Abstract
The mechanism of CPK elevation was elucidated in two groups of patients with severe acute diabetic syndrome: group A, CPK >200 IU/L; group B, CPK <200 IU/L. Group A consisted of patients with ketosis (n=1), diabetic ketoacidosis (DKA, n=8) and nonketotic hyperosmolar coma (NKHC, n=2). Group B consisted of these with ketosis (n=14), DKA (n=14) and NKHC (n=2). In each group, correlations between CPK and mean blood pressure (MBP) and other laboratory findings were evaluated. Furthermore, the amount of insulin and i.v. fluid given to control the plasma glucose (PG) level to 250 mg/dl were compared between the two groups. In group A, the mean MBP value was lower and PG, plasma osmolarity (Osm), BUN and Cr were higher compared with those in group B. In group A, there was a significant correlation between CPK and BUN (r=0.73), Cr (r=0.72), Osm (r=0.58), PG (r=0.55), SGOT (r =0.40) and MBP (r=-0.36). Although no significant change in the amount of insulin was noted, the amount of i.v. fluid was larger in group A. These results indicate that peripheral circulatory failure due to dehydration could be an important causative factor for CPK elevation in severe acute diabetic syndrome.
