Tumor lysis syndrome (TLS), hyperleukocytosis,
and disseminated intravascular coagulation (DIC) are representative oncological
emergencies that overlap mutually at the beginning of therapy for aggressive leukemia. Lately recombinant urate oxidase
(rUO) enables to control uric acid
level and its
crystallization, the most frequent risk factor for clinical TLS; therefore,
hyperphosphatemia appears to be the main risk in the rUO era. We here report an
infantile leukemia patient who developed severe hyperphosphatemia, resulting in
acute renal failure and ischemic encephalopathy. A 9-month-old female baby was
adynamic with a bulging anterior fontanel, and was diagnosed as infantile acute
lymphoblastic leukemia with a mixed lineage leukemia gene rearrangement. A laboratory
examination revealed leukocytosis, bicytopenia, hyperuricemia, a prolonged
prothrombin time, activated partial thromboplastin time, and elevated lactate
dehydrogenase level. Soon after a reduced dose of prednisolone was
administered, she developed hypoxia caused by systemic inflammatory response
syndrome and heart failure. Her white blood cell count decreased sharply,
leading to acute renal failure due to hyperphosphatemia, which required
continuous hemodiafiltration for 48 hours. Although renal function subsequently
recovered, severe ischemic encephalopathy remained. She achieved morphological
remission once, however, relapsed and passed away soon after. We have to pay
attention to the progression of hyperphosphatemia, hyperkakemia and DIC,
although hyperuricemia was controlled using rUO. Changes in electrolyte levels must be continuously monitored, and TLS,
DIC and/or hyperleukocytosis should be promptly managed especially in
patients who are sensitive to therapy.