Advanced glycation end products and chronic inflammation in adult survivors of childhood leukemia treated with hematopoietic stem cell transplantation.
Adult
Biomarkers
/ blood
Cancer Survivors
/ statistics & numerical data
Cardiovascular Diseases
/ blood
Case-Control Studies
Child
Chronic Disease
Female
Follow-Up Studies
Glycation End Products, Advanced
/ blood
Hematopoietic Stem Cell Transplantation
/ adverse effects
Humans
Inflammation
/ blood
Male
Precursor Cell Lymphoblastic Leukemia-Lymphoma
/ pathology
Prognosis
Whole-Body Irradiation
/ adverse effects
Young Adult
advanced glycation end products
cardiovascular late effects
childhood cancer survivors
chronic inflammation
hematopoietic stem cell transplantation
Journal
Pediatric blood & cancer
ISSN: 1545-5017
Titre abrégé: Pediatr Blood Cancer
Pays: United States
ID NLM: 101186624
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
06
08
2019
revised:
11
11
2019
accepted:
11
11
2019
pubmed:
11
12
2019
medline:
6
5
2020
entrez:
11
12
2019
Statut:
ppublish
Résumé
Among survivors of pediatric acute lymphoblastic leukemia (ALL), those who received hematopoietic stem cell transplantation (HSCT) conditioned with total-body irradiation (TBI) show the highest risk of late complications, including cardiovascular (CV) disease. Advanced glycation end products (AGEs) have been associated with CV disease in diabetes mellitus and other clinical conditions. This study explores AGEs plasma levels, inflammatory status, and lipid profile in survivors of pediatric ALL who received HSCT conditioned with TBI. Inclusion criteria were (a) previous diagnosis of ALL at age < 18 years, treated with HSCT conditioned with TBI; (b) age > 18 at the time of the study enrollment; (c) off-therapy for at least five years. Radiotherapy other than TBI, preexisting heart disease, glucose metabolism impairment, body mass index > 25, active graft versus host disease (GvHD), smoking, or treatment with cholesterol lowering medications were exclusion criteria. Eighteen survivors and 30 age-matched healthy controls were enrolled. AGEs plasma levels were markedly higher in ALL survivors than in healthy subjects (2.15 ± 2.21 vs 0.29 ± 0.15 pg/mL, P < 0.01). Survivors also showed higher levels of high-sensitivity C-reactive protein (2.32 ± 1.70 vs 0.88 ± 1.09 mg/dL, P < 0.05), IL-1β (7.04 ± 1.52 vs 4.64 ± 2.02 pg/mL, P < 0.001), IL17 (37.44 ± 3.51 vs 25.19 ± 6.34 pg/mL, P < 0.001), an increased glutathione/reduced glutathione ratio (0.085 ± 0.07 vs 0.041 ± 0.036, P < 0.05) and slight alterations in their lipid profile. Our data show AGEs accumulation and chronic inflammation in ALL survivors who received HSCT conditioned with TBI. These alterations may contribute to the increased risk of CV disease reported in these subjects.
Sections du résumé
BACKGROUND
Among survivors of pediatric acute lymphoblastic leukemia (ALL), those who received hematopoietic stem cell transplantation (HSCT) conditioned with total-body irradiation (TBI) show the highest risk of late complications, including cardiovascular (CV) disease. Advanced glycation end products (AGEs) have been associated with CV disease in diabetes mellitus and other clinical conditions. This study explores AGEs plasma levels, inflammatory status, and lipid profile in survivors of pediatric ALL who received HSCT conditioned with TBI.
PROCEDURE
Inclusion criteria were (a) previous diagnosis of ALL at age < 18 years, treated with HSCT conditioned with TBI; (b) age > 18 at the time of the study enrollment; (c) off-therapy for at least five years. Radiotherapy other than TBI, preexisting heart disease, glucose metabolism impairment, body mass index > 25, active graft versus host disease (GvHD), smoking, or treatment with cholesterol lowering medications were exclusion criteria. Eighteen survivors and 30 age-matched healthy controls were enrolled.
