Case Report

Tumour lysis syndrome

A 57-year-old man with relapsed non-Hodgkin’s lymphoma (NHL) was admitted for salvage chemotherapy with dexamethasone, ara-C and cisplatin. Shortly after cisplatin was initiated he developed a cough, wheeze, nausea, vomiting, tachypnoea and tachycardia. The biochemical findings are shown in Table I. He was treated by pushing intravenous fluids and potassium-binding resin, followed by allopurinol and calcium supplementation. His laboratory results improved over the next 48 hours (Table I). The patient subsequently tolerated two cycles of the same chemotherapy with aggressive hydration and allopurinol. He will have CT scan re-staging and stem cell transplantation in the future.

The main differential diagnosis was cisplatin hypersensitivity and tumour lysis syndrome (TLS). The biochemical features (hyperuricaemia, hyperkalaemia, hyperphosphataemia and hypocalcaemia) were typical of TLS. TLS is a life-threatening oncological emergency caused by rapid lysis of malignant cells, either spontaneously or induced by chemotherapy. TLS typically occurs with high-grade lymphomas and other haematological malignancies.1 Manifestations of TLS are variable, including renal failure, muscle cramps, weakness and seizures.2

The cornerstone of TLS management is to push fluids to increase excretion of urate and phosphate.3 Hyperkalaemia must be managed urgently. Drugs that lower serum urate have a key role in the management of TLS (Fig. 1). Allopurinol reduces the formation of urate, but does not affect circulating urate or crytals deposited in the tissues4 (Fig. 2). Rasburicase, a recombinant urate-oxidase enzyme, converts urate to soluble allantoin. Although rasburicase lowers uric acid more than allopurinol, there is currently no evidence of clinical benefit and it is extremely expensive.5

Mohamed Irhuma, MB ChB

Registrar, Division of Clinical Pharmacology, Department of Medicine, Groote Schuur Hospital, University of Cape Town

Zainab Mohamed, MBChB, MMed (Rad Onc)

Radiation Oncologist, Department of Radiation Oncology, Groote Schuur Hospital, University of Cape Town

Gary Maartens, MB ChB, MMed, FCP (SA), DTM&H

Professor and Head, Division of Clinical Pharmacology, Department of Medicine, Groote Schuur Hospital, University of Cape Town

Correspondence to: M Irhuma ( mohamed.irhuma@uct.ac.za )

References

1. Cairo MS, Bishop M. Tumor lysis syndrome: new therapeutic strategies and classification. Br J Haematol 2004;127(1):3-11.

2. Hande KR, Garrow GC. Acute tumor lysis syndrome in patients with high-grade non-Hodgkin’s lymphoma. Am J Med 1993;94(2):133-139.

3. Jones DP, Mahmoud H, Chesney RW. Tumor lysis syndrome: pathogenesis and management. Pediatr Nephrol 1995;9(2):206-212.

4. Hochberg J, Cairo MS. Tumor lysis syndrome: current perspective. Haematologica 2008; 3(1):9-13.

5. Cortes J, Moore JO, Maziarz RT, et al. Control of plasma uric acid in adults at risk for tumor lysis syndrome: efficacy and safety of rasburicase alone and rasburicase followed by allopurinol compared with allopurinol alone – Results of a multicenter phase III study. J Clin Oncol 2010;28(27):4207-4213.

Table I. Relevant biochemical findings during admission