肠外与肠内营养
腸外與腸內營養
장외여장내영양
PARENTERAL & ENTERAL NUTRITION
2010年
1期
8-10
,共3页
颅脑疾病%胰岛素%血糖%蛋白质代谢
顱腦疾病%胰島素%血糖%蛋白質代謝
로뇌질병%이도소%혈당%단백질대사
Craniocerebral disease%Insulin%Blood glucose%Protein metabolism
目的:研究胰岛素治疗中三种不同血糖控制目标对危重颅脑疾病病人蛋白质代谢的影响.方法:将122例危重颅脑疾病病人随机分为三组,分别给予胰岛素控制血糖于不同的目标,即A组41例,血糖控制在4.4~6.1 mmol/L);B组42例,血糖控制在6.1~8.3 mmol/L,C组39例,血糖控制在10~11.1 mmol/L.对三组病人的蛋白质代谢情况和低血糖发生率进行比较.结果:A组与B组氮平衡、PA和TF指标优于C组,差异有显著性意义(P<0.05);但低血糖发生率A组高于B组和C组(P<0.05).结论:病人血糖控制在≤8.3 mmol/L,有利于减轻严重颅脑疾病病人的高分解代谢,促进蛋白合成,改善营养状况.
目的:研究胰島素治療中三種不同血糖控製目標對危重顱腦疾病病人蛋白質代謝的影響.方法:將122例危重顱腦疾病病人隨機分為三組,分彆給予胰島素控製血糖于不同的目標,即A組41例,血糖控製在4.4~6.1 mmol/L);B組42例,血糖控製在6.1~8.3 mmol/L,C組39例,血糖控製在10~11.1 mmol/L.對三組病人的蛋白質代謝情況和低血糖髮生率進行比較.結果:A組與B組氮平衡、PA和TF指標優于C組,差異有顯著性意義(P<0.05);但低血糖髮生率A組高于B組和C組(P<0.05).結論:病人血糖控製在≤8.3 mmol/L,有利于減輕嚴重顱腦疾病病人的高分解代謝,促進蛋白閤成,改善營養狀況.
목적:연구이도소치료중삼충불동혈당공제목표대위중로뇌질병병인단백질대사적영향.방법:장122례위중로뇌질병병인수궤분위삼조,분별급여이도소공제혈당우불동적목표,즉A조41례,혈당공제재4.4~6.1 mmol/L);B조42례,혈당공제재6.1~8.3 mmol/L,C조39례,혈당공제재10~11.1 mmol/L.대삼조병인적단백질대사정황화저혈당발생솔진행비교.결과:A조여B조담평형、PA화TF지표우우C조,차이유현저성의의(P<0.05);단저혈당발생솔A조고우B조화C조(P<0.05).결론:병인혈당공제재≤8.3 mmol/L,유리우감경엄중로뇌질병병인적고분해대사,촉진단백합성,개선영양상황.
Objective: To investigate the effect of three different goals of blood glucose control by insulin therapy on protein metabolism in the patients with critically cerebral disease.Methods: We performed a prospective,randomized,controlled study.A total of 122 patients with critically cerebral disease were randomly divided into three groups according to the target glucose-control levels:Group A: 4.4-6.1 mmol/L(n=41),Group B: 6.1-8.3 mmol/L(n=42),and Group C: 10-11.1 mmol/L(n=39).The state of protein metabolism and ratio of hypoglycemia of three groups were compared.Results: The indicators of nitrogen balance,prealbumin and transferrin in group A and group B were significantly better than that in group C(P<0.05),but the ratio of hypoglycemia in group A was significantly higher than those in group B and group C(P<0.05).Conclusion: Maintaining the blood glucose level ≤8.3 mmol/L might improve the nutrition status in the patients with critically cerebral disease by decreasing catabolism and promoting synthesis of protein.