Abstract
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 and 7 after chemotherapy were collected. Data analyzed on SPSS using descriptive statistics. Independent t- test was applied to compare means and P- value<0.05 was taken as significant.Results:Ninety-one children with mean age of 6.39±3.08 years were studied. Male were 57% and 43% female. High risk ALL were 61.5%. Pre –BALL were 82.4% and 17.5% had T-cell ALL. All patients had anemia (hemoglobin7.69±2.66 g/dl) and thrombocytopenia (43.61± 18.6 x109) where as hyperleukocytosis and blast cells were observed in 20.87% and 73.6% respectively. Comparing the biochemical parameters of ALL, the difference in SCr from D0 vs D3 (0.46±0.16 vs0.54± 0.35 and D7, 0.44±0.22) was significant (p=0.001). Similarly, difference in UA (D0, 4.12±2.40 vs D3, 3.82±1.73 and D7, 3.56±1.42), SP (D0, 4.24±1.34 vs D3, 4.61±1.76 and D7,4.13±1.07mg/dl)and for K (p=0.038) was significant. There was no difference in Ca from D0 vs D3 (0.092) and D7 (0.277). TLS was found in 62.6% children, it was chemotherapy induced in 72% and spontaneous in 28%. Clinical-TLS was observed in 14% and all CTLS had AKI. Hyperuricemia and hyperphosphatemia were the most common biochemical abnormalities in laboratory-TLS and CTLS.Conclusion:TLS was found in 62.6% despite preventive measures. Early recognition and treatment is essential to avoid morbidity and mortality.
Highlights
Tumor lysis syndrome (TLS) is an oncological emergency resulting from massive lysis of malignant cells and clinically characterized by renal failure, seizures and cardiac arrhythmias that requires early recognition and management.[1]
The objective of this study was to determine the frequency of TLS in children with acute lymphoblastic leukemia (ALL) and various biochemical abnormalities in children with TLS. This retrospective cross-sectional study was conducted on 91 children with ALL who were managed in the Department of Pediatric Oncology, National Institute of Child Health, Karachi, from January 2016 to December 2017
Operational Definitions: Laboratory TLS was defined when two or more of the following biochemical abnormalities were present (i) hyperuricemia (ii) hyperkalemia (iii) hyperphosphatemia (iv) hypocalcemia, Clinical TLS was diagnosed if child had abnormality in any one end organ along with lab TLS
Summary
Tumor lysis syndrome (TLS) is an oncological emergency resulting from massive lysis of malignant cells and clinically characterized by renal failure, seizures and cardiac arrhythmias that requires early recognition and management.[1]. The massive lysis of lymphoblastic cells releases intracellular metabolites like potassium (K), uric acid (UA), phosphate (P) and products of protein and purine metabolites into systemic circulation. These high effluxes of metabolites result in abnormal accumulation in the blood and exceed the capacity of renal clearance and results hyperkalemia, hyperuricemia, hyperphosphatemia and secondary hypocalcemia. Hyperuricemia is the initial and most common abnormality, induces acute renal injury by intra-renal uric acid crystallization and It aggravates precipitation of calcium phosphate crystals in the renal tubules This crystal nephropathy causes inflammation, obstruction and renal tubular damage manifesting as acute kidney injury. There is concomitant rise of lactic dehydrogenase because of rapid cell turn over in ALL.[1,2,3,4]
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