Acute pancreatitis and diabetic ketoacidosis are unusual adverse events following chemotherapy based on L-asparaginase and prednisone as support treatment for acute lymphoblastic leukemia. We present the case of a 16-year-old Hispanic male patient, in remission induction therapy for acute lymphoblastic leukemia on treatment with mitoxantrone, vincristine, prednisone, and L-asparaginase. He was hospitalized complaining of abdominal pain, nausea, and vomiting. Hyperglycemia, acidosis, ketonuria, low bicarbonate levels, hyperamylasemia, and hyperlipasemia were documented, and the diagnosis of diabetic ketoacidosis was made. Because of uncertainty of the additional diagnosis of acute pancreatitis as the cause of abdominal pain, a contrast-enhanced computed tomography was performed resulting in a Balthazar C pancreatitis classification. 1. Introduction The long-term outcome of acute lymphoblastic leukemia (ALL) has improved dramatically during the last few decades because of the development of well-designed and effective treatment protocols. Since 1961, L-asparaginase, combined with danorubicin, vincristine, and prednisone, the cornerstone treatment for ALL. They are used in remission, induction, and intensification phases in all pediatric regimens and in the majority of adult treatment protocols [1, 2]. Long-term, event-free, survival rates in children are currently around 80% and overall survival rates are close to or exceeding 90% of pediatric patients. Although overall survival rates in adults have improved in recent years, only 38% to 50% achieve long-term survival [3]. The most common complications associated with L-asparaginase are abdominal pain and allergic reactions. Other side effects include liver dysfunction, coagulation defects and central nervous system depression. Moreover, acute pancreatitis (AP), hyperglycemia, and diabetic ketoacidosis (DKA) can also be present [4]. Even though these side effects are well known, the combination of both DKA and AP represents unusual conditions generally reported as benign and self-limited [5]. We report a case of a 16-year-old male patient who developed transient diabetes mellitus following L-asparaginase therapy with ketoacidosis and acute pancreatitis as the mode of presentation. 2. Case Presentation A 16-year-old Hispanic male patient was admitted to our hospital. He was diagnosed as having acute lymphoblastic leukemia 5 months earlier. He was during the remission induction phase of therapy with mitoxantrone, vincristine, prednisone, and L-asparaginase, receiving last dose one week prior to his
References
[1]
J. D. Broome, “Evidence that the L-asparaginase activity of guinea pig serum is responsible for its antilymphoma effects,” Nature, vol. 191, no. 4793, pp. 1114–1115, 1961.
[2]
C.-H. Pui and W. E. Evans, “Treatment of acute lymphoblastic leukemia,” The New England Journal of Medicine, vol. 354, no. 2, pp. 166–178, 2006.
[3]
J. Flores-Calderón, E. Exiga-Gonzaléz, S. Morán-Villota, J. Martín-Trejo, and A. Yamamoto-Nagano, “Acute pancreatitis in children with acute lymphoblastic leukemia treated with L-asparaginase,” Journal of Pediatric Hematology/Oncology, vol. 31, no. 10, pp. 790–793, 2009.
[4]
S. Sahu, S. Saika, S. K. Pai, and S. H. Advani, “L-asparaginase (Leunase) induced pancreatitis in childhood acute lymphoblastic leukemia,” Pediatric Hematology and Oncology, vol. 15, no. 6, pp. 533–538, 1998.
[5]
M. T. Shaw, C. C. Barnes, F. J. Madden, and K. D. Bagshawe, “L-asparaginase and pancreatitis,” The Lancet, vol. 2, no. 7675, p. 721, 1970.
[6]
A. Morimoto, T. Imamura, R. Ishii et al., “Successful management of severe L-asparaginase-associated pancreatitis by continuous regional arterial infusion of protease inhibitor and antibiotic,” Cancer, vol. 113, no. 6, pp. 1362–1369, 2008.
[7]
K. Derwich, D. Stencel, M. Warzywoda, and M. Leda, “Acute pancreatitis during L-asparaginase treatment in children with acute lymphoblastic leukemia,” Reports of Practical Oncology and Radiotherapy, vol. 4, no. 1, pp. 15–22, 1999.
[8]
S. Treepongkaruna, N. Thongpak, S. Pakakasama, P. Pienvichit, N. Sirachainan, and S. Hongeng, “Acute pancreatitis in children with acute lymphoblastic leukemia after chemotherapy,” Journal of Pediatric Hematology/Oncology, vol. 31, no. 11, pp. 812–815, 2009.
[9]
J. R. Roberson, S. Raju, J. Shelso, C.-H. Pui, and S. C. Howard, “Diabetic ketoacidosis during therapy for pediatric acute lymphoblastic leukemia,” Pediatric Blood & Cancer, vol. 50, no. 6, pp. 1207–1212, 2008.
[10]
A. Khan, M. Adachi, and J. M. Hill, “Potentiation of diabetogenic effect of L-asparaginase by prednisolone,” Hormone and Metabolic Research, vol. 2, no. 5, pp. 275–276, 1970.
[11]
R. Mondal, M. Nandi, A. Tiwari, and S. Chakravorti, “Diabetic ketoacidosis with l-asparaginase therapy,” Indian Pediatrics, vol. 48, no. 9, pp. 735–736, 2011.
[12]
C. H. Pui, G. A. Burghen, W. P. Bowman, and R. J. A. Aur, “Risk factors for hyperglycemia in children with leukemia receiving L-asparaginase and prednisone,” The Journal of Pediatrics, vol. 99, no. 1, pp. 46–50, 1981.
[13]
R. Y. Sonabend, S. V. McKay, M. F. Okcu, J. Yan, M. W. Haymond, and J. F. Margolin, “Hyperglycemia during induction therapy is associated with poorer survival in children with acute lymphocytic leukemia,” The Journal of Pediatrics, vol. 155, no. 1, pp. 73–78, 2009.