RESULTS
AGEs plasma levels were markedly higher in ALL survivors than in healthy subjects (2.15 ± 2.21 vs 0.29 ± 0.15 pg/mL, P < 0.01). Survivors also showed higher levels of high-sensitivity C-reactive protein (2.32 ± 1.70 vs 0.88 ± 1.09 mg/dL, P < 0.05), IL-1β (7.04 ± 1.52 vs 4.64 ± 2.02 pg/mL, P < 0.001), IL17 (37.44 ± 3.51 vs 25.19 ± 6.34 pg/mL, P < 0.001), an increased glutathione/reduced glutathione ratio (0.085 ± 0.07 vs 0.041 ± 0.036, P < 0.05) and slight alterations in their lipid profile.
CONCLUSIONS
Our data show AGEs accumulation and chronic inflammation in ALL survivors who received HSCT conditioned with TBI. These alterations may contribute to the increased risk of CV disease reported in these subjects.
Substances chimiques
Biomarkers
0
Glycation End Products, Advanced
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e28106Informations de copyright
© 2019 Wiley Periodicals, Inc.
Références
Essig S, Li Q, Chen Y, et al. Risk of late effects of treatment in children newly diagnosed with standard-risk acute lymphoblastic leukaemia: a report from the Childhood Cancer Survivor Study cohort. Lancet Oncol. 2014;15:841-851.
Armstrong GT, Chen Y, Yasui Y, et al. Reduction in late mortality among 5-year survivors of childhood cancer. N Engl J Med. 2016;374:833-842.
Bhakta N, Liu Q, Ness KK, et al. The cumulative burden of surviving childhood cancer: an initial report from the St Jude Lifetime Cohort Study (SJLIFE). Lancet. 2017;390:2569-2582.
Felicetti F, D'Ascenzo F, Moretti C, et al. Prevalence of cardiovascular risk factors in long-term survivors of childhood cancer: 16 years follow up from a perspective registry. Eur J Epidemiol. 2015;22:762-770.
Saultier P, Auquier P, Bertrand Y, et al. Metabolic syndrome in long-term survivors of childhood acute leukemia treated without hematopoietic stem cell transplantation: an L.E.A. study. Haematologica. 2016;101:1603-1610.
Keegan THM, Kushi LH, Li Q, et al. Cardiovascular disease incidence in adolescent and young adult cancer survivors: a retrospective cohort study. J Cancer Surviv. 2018;12:388-397.
Pommier P, Sunyach MP, Pasteuris C, Frappaz D, Carrie C. Second cancer after total-body irradiation (TBI) in childhood. Strahlenther Onkol. 2009;185(Suppl 2):13-16.
Ferry C, Gemayel G, Rocha V, et al. Long-term outcomes after allogeneic stem cell transplantation for children with hematological malignancies. Bone Marrow Transplant. 2007;40:219-224.
Armstrong GT, Kawashima T, Leisenring W, et al. Aging and risk of severe, disabling, life-threatening, and fatal events in the childhood cancer survivor study. J Clin Oncol. 2014;32:1218-1227.
Hudson MM. Clinical ascertainment of health outcomes among adults treated for childhood cancer. JAMA. 2013;309:2371-2381.
de Haas EC, Oosting SF, Lefrandt JD, Wolffenbuttel BH, Sleijfer DT, Gietema JA. The metabolic syndrome in cancer survivors. Lancet Oncology. 2010;11:193-203.
Ness KK, Kirkland JL, Gramatges MM, et al. Premature physiologic aging as a paradigm for understanding increased risk of adverse health across the lifespan of survivors of childhood cancer. J Clin Oncol. 2018;36:2206-2215.
Ness KK, Armstrong GT, Kundu M, Wilson CL, Tchkonia T, Kirkland JL. Frailty in childhood cancer survivors. Cancer. 2015;121(10):1540-1547.
Sadowska-Bartosz I, Bartosz G. Effect of glycation inhibitors on aging and age-related diseases. Mech Ageing Dev. 2016;160:1-18.
