Diabetic ketoacidosis promotes a prothrombotic state

被引:83
作者
Carl, GF
Hoffman, WH
Passmore, GG
Truemper, EJ
Lightsey, AL
Cornwell, PE
Jonah, MH
机构
[1] Vet Adm Med Ctr, Dept Neurol, Augusta, GA 30904 USA
[2] Med Coll Georgia, Sect Pediat Endocrinol, Augusta, GA 30912 USA
[3] Med Coll Georgia, Pediat Crit Care Sect, Augusta, GA USA
[4] Med Coll Georgia, Sect Pediat Hematol & Oncol, Augusta, GA USA
[5] Univ Alabama Birmingham, Dept Nutr, Sch Hlth Related Profess, Birmingham, AL USA
[6] Med Coll Georgia, Hematol Coagulat Sect, Augusta, GA USA
关键词
diabetic ketoacidosis; endothelial activation; folate; homocysteine; protein C; protein S; von Willebrand factor;
D O I
10.1081/ERC-120018678
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cerebrovascular accidents are one of the life-threatening complications of diabetic ketoacidosis,(DKA) in children and adolescents. Our-objective was to evaluate the effect of DKA and its treatment on factors known to affect thrombotic activity (protein C; protein S; von Willebrand factor; fibrinogen; homocysteine; and folate) by comparing seven adolescents with DKA prior to treatment and at 6, 24, and 120 hours after initiation of treatment. We found-that protein C activity was significantly decreased by DKA, but normalized slowly following treatment. Free protein S was low throughout the study. Protein C antigen and protein S antigen showed varying degrees of change within the first 24 hours, but remained in the normal range, with the exception of the. initial value of protein C antigen, which was elevated. von Willebrand factor (vWF) antigen and vWF activity were both significantly increased prior to treatment, but decreased with treatment However, vWF activity remained elevated at 120 hours. Fibrinogen concentrations. showed no significant changes throughout the study. Homocysteine was significantly decreased prior to treatment and increased with the initiation of treatment. Folate was significantly increased prior to treatment, and decreased to high normal levels. The increased vWF and the decreased levels of protein C activity and of free protein S support the hypothesis that DKA and its treatment results in a prothrombotic state and activation of the vascular endothelium,, which, in turn, predispose to cerebrovascular accidents.
引用
收藏
页码:73 / 82
页数:10
相关论文
共 42 条
[1]   Type I diabetes mellitus, ketoacidosis and thromboembolism in an adolescent with Prader-Willi syndrome [J].
Anhalt, H ;
Eckert, KH ;
Hintz, RL ;
Neely, EK .
ACTA PAEDIATRICA, 1996, 85 (04) :516-516
[2]   MULTIPLE CEREBRAL HEMATOMAS AND PERIPHERAL-NERVE PALSIES ASSOCIATED WITH A CASE OF JUVENILE DIABETIC-KETOACIDOSIS [J].
ATKIN, SL ;
COADY, AM ;
HORTON, D ;
SUTARIA, N ;
SELLARS, L ;
WALTON, C .
DIABETIC MEDICINE, 1995, 12 (03) :267-270
[3]   Endothelial cell damage and the development or progression of atherosclerosis [J].
Blann, AD .
CLINICAL SCIENCE, 1999, 97 (01) :119-121
[4]   Evidence for endothelial cell activation/injury in heatstroke [J].
Bouchama, A ;
Hammami, MM ;
Haq, A ;
Jackson, J ;
AlSedairy, S .
CRITICAL CARE MEDICINE, 1996, 24 (07) :1173-1178
[5]   POSSIBLE ROLE FOR INCREASED C4B-BINDING PROTEIN LEVEL IN ACQUIRED PROTEIN-S DEFICIENCY IN TYPE-I DIABETES [J].
CERIELLO, A ;
BARBANTI, M ;
GIUGLIANO, D ;
LEFEBVRE, P ;
QUATRARO, A ;
MARCHI, E .
DIABETES, 1990, 39 (04) :447-449
[6]  
CERIELLO A, 1990, THROMB HAEMOSTASIS, V64, P104
[7]   Endothelial haemostatic factors are associated with progression of urinary albumin excretion in clinically healthy subjects: a 4-year prospective study [J].
Clausen, P ;
Feldt-Rasmussen, B ;
Jensen, G ;
Jensen, JS .
CLINICAL SCIENCE, 1999, 97 (01) :37-43
[8]   MODIFICATION OF A HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHIC METHOD FOR ASSAY OF HOMOCYSTEINE IN HUMAN PLASMA [J].
CORNWELL, PE ;
MORGAN, SL ;
VAUGHN, WH .
JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS, 1993, 617 (01) :136-139
[9]  
De Cristofaro R, 2002, THROMB HAEMOSTASIS, V87, P58
[10]   RISK-FACTORS FOR CARDIOVASCULAR-DISEASE IN IDDM - A STUDY OF IDENTICAL-TWINS [J].
DUBREY, SW ;
REAVELEY, DR ;
SEED, M ;
LANE, DA ;
IRELAND, H ;
ODONNELL, M ;
OCONNOR, B ;
NOBLE, MI ;
LESLIE, RDG .
DIABETES, 1994, 43 (06) :831-835