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Year : 2021  |  Volume : 58  |  Issue : 3  |  Page : 461--462

Lipid profile during chemotherapy in children with acute lymphoblastic leukemia

Dolly Madan, Priyanka Aggarwal, Anubha Jain, Vineeta Gupta 
 Division of Pediatric Hematology Oncology, Department of Pediatrics, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India

Correspondence Address:
Vineeta Gupta
Division of Pediatric Hematology Oncology, Department of Pediatrics, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh

How to cite this article:
Madan D, Aggarwal P, Jain A, Gupta V. Lipid profile during chemotherapy in children with acute lymphoblastic leukemia.Indian J Cancer 2021;58:461-462

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Madan D, Aggarwal P, Jain A, Gupta V. Lipid profile during chemotherapy in children with acute lymphoblastic leukemia. Indian J Cancer [serial online] 2021 [cited 2021 Dec 3 ];58:461-462
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Deranged lipid profile has been reported in children with acute lymphoblastic leukemia (ALL) during and following treatment.[1] The condition is under-diagnosed in India. This study was conducted to evaluate alterations in lipid levels and levels of amylase and lipase in 82 newly diagnosed patients with ALL in the age group one to 15 years admitted in university teaching hospital from September 2017 to August 2019. Estimation of serum amylase, lipase (U/L) and lipid profile (mg/dl) including very low density lipoprotein (VLDL), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and serum cholesterol was done at 0 month (at diagnosis), 1 month (end of induction phase), and 6 months (start of maintenance phase). Patients were divided into 3 age groups: 1–4, 5–9, and ≥10 years. Lipid levels were correlated with age, gender, risk stratification, cell lineage, and nutritional status. Weight-for-age was used in patients <5 years and body mass index was used for patients ≥5 years. Treatment was as per the children oncology group (COG) protocol. Fifty age- and gender-matched children were controls. Written informed consent was taken from parents/guardians. The study protocol was approved by the institutional ethics committee.

The baseline characteristics of the patients are presented in [Table 1]. All the mean values are accompanied with standard deviation. VLDL and triglycerides levels were high (51.17 ± 22.46 versus 34.02 ± 14.18, P = 0.002; 213.42 ± 91.09 versus 144.70 ± 66.41, P = 0.005) and HDL was low (25.97 ± 18.68 versus 42.81 ± 15.38, P = 0.008) at diagnosis compared to levels at 6 months in 1-4 years. In 5-9 years also, VLDL (45.04 ± 19.43 versus 31.95 ± 13.10, P = 0.012) and triglycerides (231.42 ± 91.09 versus 144.70 ± 66.41, P = 0.005) were high and HDL levels were low (34.61 ± 35.85 versus 48.01 ± 28.57, P = 0.004). No change was observed in LDL and cholesterol levels. In ≥10 years, only HDL levels were low (32.74 ±36.48 versus 46.81 ± 27.04, P = 0.002) at diagnosis. There was no significant change in VLDL, LDL, triglycerides, and cholesterol levels. Serum lipid levels of patients at diagnosis and controls were also compared in all three age groups. VLDL levels were high in patients 1-4 years of age (51.17 ± 22.46 versus 38.90 ± 13.90, P = 0.06). In 5–9 years of age, both VLDL and triglycerides were significantly increased (45.04 ± 19.43 versus 33.41 ± 27.79, P = 0.007 and 222.06 ± 95.73 versus 136.66 ± 51.46, P = 0.006 respectively). In ≥10 years, VLDL, LDL, HDL, triglycerides, and cholesterol levels were comparable to controls. No risk factors were identified for the deranged lipid profile. Serum amylase and lipase levels increased significantly at one month in patients <10 years only which normalized at 6 months. No patient had hypertriglyceridemia, pancreatitis, or thromboembolism.{Table 1}

Dyslipidemia is part of metabolic syndrome (MS) along with obesity, insulin resistance, and hypertension in survivors of ALL.[2] Older children and those treated with higher-risk therapy are at risk for severe hypertriglyceridemia (serum triglycerides ≥1000 mg/dL). Corticosteroids increase triglyceride synthesis and also increase the activity of lipoprotein lipase, whereas asparaginases can inhibit the activity of lipoprotein lipase. When steroids and asparaginase are given together, triglyceride-rich lipoproteins may be formed rapidly which are cleared inadequately resulting in hypertriglyceridemia.[3] This may be associated with pancreatitis and thromboembolism. In our patients, VLDL and triglycerides were raised and HDL levels were low at diagnosis all of which normalized at 6 months. VLDL and triglyceride levels at diagnosis were significantly higher than controls. The results are in agreement with other studies where lipid derangement was observed at the time of diagnosis which normalized during remission.[4],[5] It was suggested that lipid abnormalities observed at diagnosis may reflect altered nutritional states or altered lipid metabolism.[3] In contrast, one of the studies reported rising triglyceride and cholesterol levels during therapy and the reason was attributed to asparaginase treatment.[6] We could not identify any risk factor for deranged lipid profile which is also similar to the findings of another study.[5] It has been suggested that triglycerides are affected more by pegylated asparaginase than by native asparaginase especially when given together with dexamethasone.[7] We did not use pegylated asparaginase due to financial constraints and prednisolone was used during induction instead of dexamethasone. This may explain the low incidence of hypertriglyceridemia and pancreatitis in our study.

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