摘要
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.
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.
