中国小儿急救医学
中國小兒急救醫學
중국소인급구의학
CHINESE PEDIATRIC EMERGENCY MEDICINE
2014年
9期
550-553
,共4页
刘萍萍%祝益民%肖政辉%张新萍%仇君%卢秀兰
劉萍萍%祝益民%肖政輝%張新萍%仇君%盧秀蘭
류평평%축익민%초정휘%장신평%구군%로수란
高血糖%β细胞功能障碍%胰岛素抵抗%脓毒症%儿童
高血糖%β細胞功能障礙%胰島素牴抗%膿毒癥%兒童
고혈당%β세포공능장애%이도소저항%농독증%인동
Hyperglycemia%Beta cell dysfunction%Insulin resistance%Sepsis%Children
目的 分析重症儿童高血糠发生与胰岛素抵抗和胰腺β细胞功能障碍之间的关系,探讨胰腺β细胞功能障碍与胰腺损伤的关系.方法 分析2012年6月至2013年3月湖南省儿童医院PICU收治的736例危重症患儿,以入住PICU 24 h内选择空腹时间点采集血标本,静脉血糖≥11.1mol/L为重度升高组(n=67);6.1～ 11.1 mmol/L为轻度升高组(n=361);≤6.1 mmol/L为血糖正常组(n =308),比较血清胰岛素、C肽、血清淀粉酶、脂肪酶、尿淀粉酶、HOMA-β指数、HOMA-IR指数、按脓毒症严重程度分非脓毒症组(n =414)、脓毒症组(n=237)、严重脓毒症组(n=64)、脓毒性休克组(n=21),比较血糖、血清胰岛索、C肽、HOMA-β指数、HOMA-IR指数差异.结果 (1)胰岛素、C肽、血淀粉酶、脂肪酶、尿淀粉酶的总体趋势随血糖升高而逐渐升高(rs值分别为0.235、0.142、0.142、0.119、0.093,P＜0.05),三组间比较差异有统计学意义(P＜0.05),血糖重度升高组血清淀粉酶(IU/L)[102.81(10.48-191.69)]、脂肪酶(U/L)[69.75(10.67-121.85)]高于正常值上限.重度升高组HOMA-β指数下降至18.75％,HOMA-β指数随血糖水平升高而下降(rs=-0.108,P ＜0.05),HOMA-IR指数随血糖升高而逐渐升高(rs=0.455,P ＜0.05).(2)非脓毒症组、脓毒症组、严重脓毒症组、脓毒性休克组患儿的血糖、胰岛素、C肽水平和HOMA-β指数差异有统计学意义(P＜0.05),HOMA-IR指数比较差异无统计学意义(P＞0.05).脓毒性休克组血糖为9.21 (6.21-19.60) mmol/L,HOMA-β指数降低至10.52％,血糖、胰岛素、C肽、HOMA-β指数与其他三组比较差异有统计学意义(P＜0.05).结论 重症儿童高血糖与胰岛素抵抗和胰岛β细胞功能障碍有关,危重症继发胰腺损伤是导致胰岛β细胞功能障碍的原因;在脓毒症儿童,胰腺β细胞功能障碍使血糖升高的作用比胰岛素抵抗更加显著.
目的 分析重癥兒童高血糠髮生與胰島素牴抗和胰腺β細胞功能障礙之間的關繫,探討胰腺β細胞功能障礙與胰腺損傷的關繫.方法 分析2012年6月至2013年3月湖南省兒童醫院PICU收治的736例危重癥患兒,以入住PICU 24 h內選擇空腹時間點採集血標本,靜脈血糖≥11.1mol/L為重度升高組(n=67);6.1～ 11.1 mmol/L為輕度升高組(n=361);≤6.1 mmol/L為血糖正常組(n =308),比較血清胰島素、C肽、血清澱粉酶、脂肪酶、尿澱粉酶、HOMA-β指數、HOMA-IR指數、按膿毒癥嚴重程度分非膿毒癥組(n =414)、膿毒癥組(n=237)、嚴重膿毒癥組(n=64)、膿毒性休剋組(n=21),比較血糖、血清胰島索、C肽、HOMA-β指數、HOMA-IR指數差異.結果 (1)胰島素、C肽、血澱粉酶、脂肪酶、尿澱粉酶的總體趨勢隨血糖升高而逐漸升高(rs值分彆為0.235、0.142、0.142、0.119、0.093,P＜0.05),三組間比較差異有統計學意義(P＜0.05),血糖重度升高組血清澱粉酶(IU/L)[102.81(10.48-191.69)]、脂肪酶(U/L)[69.75(10.67-121.85)]高于正常值上限.重度升高組HOMA-β指數下降至18.75％,HOMA-β指數隨血糖水平升高而下降(rs=-0.108,P ＜0.05),HOMA-IR指數隨血糖升高而逐漸升高(rs=0.455,P ＜0.05).(2)非膿毒癥組、膿毒癥組、嚴重膿毒癥組、膿毒性休剋組患兒的血糖、胰島素、C肽水平和HOMA-β指數差異有統計學意義(P＜0.05),HOMA-IR指數比較差異無統計學意義(P＞0.05).膿毒性休剋組血糖為9.21 (6.21-19.60) mmol/L,HOMA-β指數降低至10.52％,血糖、胰島素、C肽、HOMA-β指數與其他三組比較差異有統計學意義(P＜0.05).結論 重癥兒童高血糖與胰島素牴抗和胰島β細胞功能障礙有關,危重癥繼髮胰腺損傷是導緻胰島β細胞功能障礙的原因;在膿毒癥兒童,胰腺β細胞功能障礙使血糖升高的作用比胰島素牴抗更加顯著.
