Biomarkers Predictive of Metabolic Syndrome and Cardiovascular Disease in Childhood Cancer Survivors

Abstract

The improvement in childhood cancer treatments resulted in a marked improvement in the survival of pediatric cancer patients. However, as survival increased, it was also possible to observe the long-term side effects of cancer therapies. Among these, metabolic syndrome is one of the most frequent long-term side effects, and causes high mortality and morbidity. Consequently, it is necessary to identify strategies that allow for early diagnosis. In this review, the pathogenetic mechanisms of metabolic syndrome and the potential new biomarkers that can facilitate its diagnosis in survivors of pediatric tumors are analyzed.

Egyptian “Ful Medames” mitigates metabolic syndrome associated inflammation through regulation of resistin, leptin and adipokine mRNA expression in Wistar rats

“…Moreover, lemon juice was added and olive oil. The previously mentioned additives gave the meal a very good palatability as shown in Table (4) for sensory evaluation of the meal, in which the overall acceptability of the meal is very high accounting for 9.29 ± 0.20 out of ten for the CFBM with additives which is significantly higher compared to the CFBM with no additives which was 7.20 ± 0.24 reflecting the role of these natural additives in improving the overall acceptability of the CFBM.…”

“…It is a cluster of metabolic disorders comprising hyperglycemia, atherogenic dyslipidemia, insulin resistance, high blood pressure and central obesity [1,2] and it is characterized by prothrombotic and proinflammatory states [3]. According to the latest consensus of the American Heart Association, National Heart, Lung and Blood Institute and International Diabetes Federation, metabolic syndrome is defined if three of the following five criteria are satisfied; fasting blood glucose more than 100 mg/dl, increased triglyceride levels more than 150 mg/dl, reduced high-density lipoprotein cholesterol (HDL-C) levels less than 40 mg/dl, blood pressure more than 130/85 mmHg and increased waist circumference [4]. This collection of pathological and abnormal conditions is considered as a crucial risk factor for developing many diseases, like diabetes mellitus, cardiovascular diseases, chronic kidney disease and hypertension [5].…”

Diabetes in childhood cancer survivors: emerging concepts in pathophysiology and future directions

“…Radiation is associated with decreased subcutaneous adipose tissue, which is thought to protect against metabolic dysregulation, and increased visceral adipose tissue, which increases metabolic dysregulation including insulin resistance ( 49 , 50 ). Radiation-induced adipose tissue damage leads to inflammation and mitochondrial injury, both of which are also associated with the development of DM ( 51 , 52 ). The extent to which radiation to the pancreas affects beta-cell function, and the timing of these effects relative to the radiation exposure deserve further delineation in future studies.…”

“…Untreated growth hormone deficiency is associated with alterations in body composition, including increased waist-to-height ratio and low muscle mass, that can contribute to insulin resistance ( 54 ). Cranial radiation may also impact hypothalamic responsiveness to leptin, leading to an increase in adipose tissue and its production of leptin ( 51 ). Impaired responsiveness to leptin would be expected to lead to increased caloric intake and subsequent weight gain, further increasing insulin resistance ( 55 ).…”

“…Corticosteroids, commonly used in the treatment of ALL and many lymphomas, are associated with increased risk of treatment-induced DM. The posited mechanisms include steroid-induced inhibition of glucose uptake in peripheral tissues, increased hepatic gluconeogenesis, and excess lipid deposition in skeletal muscle ( 51 , 57 , 58 ). While not all individuals who receive corticosteroids develop DM after completion of therapy, survivors who develop treatment-induced DM during steroid therapy are at increased risk of subsequently developing DM even when off steroids ( 59 ).…”