|LETTER TO THE EDITOR
|Year : 2014 | Volume
| Issue : 4 | Page : 537
L-asparaginase induced acute parotitis during intensification therapy of acute lymphoblastic leukemia
J Kathwate, S Mundada, P Patil
Department of Pediatrics, Government Cancer hospital and Government Medical College, Aurangabad, Maharashtra, India
|Date of Web Publication||1-Feb-2016|
Dr. J Kathwate
Department of Pediatrics, Government Cancer hospital and Government Medical College, Aurangabad, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kathwate J, Mundada S, Patil P. L-asparaginase induced acute parotitis during intensification therapy of acute lymphoblastic leukemia. Indian J Cancer 2014;51:537
|How to cite this URL:|
Kathwate J, Mundada S, Patil P. L-asparaginase induced acute parotitis during intensification therapy of acute lymphoblastic leukemia. Indian J Cancer [serial online] 2014 [cited 2019 Aug 24];51:537. Available from: http://www.indianjcancer.com/text.asp?2014/51/4/537/175358
L-asparaginase (L-ASP) is commonly used during the induction and intensification therapy in acute lymphoblastic leukemia (ALL) and lymphomas along with vincristine, dexamethasone, and anthracycline derivatives. The most common complications associated with L-ASP are abdominal pain and allergic reactions. Although L-ASP is well-tolerated in most patients and causes myelosuppression, significant toxicities occur in up to 30% of patients. Other significant toxicities relate to a reduction in protein synthesis and include pancreatitis, thrombosis, central nervous system complications, and liver dysfunction., We report a 7-year-old boy with ALL, who suffered bilateral acute parotitis, during intensification phase therapy, which is a rare complication associated with L-ASP. He was receiving chemotherapy drugs regimen MCP 841 protocol including daunorubicin, vincristine, L-ASP, oral prednisone and methotrexate. He presented with fever and bilateral painful parotid enlargement. On examination, parotids were enlarged and tender. Blood culture and swab culture from the oral cavity did not grow any microorganism. Clinically mumps was ruled out as there was no history of contact, and he was vaccinated with measles, mumps, rubella at appropriate age. Serum amylase was raised, 200 (U/L) (normal range 30–110 U/L) and serum lipase was 30 U/L (normal range 5–208 U/L) was normal thus ruling out associated pancreatitis. Ultrasonography of parotids revealed enlarged, hypoechoic and hyperemiac glands with few enlarged lymph nodes. There was no glycosuria or ketonuria. He was started with broad-spectrum antibiotics and analgesics in view of bacterial parotitis. His blood and oral cavity swab cultures were negative as well as there was no evidence of parotid gland ostia inflammation on oral cavity examination so possibility of drug-induced parotitis was considered. Review of literature showed no other drugs except L-ASP can cause parotitis. After discounting L-ASP parotitits resolved within a week. Pancreatic toxicity results from direct deprivation on the protein metabolism leading to a disturbed synthesis of albumin, fibrinogen, plasma clotting factors IX and X, plasminogen, and antithrombin III, which leads to considerable toxicity particularly to organs associated with high protein production such as liver and pancreas. There are several case reports of L-ASP induced pancreatitis, but in our English language literature, only seven cases of L-ASP induced acute parotitis are reported. Probable mechanism of parotitis may be same as related to pancreatic injury as both are glands of the digestive tract, and there is a high rate of protein synthesis. This complication may be related to genetic susceptibility and needs further research as it is rarely seen in other patients receiving L-ASP. The rarely observed toxic effects of L-ASP, such as the parotitis, should be recognized as promptly as common complications of the drug to avoid the continuation of drug.
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