Acute lymphoblastic leukaemia (ALL) is the commonest type of cancer seen among children contributing to almost one fourth of all childhood cancers [1]. In developing countries, these children present late when the disease has progressed to an advanced stage with a high tumour load [2], and hence have a high risk of developing a tumor lysis syndrome. The standard treatment of hyper-leukocytosis associated with tumor lysis syndrome is hyperhydration and allopurinol along with Rasburicase (Urate oxidase) to control very high uric acid levels. If in spite of hyper-hydration the serum phosphate levels remain high, it is then treated with aluminium hydroxide [3]. Sevelamer is a non-calcium phosphate binder which is not absorbed from the gastrointestinal tract, and has proven efficacy in reducing the serum phosphate levels in chronic kidney disease and in patients on hemodialysis [4,5]. We report two children with tumor lysis syndrome where we used Sevelamer hydrochloride to treat hyperphosphatemia.

Case 1: A seven-year-old boy reported with a 10 day history of progressive fever, associated with facial swelling and bruises for 2 days. On examination he had bulky lymph nodes in the neck associated with hepatosplenomegaly. His chest X-ray was suggestive of superior mediastinal lymphadenopathy. His initial blood results showed the following: Hb 9.3 g/dL, total leukocyte count 51×10⁹/L, and platelet count 7×10⁹/L. The blood film was suggestive of acute leukemia and was later confirmed to be T-cell ALL. His other blood tests revealed: uric acid 18 mg/dL, phosphate 8 mg/dL, potassium 4.6 mmol/L, calcium 8.6 mg/dL and LDH 1932 units. He was started on hyper-hydration (3L/m²) by maintaining a urine output above 3mL/kg/hr using regular doses of furosemide. Following a dose of rasburicase (0.2 mg/kg), the uric acid levels came down to within the normal range (Fig. 1). The serum creatinine was initially 1.1 mg/dL and reached a maximum of 1.9 mg/dL. The serum phosphate level started to rise on the day 2 of admission to a maximum of 12 mg/dL, along with signs of hypocalcaemic tetany (Serum calcium 5.7 mg/dL), which was treated with calcium gluconate injections on two occasions. In addition to increasing fluids to a maximum 5 L/m², sevelamer hydrochloride 400 mg was given orally every 8 hrs, following which the phosphate levels were controlled in 48 hrs (Fig.1). The child was started on UKALL 2003 protocol and is currently 6 months from the date of diagnosis.

Fig.1 Changes in phosphate and uric acid and sesporise to Sevelamer hydrochloride in the two children.

Case 2: A 10-year-old boy presented with fever for 2 weeks associated with skin rashes, and facial swelling for 5 days. He had generalized lymphadenopathy with large cervical, parotid gland swelling and hepatosplenomegaly. The chest X-ray showed mediastinal widening. His initial blood results showed the following: Hb 3g/dL, total leukocyte count 395 ×10⁹/L cells/cc, and platelets count of 40×10⁹/L. The initial uric acid was 26.5 mg/dL (Fig. 1), LDH 5674 units, potassium 6.4 mmol/l, calcium 9 mg/dL, phosphate 5.5 mg/dL and the serum creatinine was 2.0 mg/dL. He was started on intravenous fluids at 3 L/m²/day. A single dose of rasburicase (3mg) controlled the hyperuricemia within 2 hours. However, serum phosphate and creatinine level started to rise by day-2, to 22 mg/dL and 2.4 mg/dL, respectively. Intravenous fluids were increased to 5 L/m²/d and urine output was maintained throughout with regular furosemide doses. He also developed hypocalcemic tetany which was treated with calcium gluconate injection. Oral Sevelamer hydrochloride 400 mg, every 8 hrs, was given following which his serum phosphate levels came to within normal levels in 48 hours. The flow cytometry result confirmed T cell Acute Lymphoblastic Leukemia and the child was subsequently started on chemotherapy as per the UKALL 2003 protocol.