Abstract
A 60-yr-old woman with diabetic ketoacidosis and with a markedly increased level of serum creatine phosphokinase (CPK) is described. She had been treated with insulin after a diagnosis of diabetes mellitus had been made at the age of 49. On January 12, 1979, she experienced thirst, polydipsia, and polyuria. Two days later, she became somnolent. On January 15, she was admitted to hospital due to loss of consciousness. On admission the patient was in a state of shock. Her blood pressure was 55/30 mmHg, and she had cold extremities and a pulse rate of 116 per min. The body temperature was under 35°C. Respiration was rapid and deep at 24 per min. The blood glucose level was 1672 mg/dl, and the serum Na, K, and Cl values were 124 mEq/L, 7.1 mEq/L, and 81mEq/L, respectively. Serum ketone bodies were positive. Being diagnosed as having diabetic ketoacidosis, she was treated with a continuous low-dose intravenous infusion of Actrapid insulin at 6 U per hr and infusion of saline. The next morning, her consciousness became clear. On January 16, the serum CPK increased to 1710 IU/L despite its having been normal on admission. Two days later, it attained a peak value of 2888 IU/L, and thereafter gradually declined to the normal range by the 12th day after admission. The serum GOT, GPT, and LDH had peak values of 180 IU/L, 96 IU/L, and 768 U, respectively. Electrocardiograms taken during and after the treatment for diabetic ketoacidosis revealed no changes suggestive of myocardial infarction. Examinations for CPK isozymes showed an increased percentage of the MM type (97%) with a small percentage of the MB type (1-2%), As myositis, trauma, and intramuscular injection could be excluded, we concluded that the increase in serum CPK resulted from abnormalities of the muscle cell membrane. The mechanisms governing an increase in serum CPK in diabetic ketoacidosis are discussed.
