中华内科杂志
中華內科雜誌
중화내과잡지
CHINESE JOURNAL OF INTERNAL MEDICINE
2012年
2期
108-113
,共6页
范慧%张鹏睿%刘佳%徐援
範慧%張鵬睿%劉佳%徐援
범혜%장붕예%류가%서원
糖尿病%糖尿病酮症酸中毒%分型%β细胞功能%蜜月期
糖尿病%糖尿病酮癥痠中毒%分型%β細胞功能%蜜月期
당뇨병%당뇨병동증산중독%분형%β세포공능%밀월기
Diabetes mellitus%Diabetic ketoacidosis%Classification%β cell function%Remission period
目的 观察进入“蜜月期”的初发糖尿病合并酮症患者的胰岛功能恢复情况及对糖尿病分型的意义.方法 初发糖尿病合并酮症患者住院胰岛素强化治疗后,对其中206例进入“蜜月期”患者随访36个月,依据是否需要长期胰岛素强化治疗分为2组,其中19例在“蜜月期”后必须应用强化胰岛素治疗才能良好控制血糖(A组),界定为1型糖尿病；其他187例在“蜜月期”结束后不需要应用胰岛素强化治疗(B组),界定为2型糖尿病.比较两组胰岛素强化治疗前后胰岛功能的变化、“蜜月期”持续时间,并分析其对糖尿病分型及预后治疗方案选择的意义.结果 胰岛素强化治疗前和治疗后A组胰岛素曲线下面积( AUCI)、C肽曲线下面积(AUCC)及稳态模型评估法(HOMA)评价的胰岛β细胞基础功能(HOMA-β)和胰岛素抵抗指数(HOMA-IR)均明显低于B组[治疗前分别为(10.18±2.36)mIU·h·L-1比(20.28 ±6.89)mIU·h·L-1,(1.56 ±0.53) μg·h·L-1比(3.75±0.67) μg·h·L-1,3.68±1.08比18.20±6.59,1.22 ±0.49比3.06 ±1.54;治疗后分别为(29.86±8.65)mIU·h·L-1比( 93.35 ±19.42) mIU·h·L-1,(3.99±0.79)μg·h·L-1比(12.54 ±3.83)μg·h·L-1,8.50±2.46比56.17±19.42,0.63±0.56比1.42 ±0.78],A组年龄、BMI、有糖尿病家族史比例更低,无合并高血压、高脂血症等代谢综合征情况.A组“蜜月期”持续时间明显短于B组[(7.9±5.2)个月比(20.9±9.9)个月].糖尿病相关抗体检测的阳性率不高,与临床结局符合率低.强化治疗后复查胰岛素释放试验:A组胰岛素、C肽释放高峰提前,出现在服葡萄糖水后0.5～1 h,但在口服葡萄糖刺激后的胰岛素、C肽释放最高峰不到基础值的2倍；而B组的胰岛素、C肽释放高峰出现在口服葡萄糖水后1h或2h,在口服葡萄糖刺激后的胰岛素、C肽释放最高峰是基础值的4～10倍.结论 进入“蜜月期”的初发糖尿病合并酮症患者中91％为2型糖尿病；强化胰岛素治疗前胰岛功能差、强化治疗后恢复不充分、“蜜月期”持续的时间短暂是1型糖尿病的标志.
目的 觀察進入“蜜月期”的初髮糖尿病閤併酮癥患者的胰島功能恢複情況及對糖尿病分型的意義.方法 初髮糖尿病閤併酮癥患者住院胰島素彊化治療後,對其中206例進入“蜜月期”患者隨訪36箇月,依據是否需要長期胰島素彊化治療分為2組,其中19例在“蜜月期”後必鬚應用彊化胰島素治療纔能良好控製血糖(A組),界定為1型糖尿病；其他187例在“蜜月期”結束後不需要應用胰島素彊化治療(B組),界定為2型糖尿病.比較兩組胰島素彊化治療前後胰島功能的變化、“蜜月期”持續時間,併分析其對糖尿病分型及預後治療方案選擇的意義.結果 胰島素彊化治療前和治療後A組胰島素麯線下麵積( AUCI)、C肽麯線下麵積(AUCC)及穩態模型評估法(HOMA)評價的胰島β細胞基礎功能(HOMA-β)和胰島素牴抗指數(HOMA-IR)均明顯低于B組[治療前分彆為(10.18±2.36)mIU·h·L-1比(20.28 ±6.89)mIU·h·L-1,(1.56 ±0.53) μg·h·L-1比(3.75±0.67) μg·h·L-1,3.68±1.08比18.20±6.59,1.22 ±0.49比3.06 ±1.54;治療後分彆為(29.86±8.65)mIU·h·L-1比( 93.35 ±19.42) mIU·h·L-1,(3.99±0.79)μg·h·L-1比(12.54 ±3.83)μg·h·L-1,8.50±2.46比56.17±19.42,0.63±0.56比1.42 ±0.78],A組年齡、BMI、有糖尿病傢族史比例更低,無閤併高血壓、高脂血癥等代謝綜閤徵情況.A組“蜜月期”持續時間明顯短于B組[(7.9±5.2)箇月比(20.9±9.9)箇月].糖尿病相關抗體檢測的暘性率不高,與臨床結跼符閤率低.彊化治療後複查胰島素釋放試驗:A組胰島素、C肽釋放高峰提前,齣現在服葡萄糖水後0.5～1 h,但在口服葡萄糖刺激後的胰島素、C肽釋放最高峰不到基礎值的2倍；而B組的胰島素、C肽釋放高峰齣現在口服葡萄糖水後1h或2h,在口服葡萄糖刺激後的胰島素、C肽釋放最高峰是基礎值的4～10倍.結論 進入“蜜月期”的初髮糖尿病閤併酮癥患者中91％為2型糖尿病；彊化胰島素治療前胰島功能差、彊化治療後恢複不充分、“蜜月期”持續的時間短暫是1型糖尿病的標誌.
