin. Moreover, the TLS can be observed before starting the treatment due to spontaneous tumor cell death, and frequently worsens when chemotherapy is initiated. TLS has high mortality, so that its prevention continues to be the most important therapeutic measure. In the intensive care unit (ICU), physicians should be aware of the clinical characteristics of TLS, which results in severe electrolyte metabolism disorders, especially hyperkalemia, hyperphosphatemia and hypocalcemia, and acute kidney injury which is a major cause of ICU mortality. An adequate strategy for the management of the TLS, combining hydration, urate oxidase, and an early admission to ICU can control this complication in most patients. The aim of this review is to provide diagnostic tools that allow to the ICU physician to recognize the population at high risk for developing the TLS, and outline a proper strategy for treating and preventing this serious complication.

Topics: Acute Kidney Injury; Allopurinol; Antineoplastic Agents; Arrhythmias, Cardiac; Chelation Therapy; Clinical Trials as Topic; Combined Modality Therapy; Critical Care; Fluid Therapy; Humans; Hyperkalemia; Hyperphosphatemia; Hypocalcemia; Incidence; Multicenter Studies as Topic; Prognosis; Renal Replacement Therapy; Risk Factors; Severity of Illness Index; Tumor Lysis Syndrome; Urate Oxidase

Tumor lysis syndrome (TLS) is a serious complication of malignancies and can result in renal failure or death.. In tumors with a high proliferative rate with a relatively large mass and a high sensitivity to cytotoxic agents, the initiation of therapy often results in the rapid release of intracellular anions, cations and the metabolic products of proteins and nucleic acids into the bloodstream. The increased concentrations of uric acid, phosphates, potassium and urea can overwhelm the body's homeostatic mechanisms to process and excrete these materials and result in the clinical spectrum associated with TLS. Typical clinical sequelae include gastrointestinal disturbances, neuromuscular effects, cardiovascular complications, acute renal failure and death. Tumor lysis syndrome can also compromise the efficacy or administration of curative therapies. Available evidence suggests that the incidence of clinical TLS is approximately 3-7% for acute leukemias and 4-11% for lymphomas. Pediatric cancers are the leading cause of death by disease in children. The most common pediatric cancers include the leukemias, lymphomas, central nervous system tumors and neuroblastoma. Thus, TLS is a major concern to practitioners caring for pediatric oncology patients. Given the complexity of TLS prevention and treatment, a multidisciplinary approach involving the collaboration of medical oncologists/ hematologists and nephrologists has the greatest potential of ensuring optimal patient outcomes. Rehydration is fundamental in the management of TLS in addition to the current standard therapy for hyperuricemia which include rasburicase and allopurinol.. The early recognition and treatment of metabolic abnormalities often prevents the severe and life-threatening complications associated with tumor lysis syndrome.

Topics: Acute Kidney Injury; Allopurinol; Child; Fluid Therapy; Gout Suppressants; Humans; Hyperkalemia; Hyperphosphatemia; Hyperuricemia; Hypocalcemia; Tumor Lysis Syndrome; Urate Oxidase

To identify patients with lymphoma at risk for tumor lysis after chemotherapy.. The case records of 102 patients receiving combination chemotherapy for non-Hodgkin's lymphoma (intermediate to high-grade histology) were reviewed. Patients were considered to have "laboratory tumor lysis" if two of the following metabolic changes occurred within 4 days of treatment: a 25% increase in the serum phosphate, potassium, uric acid, or urea nitrogen concentrations, or a 25% decline in the serum calcium concentration. "Clinical tumor lysis" was defined as laboratory tumor lysis plus one of the following: a serum potassium level greater than 6 mmol/L, a creatinine level greater than 221 mumol/L, or a calcium level less than 1.5 mmol/L, the development of a life-threatening arrhythmia, or sudden death.. Laboratory tumor lysis occurred in 42% of patients and clinical tumor lysis in 6%. There was no statistical difference in the frequency of either tumor lysis syndrome among lymphoma subgroups. Clinical tumor lysis occurred more frequently in patients with pretreatment renal insufficiency (serum creatinine level greater than 132 mumol/L) than in patients with normal renal function (36% versus 2%; p = 0.01). The development of azotemia correlated with high pretreatment serum lactate dehydrogenase concentrations (p < 0.01; r2 = 0.11).. Clinically significant tumor lysis is a rare occurrence in patients with lymphoma when they are receiving allopurinol. However, tumor lysis can occur in patients with all types of moderate to high-grade non-Hodgkin's lymphoma. Patients with a high serum lactate dehydrogenase level or renal insufficiency are at increased risk for metabolic complications after chemotherapy and should be closely monitored.

