Acute tumour lysis syndrome following a single-dose corticosteroid in children with acute lymphoblastic leukaemia (original) (raw)

Tumor lysis syndrome in pediatric acute lymphoblastic leukemia at tertiary care center

Pakistan Journal of Medical Sciences

Objectives: Tumor lysis syndrome (TLS) is common complication of acute lymphoblastic leukemia (ALL). It is characterized by presence of two or more of hyperkalemia, hyperuricemia, hyperphosphatemia and hypocalcemia. TLS may cause acute kidney injury (AKI), arrhythmias and seizures. Our objective was to determine the frequency of TLS and its biochemical abnormalities in children with ALL. Methods: A retrospective study on 91 children, aged 2-13 years with ALL was carried out in Nephrology and Oncology departments of National Institute of Child Health, Karachi from January 2016 to December 2017. Patients already received chemotherapy were excluded. Data including risk categories, immunophenotyping, laboratory parameters like complete blood picture, serum creatinine (SCr), potassium (K), calcium (Ca), phosphorus (P) and uric acid (UA) on day 0,3 and7 after chemotherapy were collected. Data analyzed on SPSS using descriptive statistics. Independent t- test was applied to compare means a...

Hyperuricemia and tumor lysis syndrome in children with non-Hodgkin’s lymphoma and acute lymphoblastic leukemia

Turkish Journal of Hematology, 2011

Objective: This study aimed to examine the incidence, clinical characteristics, and outcome of hyperuricemia and tumor lysis syndrome (TLS) in children with non-Hodgkin's lymphoma (NHL) and acute lymphoblastic leukemia (ALL). Materials and Methods: This retrospective study included data from 327 patients (113 NHL and 214 ALL). Results: Hyperuricemia occurred in 26.5% and 12.6% of the patients with NHL and ALL, respectively. The corresponding figures for TLS were 15.9% and 0.47% (p=0.001). All hyperuricemic NHL patients had advanced disease and renal involvement was present in 53%. All hyperuricemic ALL patients had a leukocyte count >50,000 mm 3 at the time of diagnosis. Among the hyperuricemic NHL and ALL patients, 96.6% and 66.6% had LDH ≥500 UI/L, respectively. Treatment consisted of hydration and allopurinol; none of the patients received urate oxidase. Among the patients that developed TLS, 26.3% had laboratory TLS, 42.1% had grade I or II TLS, and 31.6% had grade III or IV TLS. Uric acid levels returned to normal after a mean period of 3.5±2.5 and 3.05±0.8 d in NHL and ALL groups, respectively. In all, 7% of the patients with hyperuricemia required hemodialysis. None of the patients died. Conclusion: In this series the factors associated with a high-risk for TLS were renal involvement in NHL and high leucocyte count in ALL. Management with allopurinol and hydration was effective in this group of patients with high tumor burden. (Turk J Hematol 2011; 28: 52-9)

T‑cell Acute Lymphoblastic Leukaemia, Mild Leucocytosis Causes Severe Tumour Lysis Syndrome

Advances in Human Biology, 2019

Tumour lysis syndrome (TLS) is a potentially life-threatening complication of the tumour. This syndrome consists of laboratory parameters such as hyperuricaemia, hyperkalaemia, hyperphosphataemia and hypocalcaemia and clinical complications such as acidosis, seizures, acute renal failure, cardiac arrhythmias and ultimately even death. TLS is especially standard in patients with haematological malignancies with rapid cellular turnover rates such as acute lymphocytic leukaemia, Burkitt lymphoma and diffuse large cell lymphoma, but is very rare in patients with solid tumours. T‑cell acute lymphoblastic leukaemia is aggressive leukaemia, a subtype of acute lymphoblastic leukaemia accounts for 15% of children and 25% of adult acute lymphoblastic leukaemia. Diagnostic confirmation of T‑cell acute lymphoblastic leukaemia (T‑ALL) in this case done through utilising flow cytometry which is one of the best diagnostic tools for acute leukaemia, further diagnosed with a cortical T‑ALL, a subtype of T‑ALL, initially responded well in pre‑phase induction chemotherapy (oral prednisolone 40 mg for 7 days). TLS developed after the 2nd day of 40 mg oral prednisolone with hyperkalaemia and hyperphosphataemia. The prevention of TLS now considered more effective than the treatment and identification of the high‑risk patient and taking preventive support is a crucial research area. Herein, this manuscript discusses a case of the TLS the acute management

Acute renal failure due to tumor lysis syndrome in a patient with non-Hodgkin’s lymphoma

Annals of Hematology, 2005

Tumor lysis syndrome is characterized by multiple metabolic derangements resulting from the release of intracellular components into the bloodstream due to abrupt malignant cell death, spontaneously or following antineoplastic therapy. The syndrome is characterized by hyperkalemia, hyperuricemia, hyperphosphatemia, and hypocalcemia, while deposition of uric acid and calcium phosphate crystals may result in acute renal failure, which is often exacerbated by concomitant intravascular volume depletion. A case of tumor lysis syndrome complicated by acute renal failure in a patient with non-Hodgkin’s lymphoma is reported and the pathophysiology, the clinical features, and the treatment options are discussed.

Tumor Lysis Syndrome in Chronic Lymphocytic Leukemia: A Rare Case Report from Nephrology

American Journal of Case Reports, 2019

Unusual clinical course Background: Tumor lysis syndrome is common in hematological malignancy, but less frequent in chronic and solid tumors. Almost always it is observed after chemotherapy or radiotherapy initiation, but rarely occurs spontaneously. Case Report: A 89-year-old female with stable chronic lymphocytic leukemia was admitted to the hospital because of worsening dyspnea and dry cough. Her vital signs were normal, except for sinus tachycardia. On physical examination, she appeared distressed, dyspneic, sweaty but afebrile, anxious, but alert and well oriented. Lung examination revealed reduced air entry with bibasilar crackles. No peripheral edema was seen, pulses were normal, and no signs of deep vein thrombosis were observed. Laboratory analysis revealed leukocytosis; but normal hematological and biochemical parameters. Intravenous (IV) furosemide and antibiotics (IV ceftriaxone and orally azithromycin) were started along with steroid therapy (methylprednisolone 62.5 mg, IV). The treatment with steroids lasted for 1 day only, and in the following day, the patient was switched to prednisone (20 mg/day orally) for only 1 additional day. White blood cell count increased on day 1, 2 and 3 after admission, along development of hyperuricemia, hyperphosphatemia, hyperkalemia, acute renal failure and elevated troponin levels. Hemodiafiltration/hemodialysis was initiated, and the patient was discharged after serum concentrations of these electrolytes and kidney function were restored. One month after discharge, the patient denied any malaise and was at stable condition. Conclusions: Herein, we present a case of a patient with stable chronic lymphocytic leukemia, who developed spontaneous tumor lysis syndrome after short low dose of steroid therapy. This case highlights the importance of including spontaneous tumor lysis syndrome in the differential diagnosis of any acute renal failure in the constellation of any malignancy.