Fournet M, Bonté F, Desmoulière A. Glycation damage: a possible hub for major pathophysiological disorders and aging. Aging Dis. 2018;9:880-900.
Fishman SL, Sonmez H, Basman C, Singh V, Poretsky L. The role of advanced glycation end-products in the development of coronary artery disease in patients with and without diabetes mellitus: a review. Mol Med. 2018;24:59.
Reynaert NL, Gopal P, Rutten EPA, Wouters EFM, Schalkwijk CG. Advanced glycation end products and their receptor in age-related, non-communicable chronic inflammatory diseases: overview of clinical evidence and potential contributions to disease. Int J Biochem Cell Biol. 2016;81:403-418.
Wendt T, Harja E, Bucciarelli L, et al. RAGE modulates vascular inflammation and atherosclerosis in a murine model of type 2 diabetes. Atherosclerosis. 2006;185:70-77.
Schalkwijk CG, Miyata T. Early- and advanced non-enzymatic glycation in diabetic vascular complications: the search for therapeutics. Amino Acids. 2012;42:1193-1204.
Collotta D, Lucarini L, Chiazza F, et al. Reduced susceptibility to sugar-induced metabolic derangements and impairments of myocardial redox signaling in mice chronically fed with D-tagatose when compared to fructose. Oxid Med Cell Longev. 2018;2018:5042428.
Kanauchi M, Tsujimoto N, Hashimoto T. Advanced glycation end products in nondiabetic patients with coronary artery disease. Diabetes Care. 2001;24:1620-1623.
Mastrocola R, Nigro D, Chiazza F, et al. Fructose-derived advanced glycation end-products drive lipogenesis and skeletal muscle reprogramming via SREBP-1c dysregulation in mice. Free Radic Biol Med. 2016;91:224-235.
Brignardello E, Runzo C, Aragno M, et al. Dehydroepiandrosterone administration counteracts oxidative imbalance and advanced glycation end product formation in type 2 diabetic patients. Diabetes Care. 2007;30:2922-2927.
Aragno M, Mastrocola R. Dietary sugars and endogenous formation of advanced glycation endproducts: emerging mechanisms of disease. Nutrients. 2017;9(4):pii E385.
Mastrocola R, Nigro D, Cento AS, Chiazza F, Collino M, Aragno M. High-fructose intake as risk factor for neurodegeneration: key role for carboxy methyllysine accumulation in mice hippocampal neurons. Neurobiol Dis. 2016;89:65-75.
Vatanen A, Hou M, Huang T, et al. Clinical and biological markers of premature aging after autologous SCT in childhood cancer. Bone Marrow Transplant. 2017;52:600-605.
Ariffin H, Azanan MS, Abd Ghafar SS, et al. Young adult survivors of childhood acute lymphoblastic leukemia show evidence of chronic inflammation and cellular aging. Cancer. 2017;123:4207-4214.
Sulicka J, Surdacki A, Mikołajczyk T, et al. Elevated markers of inflammation and endothelial activation and increased counts of intermediate monocytes in adult survivors of childhood acute lymphoblastic leukemia. Immunobiology. 2013;218:810-816.
Rosen GP, Nguyen HT, Shaibi GQ. Metabolic syndrome in pediatric cancer survivors: a mechanistic review. Pediatr Blood Cancer. 2013;60:1922-1928.
Ketterl TG, Chow EJ, Leisenring WM, et al. Adipokines, inflammation, and adiposity in hematopoietic cell transplantation survivors. Biol Blood Marrow Transplant. 2018;24:622-626.
Ridker PM. From C-reactive protein to interleukin-6 to interleukin-1: moving upstream to identify novel targets for atheroprotection. Circ Res. 2016;118:145-156.
Robert M, Miossec P. Effects of interleukin 17 on the cardiovascular system. Autoimmun Rev. 2017;16:984-991.
Zielinski CE, Mele F, Aschenbrenner D, et al. Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β. Nature. 2012;484:514-518.
