摘要
目的探讨导致糖尿病酮症(DK)及酮症酸中毒(DKA)患者肝损害的相关因素.方法DK或DKA患者99例,其中ALT及AST均异常升高11例(A组),单项ALT异常升高13例(B组),肝功能正常75例(C组),对以上各组患者的血二氧化碳结合力(CO2CP)、尿素氮(BUN)、血糖(BG)和血浆渗透压(OSM)进行了统计分析.结果A,B两组患者的CO2CP明显低于C组(P<001,t=633和t=643),而BUN则明显升高(P<001,t=361,AvsC;P<001,t=435,BvsC),A组的BG(P<005,t=284)和血浆OSM(P<005,t=310)水平也显著高于C组,而B组患者的BG及血浆OSM与C组比较无差异;与B组相比,A组患者的CO2CP明显降低(P<002,t=271),BG(P<005,t=289)和血浆OSM(P<005,t=236)明显升高.此外,Ⅰ型糖尿病患者血清转氨酶异常升高的发生率明显高于Ⅱ型糖尿病患者(P<005,χ2=438).结论酸中毒和脱水是导致糖尿病酮症及酮症酸中毒患者肝损害的重要因素,酸中毒及脱水程度与肝损害程度相关.
AIM To study the factors causing hepatic damage in patients with diabetic ketoacidosis. METHODS Ninety nine patients with diabetic ketosis or ketoacidosis, including 11 patients with an elevation of serum ALT and AST activity (group A), 13 patients with an elevation of the serum ALT activity (group B) and 75 with normal liver function (group C), were enrolled in this study. The values of the serum carbon dioxide content (CO 2CP), urea nitrogen (BUN), glucose (BG) and the plasma osmolarity (OSM) in the three groups were analysed statistically. RESULTS The values of CO 2CP in groups A and B were lower than those in group C ( P <0 01, t =6 33 and t =6 43), and serum levels of BUN ( P <0 01, t =3 61), BG ( P <0 05, t =2 84) and OSM ( P <0 05, t =3 10) in group A were higher than those in group C. The values of CO 2CP ( P <0 02, t =2 71), BG ( P <0 05, t =2 89) and OSM ( P <0 05, t =2 36) in group A were also statistically different from those in group B. In addition, the incidence of the hepatic injury in type Ⅰ diabetic patients was significantly higher than those in type Ⅱ diabetic patients ( P <0 05, χ 2=4 38). CONCLUSION The acidosis and dehydration play an important role in the mechanism of the hepatic damage in patients with diabetic ketosis and ketoacidosis, the degree of decline in the serum CO 2CP is correlated with the severity of hepatic injury.
出处
《世界华人消化杂志》
CAS
1999年第1期66-67,共2页
World Chinese Journal of Digestology
关键词
糖尿病
酮症酸中毒
病理生理学
肝疾病
病因学
diabetic ketoacidosis/complications
diabetic ketoacidosis/physiopathology
liver disease/etiology