목적 분석중증인동고혈강발생여이도소저항화이선β세포공능장애지간적관계,탐토이선β세포공능장애여이선손상적관계.방법 분석2012년6월지2013년3월호남성인동의원PICU수치적736례위중증환인,이입주PICU 24 h내선택공복시간점채집혈표본,정맥혈당≥11.1mol/L위중도승고조(n=67);6.1～ 11.1 mmol/L위경도승고조(n=361);≤6.1 mmol/L위혈당정상조(n =308),비교혈청이도소、C태、혈청정분매、지방매、뇨정분매、HOMA-β지수、HOMA-IR지수、안농독증엄중정도분비농독증조(n =414)、농독증조(n=237)、엄중농독증조(n=64)、농독성휴극조(n=21),비교혈당、혈청이도색、C태、HOMA-β지수、HOMA-IR지수차이.결과 (1)이도소、C태、혈정분매、지방매、뇨정분매적총체추세수혈당승고이축점승고(rs치분별위0.235、0.142、0.142、0.119、0.093,P＜0.05),삼조간비교차이유통계학의의(P＜0.05),혈당중도승고조혈청정분매(IU/L)[102.81(10.48-191.69)]、지방매(U/L)[69.75(10.67-121.85)]고우정상치상한.중도승고조HOMA-β지수하강지18.75％,HOMA-β지수수혈당수평승고이하강(rs=-0.108,P ＜0.05),HOMA-IR지수수혈당승고이축점승고(rs=0.455,P ＜0.05).(2)비농독증조、농독증조、엄중농독증조、농독성휴극조환인적혈당、이도소、C태수평화HOMA-β지수차이유통계학의의(P＜0.05),HOMA-IR지수비교차이무통계학의의(P＞0.05).농독성휴극조혈당위9.21 (6.21-19.60) mmol/L,HOMA-β지수강저지10.52％,혈당、이도소、C태、HOMA-β지수여기타삼조비교차이유통계학의의(P＜0.05).결론 중증인동고혈당여이도소저항화이도β세포공능장애유관,위중증계발이선손상시도치이도β세포공능장애적원인;재농독증인동,이선β세포공능장애사혈당승고적작용비이도소저항경가현저.
Objective To analyse the relationship between insulin resistance and the pancreatic beta cell dysfunction in critically ill children with hyperglycemia,to investigate the relationship between the pancreas injury and pancreatic beta cells dysfunction.Methods Seven hundred and thirty-six critically ill children admitted in PICU of Hunan Children's Hospital from Nov 2012 to Mar 2013 were reviewed and analyzed.According to the maximum intravenous blood glucose within 24 h after admission,they were divided into severely elevated group (blood glucose ≥11.1 mmol/L,n =67),slightly elevated group(blood glucose 6.1 ～ 11.1 mmol/L,n =361) and control group (blood glucose ≤ 6.1 mmo/L,n =308).Serum insulin,C peptide,serum amylase,lipase,urinary amylase,HOMA-β,HOMA-IR were compared among 3 groups.According to the severity of sepsis,they were divided into non-sepsis group (n =414),sepsis group (n =237),severe sepsis group (n =64),septic shock group (n =21).Blood glucose,serum insulin,C peptide,HOMA-βand HOMA-IR were compared among 4 groups.Results (l)The levels of insulin,C peptide,blood amylase,lipase and urine amylase were gradually increased with elevated blood sugar(rs =0.235,P ＜ 0.05;C =0.142,P ＜ 0.05 ; rs =0.142,P ＜ 0.05 ; rs =0.119,P ＜ 0.05 ; r.s =0.093,P ＜ 0.05).The differences among 3 groups were significant (P ＜ 0.05).The levels of serum amylase (IU/L) [102.81 (10.48-191.69)],lipase(U/L) [69.75(10.67-121.85)] were higher than upper limit of normal in severely elevated group.HOMA-β fell to 18.75％ in severely elevated group.The level of HOMA-β was decreased with the increase of blood sugar level (rs =-0.108,P ＜ 0.05).The level of HOMA-IR was increased with the elevated blood sugar level(rs =0.455,P ＜ 0.05).(2) The levels of blood glucose,insulin,C peptide and HOMA-β were significantly different among 4 groups of non-sepsis,sepsis,severe sepsis and septic shock group (P ＜ 0.05),HOMA-IR showed no significant difference among 4 groups (P ＞ 0.05).The levels of blood sugar increased to 9.21 (6.21-19.60) mmol/L,HOMA-β declined to 10.52％ in septic shock group,and blood glucose,insulin,C peptide,HOMA-β were significantly different compared with the other 3 groups (P ＜ 0.05).Conclusion Hyperglycemia is associated with insulin resistance and pancreatic β cells dysfunction in critically ill children,the cause of beta cell dysfunction is secondary to pancremic injury.Pancreatic beta cells dysfunction inducing hyperglycemia is more significant than insulin resistance in sepsis children.
