Abnormal Glucose Metabolism and Body Composition Changes in Childhood Acute Lymphoblastic Leukemia Survivors during Their Adolescence
1
Issued Date
2025-01-01
Resource Type
ISSN
10774114
eISSN
15363678
Scopus ID
2-s2.0-86000648949
Pubmed ID
40013840
Journal Title
Journal of Pediatric Hematology/Oncology
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SCOPUS
Bibliographic Citation
Journal of Pediatric Hematology/Oncology (2025)
Suggested Citation
Supho W., Anurathapan U., Mahachoklertwattana P., Khlairit P., Pongratanakul S., Wongdaeng A., Poomthavorn P. Abnormal Glucose Metabolism and Body Composition Changes in Childhood Acute Lymphoblastic Leukemia Survivors during Their Adolescence. Journal of Pediatric Hematology/Oncology (2025). doi:10.1097/MPH.0000000000003013 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/106781
Title
Abnormal Glucose Metabolism and Body Composition Changes in Childhood Acute Lymphoblastic Leukemia Survivors during Their Adolescence
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Abstract
Childhood acute lymphoblastic leukemia survivors (ALL-S) face an increased risk of abnormal glucose metabolism (AGM). This study aimed to assess glucose metabolism in 141 ALL-S. All underwent an oral glucose tolerance test (OGTT) and were classified into AGM and normal glucose tolerance (NGT) groups. Insulin sensitivity and secretion indices were calculated from plasma glucose and serum insulin derived from the OGTT. Fat mass index (FMI) was derived from body composition analysis. Sixty-seven of 141 (48%) ALL-S had AGM. AGM was demonstrated in 33 of 98 nonobese ALL-S. ALL-S with AGM had a greater waist circumference percentile and FMI SD score than those with NGT. In addition, ALL-S with AGM had lower insulin sensitivity (greater homeostasis model assessment of insulin resistance: 2.3 [1.4, 3.3] vs. 1.0 [0.5, 1.4], P<0.001 and lower whole-body insulin sensitivity index: 3.5 [2.3, 4.1] vs. 7.9 [5.3, 10.9], P<0.001) and lower insulin secretion relative to insulin sensitivity (disposition index: 5.8 [4.2, 10.2] vs. 10.0 [6.1, 14.6], P<0.001) than those with NGT. Therefore, ALL-S could develop AGM regardless of their body mass index status. AGM in ALL-S stemmed from both insulin resistance and impaired insulin secretion.