In the 2003 American Diabetes Association Clinical Practice Recommendations, some statements in the Position Statement “Hyperglycemic Crises in Patients With Diabetes Mellitus” (1) lack support in the literature.

1) On p. S109, the authors write “The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies… with resulting ketonemia and metabolic acidosis.” According to Mayes (2) and Watkins et al. (3), there is no relationship between the plasmatic levels of free fatty acids and ketone bodies.

2) On p. S110, the authors write “Successful treatment of DKA… requires correction of hyperglycemia…” Both Watkins et. al. (3) and Malchoff et al. (4) have observed no correlation between serum glucose and serum ketoacid concentrations in acutely decompensated diabetic patients. In other words, serum ketoacid concentration is glucose independent, and, thus, not influenced by the decrease of hyperglycemia toward normal values.

An explanation for the readers of Diabetes Care would be useful.

1
American Diabetes Association: Hyperglycemic Crises in Patients With Diabetes Mellitus.
Diabetes Care
26 (Suppl. 1)
:
S109
–S117,
2003
2
Mayes PA: Absence of a relation between lipogenesis and ketogenesis in vivo.
Nature
183
:
540
–541,
1959
3
Watkins PJ, Hill DM, Fitzgerald MG, Malins JM: Ketonaemia in uncontrolled diabetes mellitus.
BMJ
4
:
522
–525,
1970
4
Malchoff CD, Pohl SL, Kaiser DL, Carey RM: Determinants of glucose and ketoacid concentrations in acutely hyperglycemic diabetic patients.
Am J Med
77
:
275
–285,
1984