Tumour lysis syndrome, case report and review of the literature (Clinical Case)

Tumour lysis syndrome is characterised by the development of hyperuricaemia, hyperkalaemia, anaemia, hyperphosphataemia and hypocalcaemia as a result ofthe destruction of a large number of rapidly proliferating neoplastic cells. Frequently, acute renal failure occurs. The syndrome has most often been associated with rapidly dividing myeloproliferative and lymphoproliferative disorders, classically Burkitts lymphomaand acute lymphoblastic leukaemia, but has also been documented in chronic leukaemia, breast carcinoma, germ cell rumours, neuroendocrine rumours and smallcell lung carcinoma [1-5]. It is usually associated withthe initiation of chemotherapy but may occur with radiotherapy, surgery, endocrine therapy, glucocorticoids, interferon, hyperthermia or spontaneously [6-13]. With the introduction of increasingly effective drugs and high dose chemotherapy regimes there is potentially increased risk of the development of tumour lysis syndrome because of the rapid cell breakdown. For this reason, it is also being seen in a wider range of malignant diseases [14,15]. Tumour lysis leads to the release into the systemic circulation of large quantities of potassium from the cytoplasm, urate from purine degradation and phosphate from nucleoproteins. Clearance of the products of tumour lysis depends on renal excretion, hepatic metabolism and phagocytosis by the reticulo-endothelial system. Renal clearance is the primary mechanism for the excretion ofuric acid, potassium and phosphate and the metabolic derangements of tumour lysis will be exacerbated by the development of renal failure.