中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2011年
3期
215-218
,共4页
陈显英%于明香%周俭%高键%高鑫
陳顯英%于明香%週儉%高鍵%高鑫
진현영%우명향%주검%고건%고흠
肝移植%移植后糖尿病%发生率%发病机制
肝移植%移植後糖尿病%髮生率%髮病機製
간이식%이식후당뇨병%발생솔%발병궤제
Liver transplantation%Post-transplant diabetes mellitus%Prevalence%Pathogenesis
目的 评估肝移植术后3年及以上患者糖代谢异常情况,初步探讨移植后糖尿病的发病机制.方法 收集2001年4月至2008年12月在中山医院进行肝移植患者的临床资料,排除术前已确诊糖尿病、死亡及失访患者,对肝移植术后≥3年的199例患者完成随访,统计根据空腹血糖诊断的移植后糖尿病(PTDM)发生率;对肝移植≥3年且根据空腹血糖未达到糖尿病诊断标准的的32例患者进行口服75 g葡萄糖耐量试验(OGTT),检测其空腹及糖负荷后2 h血糖和胰岛素,根据血糖情况分为血糖正常组、糖调节受损(IGR)组和PTDM组,计算其PTDM构成比和稳态模型评估(HOMA)指数.结果 肝移植术后≥3年的患者中,根据空腹血糖诊断的PTDM发生率为34.67%.对肝移植≥3年且根据空腹血糖未达到糖尿病诊断标准的32例患者进行OGTT得到:PTDM构成比为9.38%,IGR[包括空腹血糖受损和(或)糖耐量受损]为56.25%,血糖正常为34.37%.稳态模型评估胰岛β细胞功能指数(HOMA-β)在血糖正常组、IGR组、PTDM组依次递减,且PTDM组与血糖正常组、IGR组比较均有显著下降(均P<0.01).稳态模型评估胰岛素抵抗指数(HOMA-IR)在IGR组最高,PTDM组次之,IGR组相对血糖正常组升高有统计学意义.结论 本院肝移植≥3年患者PTDM总发生率为44.05%,肝移植患者在糖代谢异常早期即存在胰岛素抵抗,胰岛β细胞功能则随糖代谢异常加重而进行性衰退.
目的 評估肝移植術後3年及以上患者糖代謝異常情況,初步探討移植後糖尿病的髮病機製.方法 收集2001年4月至2008年12月在中山醫院進行肝移植患者的臨床資料,排除術前已確診糖尿病、死亡及失訪患者,對肝移植術後≥3年的199例患者完成隨訪,統計根據空腹血糖診斷的移植後糖尿病(PTDM)髮生率;對肝移植≥3年且根據空腹血糖未達到糖尿病診斷標準的的32例患者進行口服75 g葡萄糖耐量試驗(OGTT),檢測其空腹及糖負荷後2 h血糖和胰島素,根據血糖情況分為血糖正常組、糖調節受損(IGR)組和PTDM組,計算其PTDM構成比和穩態模型評估(HOMA)指數.結果 肝移植術後≥3年的患者中,根據空腹血糖診斷的PTDM髮生率為34.67%.對肝移植≥3年且根據空腹血糖未達到糖尿病診斷標準的32例患者進行OGTT得到:PTDM構成比為9.38%,IGR[包括空腹血糖受損和(或)糖耐量受損]為56.25%,血糖正常為34.37%.穩態模型評估胰島β細胞功能指數(HOMA-β)在血糖正常組、IGR組、PTDM組依次遞減,且PTDM組與血糖正常組、IGR組比較均有顯著下降(均P<0.01).穩態模型評估胰島素牴抗指數(HOMA-IR)在IGR組最高,PTDM組次之,IGR組相對血糖正常組升高有統計學意義.結論 本院肝移植≥3年患者PTDM總髮生率為44.05%,肝移植患者在糖代謝異常早期即存在胰島素牴抗,胰島β細胞功能則隨糖代謝異常加重而進行性衰退.
목적 평고간이식술후3년급이상환자당대사이상정황,초보탐토이식후당뇨병적발병궤제.방법 수집2001년4월지2008년12월재중산의원진행간이식환자적림상자료,배제술전이학진당뇨병、사망급실방환자,대간이식술후≥3년적199례환자완성수방,통계근거공복혈당진단적이식후당뇨병(PTDM)발생솔;대간이식≥3년차근거공복혈당미체도당뇨병진단표준적적32례환자진행구복75 g포도당내량시험(OGTT),검측기공복급당부하후2 h혈당화이도소,근거혈당정황분위혈당정상조、당조절수손(IGR)조화PTDM조,계산기PTDM구성비화은태모형평고(HOMA)지수.결과 간이식술후≥3년적환자중,근거공복혈당진단적PTDM발생솔위34.67%.대간이식≥3년차근거공복혈당미체도당뇨병진단표준적32례환자진행OGTT득도:PTDM구성비위9.38%,IGR[포괄공복혈당수손화(혹)당내량수손]위56.25%,혈당정상위34.37%.은태모형평고이도β세포공능지수(HOMA-β)재혈당정상조、IGR조、PTDM조의차체감,차PTDM조여혈당정상조、IGR조비교균유현저하강(균P<0.01).은태모형평고이도소저항지수(HOMA-IR)재IGR조최고,PTDM조차지,IGR조상대혈당정상조승고유통계학의의.결론 본원간이식≥3년환자PTDM총발생솔위44.05%,간이식환자재당대사이상조기즉존재이도소저항,이도β세포공능칙수당대사이상가중이진행성쇠퇴.
Objective To evaluate the status of abnormal glucose metabolism in patients being alive over 3years after liver transplantation and discuss the possible mechanism of post-transplant diabetes mellitus ( PTDM ).Methods In this study, the clinical data of patients with liver transplantation were collected from April 2001 to December 2008. Patients with diabetes mellitus before operation and those who had died and failed to appear during follow-up were exluded. 199 patients living over 3 years after liver transplantation were follow-up. The prevalence of PTDM was evaluated according to fasting plasma glucose(FPG). Among those without diabetes according to FPG,32patients underwent 75 g oral glucose tolerance test (OGTT) , and fasting and 2 h plasma glucose and insulin were determined. 32 patients were divided into three groups [normal, impaired glucose regulation ( IGR ) , and PTDM groups], proportion of PTDM and homeostasis model assessment ( HOMA ) index were calculated. Results In patients alive over 3 years after liver transplantation, the prevalence of PTDM was 34.67% according to FPG. The OGTT result showed that the proportion of PTDM was 9.38%, IGR, including impaired fasting glucose(IFG) and impaired glucose tolerance ( IGT ) , was 56. 25% , while 34. 37% remained normal. The homeostasis model assessment β cell function index( HOMA-β ) decreased progressively from normal group, IGR group to PTDM group,and that in PTDM group was significantly lower than those in normal and IGR group( P<0.01 ). IGR group had the highest homeostasis model assessment for insulin resistance (HOMA-IR) and PTDM group the next, and HOMA-IR in IGR group was significantly higher than normal group. Conclusion In patients alive over 3 years after liver transplantation, the prevalence of PTDM reached 44.05%. Insulin resistance existed during early period of impaired glucose regulation, while the degeneration of β cell progressed with the worsening of impaired glucose regulation.