[Perioperative management of total laryngectomy for a patient with cold agglutinin disease].

Cold agglutinin disease is possible to cause thromboembolism of various organs due to changes in red blood cells by exposure to low temperature. Safety standards for perioperative management of patients with cold agglutinin have not been established. A patient with cold agglutinin disease was scheduled to undergo total laryngectomy and greater pectoral muscle flap. We thought it important to perform intensive temperature control to prevent a decrease in temperature below the thermal amplitude, which induces agglutinin in the vessel. We tried to keep the temperature of the patient with the warming equipment aggressively and monitored the shift of temperature in detail. It was also important to shorten the surgery with less hemorrhage and anesthetic management which can avoid a large shift in body temperature. We could keep peripheral and deep temperature above the critical point causing agglomeration. We did not find any symptoms of microembolism due to cold agglutination during the operation.

The ex vivo production of ammonia predicts L-asparaginase biological activity in children with acute lymphoblastic leukemia.

Patients with acute lymphoblastic leukemia (ALL), who develop antiasparaginase antibodies without clinical allergic reactions ("silent inactivation") during L: -asparaginase (L: -Asp) treatment, have poor outcomes. Ammonia is produced by hydrolysis of asparagine by L: -Asp. We postulated that plasma ammonia level might reflect the biological activity of L: -Asp. Five children with ALL treated according to the Tokyo Children's Cancer Study Group (TCCSG) protocol were enrolled. Plasma ammonia levels were analyzed immediately and 1 h after incubation at room temperature and "ex vivo ammonia production" was defined as increase in ammonia concentration. Ex vivo ammonia production well correlated with L: -Asp activity (r = 0.882, P < 0.01, n = 23). It always exceeded 170 microg/dL (170-345 microg/dL) in induction therapy. We found 3 patients whose ammonia production was negligible during later phases of therapy. Antiasparaginase antibody was detected and L: -Asp activity decreased in these patients. Ex vivo ammonia production is a surrogate marker of L: -Asp biological activity.