Cellular and physiological mechanisms of new-onset diabetes mellitus after solid organ transplantation

被引:36
作者
Dong, M. [1 ,3 ]
Parsaik, A. K. [1 ]
Eberhardt, N. L. [1 ]
Basu, A. [1 ]
Cosio, F. G. [2 ]
Kudva, Y. C. [1 ]
机构
[1] Mayo Clin, Div Endocrinol Diabet Metab & Nutr, Rochester, MN USA
[2] Mayo Clin, Div Nephrol & Hypertens, Rochester, MN USA
[3] Shandong Univ, Qilu Hosp, Dept Endocrinol & Metab, Jinan 250100, Shandong, Peoples R China
关键词
diabetes mellitus; mechanism; new onset; organ transplantation; RENAL-ALLOGRAFT RECIPIENTS; ISOLATED RAT ISLETS; BETA-CELL; INSULIN-SECRETION; CYCLOSPORINE-A; KIDNEY-TRANSPLANTATION; RISK-FACTORS; CARDIOVASCULAR RISK; STEROID WITHDRAWAL; PANCREATIC-ISLETS;
D O I
10.1111/j.1464-5491.2012.03617.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Diabet. Med. 29, e1e12 (2012) Abstract New-onset diabetes after transplantation is recognized as one of the metabolic consequences which may increase the risk of morbidity and mortality after solid organ transplantation. The pathophysiology of new-onset diabetes after transplantation has not been clearly defined and may resemble that of Type 2 diabetes, characterized by predominantly insulin resistance or defective insulin secretion, or both. This review aims to summarize the current state of knowledge regarding the prevalence, consequences, pathogenesis, and management of new-onset diabetes after transplantation, with a major focus on the possible mechanisms involved in the pathogenesis of the disorder. The aetiology of new-onset diabetes after transplantation is multifactorial, with diabetogenic immunosuppressive drugs playing a major role. Multiple cellular and physiologic mechanisms are involved in the process. Selection of an appropriate maintenance immunosuppressive regimen should involve balancing the risk of patient and graft survival vs. the potential for new-onset diabetes after transplantation.
引用
收藏
页码:E1 / E12
页数:12
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