Topics: Acute Disease; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Blood Urea Nitrogen; Burkitt Lymphoma; Creatinine; Humans; Hyperkalemia; Hypocalcemia; L-Lactate Dehydrogenase; Leukemia, Lymphocytic, Chronic, B-Cell; Lymphoma, Large B-Cell, Diffuse; Lymphoma, Non-Hodgkin; Lymphoma, T-Cell; Phosphates; Renal Insufficiency; Retrospective Studies; Risk Factors; Tumor Lysis Syndrome; Uric Acid

Topics: Allopurinol; Causality; Fluid Therapy; Gout Suppressants; Humans; Hyperkalemia; Hyperphosphatemia; Hypocalcemia; Neoplasms; Nurse's Role; Nursing Assessment; Oncology Nursing; Patient Education as Topic; Risk Assessment; Tumor Lysis Syndrome; Urate Oxidase

Metabolic abnormalities occur relatively frequently in lymphoma patients undergoing chemotherapy. These abnormalities include hyperuricemia, hypercalcemia, hyperphosphatemia, hypocalcemia, hypomagnesemia, hyponatremia, and hyperkalemia. In addition, tumor lysis syndrome can result in several metabolic abnormalities, leading to potential renal failure. If these syndromes are identified promptly, they can be corrected. Guidelines for identifying metabolic abnormalities in lymphoma patients, as well as management suggestions, are presented

Topics: Adult; Allopurinol; Anthracyclines; Cell Division; Creatinine; Enzyme Inhibitors; Humans; Hypocalcemia; Hypophosphatemia; Lymphoma; Male; Renal Insufficiency; Time Factors; Tumor Lysis Syndrome; Urate Oxidase; Uric Acid

In two patients, metabolic complications, previously unreported to our knowledge, of severe hyperphosphatemia and hypocalcemia in addition to hyperkalemia nad hyperuricemia were demonstrated after treatment with cyclophosphamide. In one patient, elevated blood and ascites lactate levels were measured. The levels decreased rapidly to normal following chemotherapy. The hyperphosphatemia and hyperkalemia may have been due to rapid tumor lysis and the hypocalcemia may have been caused by the hyperphosphatemia. The reduction in blood and aseties lactate levels may reflect the lysis of anaerobically metabolising tumor cells. Renal dialysis was required in the management of both cases. Because of the potential for cardiac arrythmias related to electrolyte imbalance, it is recommended that whenever possible reanl dialysis be available before treating cases of Burkitt lymphoma with large tumor burden.

Topics: Abdominal Neoplasms; Allopurinol; Burkitt Lymphoma; Calcium; Child; Child, Preschool; Cyclophosphamide; Humans; Hypocalcemia; Lactates; Male; Methotrexate; Phosphates

Topics: Acute Disease; Allopurinol; Child, Preschool; Humans; Hyperkalemia; Hypocalcemia; Leukemia, Lymphoid; Male; Methotrexate; Prednisone; Uric Acid

Topics: Adolescent; Allopurinol; Asparaginase; Blood Urea Nitrogen; Calcium; Calcium, Dietary; Child; Creatinine; Humans; Hypocalcemia; Kidney Tubules; Leukemia, Lymphoid; Leukocyte Count; Lymphocytes; Male; Phosphates; Prednisone; Prospective Studies; Uric Acid; Vincristine