Lee S, Piao C, Kim G, Kim JY, Choi E, Lee M. Production and application of HMGB1 derived recombinant RAGE-antagonist peptide for anti-inflammatory therapy in acute lung injury. Eur J Pharm Sci. 2018;114:275-284.
Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129:S1-45.
Gidez LI, Miller GJ, Burnstein M, Slagle S, Eder HA. Separation and quantitation of subclasses of human plasma HDL by a single precipitation procedure. J Lipid Res. 1982;23:1206-1216.
Leahy J, Spahis S, Bonneil E, et al. Insight from mitochondrial functions and proteomics to understand cardiometabolic disorders in survivors of acute lymphoblastic leukemia. Metabolism. 2018;85:151-160.
Friedman DN, Hilden P, Moskowitz CS, et al. Cardiovascular risk factors in survivors of childhood hematopoietic cell transplantation treated with total body irradiation: a longitudinal analysis. Biol Blood Marrow Transplant. 2017;23:475-482.
Schmidt AM, Hori O, Chen JX, et al. Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes. J Clin Invest. 1995;96:1395-1403.
Lyons TJ, Jenkins AJ. Lipoprotein glycation and its metabolic consequences. Curr Opin Lipidol. 1997;8:174-180.
Rojas A, Mercadal E, Figueroa H, Morales MA. Advanced glycation and ROS: a link between diabetes and heart failure. Curr Vasc Pharmacol. 2008;6:44-51.
Palanissami G, Solomon P. Rage and its ligands: molecular interplay between glycation, inflammation, and hallmarks of cancer - a review. Horm Cancer. 2018;9:295-325.
Azzam EI, Jay-Gerin JP, Pain D. Ionizing radiation-induced metabolic oxidative stress and prolonged cell injury. Cancer Lett. 2012;327:48-60.
Cappetta D, De Angelis A, Sapio L, et al. Oxidative stress and cellular response to doxorubicin: a common factor in the complex milieu of anthracycline cardiotoxicity. Oxid Med Cell Longev. 2017;2017:1521020.
Ramasamy R, Vannucci SJ, Yan SS, Herold K, Yan SF, Schmidt AM. Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation. Glycobiology. 2005;15:16R-28R.
Ceriello A. Hypothesis: the “metabolic memory”, the new challenge of diabetes. Diabetes Res Clin Pract. 2009;86:S2-S6.
Bevilacqua MP, Pober JS, Wheeler ME, Cotran RS. Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines. J Clin Invest. 1985;76:2003-2011.
Libby P, Warner SJ, Friedman GB. Interleukin 1: a mitogen for human vascular smooth muscle cells that induces the release of growth-inhibitory prostanoids. J Clin Invest. 1988;81:487-498.
Arida A, Protogerou AD, Kitas GD, Sfikakis PP. Systemic inflammatory response and atherosclerosis: the paradigm of chronic inflammatory rheumatic diseases. Int J Mol Sci. 2018;19(7):E1890.
Chow EJ, Wong K, Lee SJ, et al. Late cardiovascular complications after hematopoietic cell transplantation. Biol Blood Marrow Transplant. 2014;20:794-800.
Duncan CN, Brazauskas R, Huang J, et al. Late cardiovascular morbidity and mortality following pediatric allogeneic hematopoietic cell transplantation. Bone Marrow Transplant. 2018;53:1278-1287.
Abe R, Yamagishi S. AGE-RAGE system and carcinogenesis. Curr Pharm Des. 2008;14:940-945.
Lin JA, Wu CH, Lu CC, Hsia SM, Yen GC. Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: an emerging biological factor in cancer onset and progression. Mol Nutr Food Res. 2016;60:1850-1864.
Ahmad S, Khan H, Siddiqui Z, et al. AGEs, RAGEs and s-RAGE; friend or foe for cancer. Semin Cancer Biol. 2018;49:44-55.
Niall DK, Des CW. Advanced glycation end products and tumorigenesis. J Tumor Med Prev. 2017;1:555558.