목적 관찰진입“밀월기”적초발당뇨병합병동증환자적이도공능회복정황급대당뇨병분형적의의.방법 초발당뇨병합병동증환자주원이도소강화치료후,대기중206례진입“밀월기”환자수방36개월,의거시부수요장기이도소강화치료분위2조,기중19례재“밀월기”후필수응용강화이도소치료재능량호공제혈당(A조),계정위1형당뇨병；기타187례재“밀월기”결속후불수요응용이도소강화치료(B조),계정위2형당뇨병.비교량조이도소강화치료전후이도공능적변화、“밀월기”지속시간,병분석기대당뇨병분형급예후치료방안선택적의의.결과 이도소강화치료전화치료후A조이도소곡선하면적( AUCI)、C태곡선하면적(AUCC)급은태모형평고법(HOMA)평개적이도β세포기출공능(HOMA-β)화이도소저항지수(HOMA-IR)균명현저우B조[치료전분별위(10.18±2.36)mIU·h·L-1비(20.28 ±6.89)mIU·h·L-1,(1.56 ±0.53) μg·h·L-1비(3.75±0.67) μg·h·L-1,3.68±1.08비18.20±6.59,1.22 ±0.49비3.06 ±1.54;치료후분별위(29.86±8.65)mIU·h·L-1비( 93.35 ±19.42) mIU·h·L-1,(3.99±0.79)μg·h·L-1비(12.54 ±3.83)μg·h·L-1,8.50±2.46비56.17±19.42,0.63±0.56비1.42 ±0.78],A조년령、BMI、유당뇨병가족사비례경저,무합병고혈압、고지혈증등대사종합정정황.A조“밀월기”지속시간명현단우B조[(7.9±5.2)개월비(20.9±9.9)개월].당뇨병상관항체검측적양성솔불고,여림상결국부합솔저.강화치료후복사이도소석방시험:A조이도소、C태석방고봉제전,출현재복포도당수후0.5～1 h,단재구복포도당자격후적이도소、C태석방최고봉불도기출치적2배；이B조적이도소、C태석방고봉출현재구복포도당수후1h혹2h,재구복포도당자격후적이도소、C태석방최고봉시기출치적4～10배.결론 진입“밀월기”적초발당뇨병합병동증환자중91％위2형당뇨병；강화이도소치료전이도공능차、강화치료후회복불충분、“밀월기”지속적시간단잠시1형당뇨병적표지.
Objective To observe β cell function in newly diagnosed diabetic patients with ketosis before and in remission period and evaluate its classification and predictive value.Methods A total of 206 patients newly diagnosed as diabetic ketosis who had been treated with intensive insulin therapy in our hospital and entered in the "honeymoon" after the withdraw of insulin therapy were followed for 36 months from onset of diabetes.They were divided into two groups of type 1 and type2 diabetes ( group A and B),according to the dependence or independence on insulin treatment. The β cell function of the two groups before and in remission period was compared by oral glucose tolerance test (OGTF).β cell function was measured with the AUC of insulin and C-peptide and homeostatic model assessment β-cell function (HOMA-β),while homeostatic model assessment insulin resistant (HOMA-IR) for insulin resistant.The duration of the "honeymoon" and the change of insulin and C-peptide curve before and in "honeymoon" were also observed.Results The AUC of insulin and C-peptide,the HOMA-β and the HOMA-IR before and after the intensive insulin treatment were lower in group A than that in group B [ before the insulin treatment:(10.18 ±2.36)mIU · h · L-1 vs (20.28 ±6.89)mIU · h · L-1,(1.56 ±0.53) μg · h · L-1 vs (3.75 ±0.67) μg · h · L-1,3.68 ± 1.08 vs 18.20 ±6.59,1.22 ±0.49 vs 3.06 ± 1.54,respectively;after the insulin treatment:(29.86 ± 8.65 ) mIU · h · L-1 vs (93.35 ± 19.42 ) mIU · h · L-1,( 3.99 ± 0.79 )μg · h · L-1 vs ( 12.54 ±3.83) μg · h · L-1,8.50 ±2.46 vs 56.17 ± 19.42,0.63 ±0.56 vs 1.42 ±0.78,respectively ].The duration of the "honeymoon" in group A was significantly shorter than in group B [ (7.9 ±5.2) months vs (20.9 ± 9.9 ) months ].In oral glucose insulin and C-peptide release test,the peak of insulin and C-peptide releasing curve in group A was brought forward by a half to 1 hour after intensive treatment while delayed in group B by 1 or 2 hours.The releasing peak of insulin and C-peptide in group A was less than two folds of the basic value,while four to ten fold of the basic value in group B.The positive ratio of glutamic acid decarboxylase antibody,insulin autoantibody and insular cellular antibody in group A and group B were 21.2％ vs 4.8％,18.1％ vs 3.3％,9.2％ vs 10.6％,respectively.Conclusions Of all the patients newly diagnosed as diabetes ketosis who had entered into the honeymoon after intensive insulin therapy,91％ were type 2 diabetes.Inferior β cell function before insulin therapy,weaker remission after insulin therapy and shorter duration of remission period suggest the classification of type 1 diabetes.
