Abstract
In the last decade, the survival of subjects affected by cancer in childhood has significantly improved. The increased lifespan of childhood cancer survivors (CCS) led to a greater risk for long-term, therapy-related morbidity. To identify the clinical predictors of metabolic adverse outcomes in CCS (average off-therapy period: 12 years), we recruited 126 survivors of different childhood cancers (86.5% hematological cancers) who received at least anticancer chemotherapy, consecutively approached during their annual oncohematological outpatient visit. At examination, anthropometric measures and cancer-related history were collected. Moreover, a fasting venous sample was carried out for measuring fasting plasma glucose and insulin, glycated hemoglobin, lipid panel, and transaminases. We calculated the indexes of insulin resistance (HOMA-IR, McAuley, and QUICKI) and secretion (HOMA-β), liver steatosis (Hepatic Steatosis Index) and fibrosis (FIB-4 and NAFLD fibrosis score), and visceral fat dysfunction (Visceral Adiposity Index). More than one-third of the subjects (37.3%) did not have normal weight, with 11.1% of them affected by obesity. At recruitment, obese subjects were at significantly higher risk for impaired fasting glucose, metabolic syndrome, visceral adipose dysfunction, and liver steatosis/fibrosis. Subjects who received bone marrow transplantation were prone to insulin resistance, while survivors of lymphoma presented a visceral adipose dysfunction These results suggest a carefully metabolic monitoring of CCS, particularly in subgroups at higher risk, to early detect these conditions, promptly begin therapeutic interventions, and mitigate the dysmetabolic-related health burden.
Highlights
Cancers affecting pediatric and adolescent age represent 1–2% of all cancer [1]
In our cohort, we explored various biochemical metabolic variables and derived parameters to determine the prevalence in the recruited cancer survivors (CCS) of adipose tissue dysfunction, glucose and lipid impairment, hypertension, and liver metabolic disease (NAFLD, NASH, and liver fibrosis/cirrhosis)
In subjects who underwent bone marrow transplantation (BMT), we found a trend for an increase of ALT and aspartate transaminase (AST) value, regardless of body mass index (BMI), but no significant difference in terms of Hepatic Steatosis Index (HSI), FIB-4, and NAFLD fibrosis score (NFS) among the BMT, only chemotherapy (OC), and chemotherapy plus radiotherapy (CR) groups was observed (Table 4). (Table 3)
Summary
Cancers affecting pediatric and adolescent age represent 1–2% of all cancer [1]. Leukemia is the most common (33% of childhood tumors), followed by brain tumors, lymphomas, neuroblastoma, bone tumors (osteosarcoma and Ewing’s sarcoma), hepatoblastoma, Wilms’ tumor, rhabdomyosarcoma, and retinoblastoma [1]. The anticancer therapeutic protocols have been improved in terms of toxicity, the high survival rate and lifespan of childhood cancer survivors (CCS) led to a greater risk for long-term, treatment-related morbidity: cardiac damage (heart failure and coronary and valvular diseases), dysmetabolic conditions, bone loss, neuropathy, gonadal failure, infertility, sexual dysfunction, chronic pain and fatigue, insomnia, and accelerated aging [3–8]. Anticancer therapies induce long-term insulin resistance (IR) and hyperinsulinemia, affecting carbohydrate and lipid metabolism. Both chemotherapy and radiotherapy cause the release of inflammatory molecules (e.g., IL-6, IL-1β, and TNF-a) and the activation of macrophages that contribute to the development of IR, mainly responsible for the long-term onset of metabolic changes [7,9]. Glucocorticoids, often used in the different stages of treatment, contribute to the accumulation of body fat and increase of insulin resistance, favoring the occurrence of dysmetabolic conditions [9,12]
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