Abstract
Childhood survivors of acute lymphoblastic leukemia (ALL) are increased risk of several chronic complications, such as second cancers, pulmonary, metabolic complications and cardiovascular disease. Obesity and metabolic syndrome is one of the most common treatment related complication in children surviving cancer, which concurs with our nations childhood epidemic [1-3] Recent research has identified the role of genetics in the development of obesity and metabolic syndrome in childhood survivors of ALL. Growth hormone deficiency, Leptin regulation, fat mass obesity (FTO) gene and the insulin resistant ENPP1 variants disorders has been associated adverse effects of chemotherapeutic treatment and the cause of clinical manifestations of metabolic syndrome [4-8]. The illumination of the role of genetic variants can shed insights into obesity within high risk population, as well as, a target to prevent disease.
Highlights
Acute lymphoblastic leukemia is the most common form of childhood cancer with an 80% cure rate [9]
Obesity and metabolic syndrome is one of the most common treatment related complication in children surviving cancer, which concurs with our nations childhood epidemic [1,2,3] Recent research has identified the role of genetics in the development of obesity and metabolic syndrome in childhood survivors of acute lymphoblastic leukemia (ALL)
A number of endocrine/metabolic adverse effects have been described in the literature in childhood survivors of ALL, which include obesity, dyslipidemia, insulin resistance, hypertension and eventually cardiac disease [2,3,5]
Summary
Acute lymphoblastic leukemia is the most common form of childhood cancer with an 80% cure rate [9]. Tion in North American survivors of childhood ALL, who were a mean age of 32 years at follow-up, the studied reported an increased risk of obesity, but a significantly greater rate of change in BMI over time, as compared with a noncancer comparison population [13]. Studies of childhood survivors showed an increase risk for obesity in metabolic syndrome especially due to particular treatment methods [7,10,11,12,13,14]. The early adipose rebound is thought to be a consequence of treatment with cranial radiation and, glucocorticoid steroids which alters body composition and increased risk of developing obesity/metabolic syndrome [8,16].
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