 Leukemia & Lymphoma, June 2012; 53(6): 1245–1246 © 2012 Informa UK, Ltd. ISSN: 1042-8194 print / 1029-2403 online DOI: 10.3109/10428194.2011.647312 Correspondence: Dr. Matthew Tan, MBBS, MRCP, Singapore General Hospital, Endocrinology, Outram Rd, 169608 Singapore. E-mail: matthew.tan.z.w@ singhealth.com.sg Received 13 September 2011; revised 13 November 2011; accepted 4 December 2011 LETTER TO THE EDITOR Acarbose is an effective treatment for severe hypertriglyceridemia secondary to L-asparaginase and dexamethasone Matthew Tan 1 , Daniel Wai 1 , Chiaw Ling Chng 1 & William Hwang 2 1 Department of Endocrinology and 2 Department of Hematology, Singapore General Hospital, Singapore l-asparaginase is a drug used in the treatment of childhood acute lymphoblastic leukemia (ALL). Its action is the hydro- lysis of l-asparagine, which depletes the supply of this amino acid needed for protein synthesis and cell functioning, in cancer cells. It is documented to cause lipid abnormalities, especially hypertriglyceridemia, in as many as 67–72% [1,2] of treated patients. In a retrospective analysis [2] of 65 chil- dren and adolescents with ALL treated with l-asparaginase, it was noted that fve (12%) patients developed severe hyper- triglyceridemia (triglyceride level more than 1000 mg/dL or more than 11.4 mmol/L). Te postulated mechanism is the inhibition of lipoprotein lipase (LPL) [3,4], which is a vital enzyme in the removal of triglyceride (TG) from the TG- rich lipoproteins, which results in high levels of exogenous chylomicron bound triglycerides found during the period of l-asparaginase treatment [5]. Corticosteroids, especially dex- amethasone, are also an integral component of chemother- apy, which exacerbates the severity of hypertriglyceridemia with increased endogenous production of very-low-density lipoprotein (VLDL) [6,7]. Te concern with severe hyper- triglyceridemia is the induction of acute pancreatitis and complications of hyperviscosity syndrome. In the literature various modalities of treatment have been described, which include plasmapheresis or insulin infusion for symptomatic cases. For asymptomatic individuals a more conservative approach has been described, which may involve fasting and judicious use of fbrates. In this case report, we highlight the novel use of acarbose in the treatment of l-asparaginase and dexamethasone induced severe hypertriglyceridemia. A 25-year-old Bangladeshi woman, who originally pre- sented with a history of bleeding tendency for several years and subsequently developed fever of a month ’ s duration, was diagnosed with ALL in Bangladesh and referred to Singapore General Hospital for further assessment and treatment. Te patient did not attain complete remission after cycle 1B of HyperCVAD (hyperfractionated cyclophosphamide, vincristine, doxorubicin, dexamethasone alternating with methotrexate, cytarabine) and had some residual blast cells on fow cytometry. She then received a third round while a matched unrelated donor search was performed. However, she did not have a matching donor, and hence the decision was made to switch to a locally adapted form of the Berlin–Frankfurt–Münster (BFM) regimen known as the Hong Kong–Singapore ALL 97 (HK-SG ALL 97) chemotherapy regimen. As part of this regimen, l-asparaginase is utilized during reinduction phase IIA, dosed to body surface area (10 000 units/m 2 ), and given on days 8, 11, 15 and 18. Te other medications included vincristine (1.5 mg/m 2 on days 8, 15, 22 and 29), doxorubicin (30 mg/m 2 on days 8, 15, 22 and 29) and dexamethasone (10 mg/m 2 /day from day 1 to day 21 and tapered to 5 mg/m 2 /day on days 22–24, 2.5 mg/m 2 /day on days 25–27 and 1.25 mg/m 2 /day on days 28–30). She tolerated the chemotherapy fairly well until day 19 of reinduction phase IIA, when she started having mild abdominal pain which gradually became worse, resulting in hospital readmission on day 21. Her amylase and lipase lev- els were noted to be normal. Tere was transaminitis about two to three times the upper limit of normal. An ultrasono- graphic examination was performed subsequently, which did not reveal pancreatitis or biliary duct dilatation, although fatty liver was noted. She was continued on lamivudine that was empirically started prior to her frst initiation of chemo- therapy in view of hepatitis B core antibody positivity; the hepatitis B DNA level at this admission was undetectable. She was determined to have cytomegalovirus (CMV) associ- ated hepatitis in view of CMV viremia, and she was started on ganciclovir, which resulted in some improvement of the transaminitis. On day 27 her serum was highlighted by the laboratory to be very lipemic, and blood for fasting lipids was performed the next day, showing severe hypertriglyceridemia of more than 56 mmol/L (upper limit of detection is 56 mmol/L in our laboratory); total cholesterol was 20.9 mmol/L. A Beck- man UniCel DxC 800 Synchron Clinical System was used to measure triglycerides and total cholesterol. Te fasting lipid test was repeated on day 29, and again severe hypertriglyc- eridemia of more than 56 mmol/L was reported. Fasting venous glucose was 3.7 mmol/L. Te patient at this time was recovering from the CMV hepatitis and there was no evi- dence to suggest acute pancreatitis. She was euthyroid with no goiter, with no evidence of xanthelasma or eruptive xan- thomata and no stigmata of chronic liver disease. Endocrine