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Review:
Jean-Louis Chiasson, Nahla Aris-Jilwan, Raphaël Bélanger, Sylvie Bertrand, Hugues Beauregard, Jean-Marie Ékoé, Hélène Fournier, and Jana Havrankova
Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state
CMAJ 2003; 168: 859-866 [Abstract] [Full text] [PDF]
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[Read eLetter] Question to the authors
Viktor Rosival   (21 May 2003)
[Read eLetter] Thank you very much
Antonio P. Ligot   (3 April 2003)

Question to the authors 21 May 2003
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Viktor Rosival,
physician
Derers Hospital, Bratislava, Slovakia

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Re: Question to the authors

rosivalv{at}hotmail.com Viktor Rosival

In the review „Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state“ by Chiasson et al(1) are several discrepancies with the literature.

1. „Low insulin and high catecholamine concentration will reduce glucose uptake by peripheral tissues“ (p 859). According to Sonksen and Sonksen(2) glucose uptake by peripheral tissues is insulin independent.

2. „Relative insulin deficiency is the cause of HHS, absolute is the cause of DKA“ (fig 1 on p 860). According to Gerich et al(3) there is no difference in the plasmatic concentration of insulin in patients with DKA and HHS.

3. „The use of bicarbonate in the treatment of DKA remains controversial. The rationale for bicarbonate therapy is the theoretical assumption that severe acidosis could contribute to organ malfunction, such as of the ...brain“ (p 865). In DKA, life threatening is only its most severe stage, coma (4,5), and the immediate cause of coma is low blood pH(6): the glycolytic enzyme phosphofructokinase is inactivated by decreasing pH and the consequence is impaired glucose utilisation in brain cells. Lever and Jaspan(7) have reported 27 comatose patients with DKA and blood pH below 7.10. They were treated with sodium bicarbonate: all recovered to full alertness, and no adverse effects of the therapy have been registered. Where is there a published report on a similar number of comatose patients with DKA with zero lethality, without sodium bicarbonate and without increase of the low blood pH?

An explanation of these discrepancies for the readers of CMAJ would be useful.

Sincerely, yours

Viktor Rosival, Department of Clinical Biochemistry Dérer's Hospital, Limbová 5, SK-833 05 Bratislava Slovakia, Europe, e-mail address: rosivalv@hotmail.com

References 1. Chiasson J-L et al.,Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ 2003;168(7):859-66. 2. Sonksen P, Sonksen J. Insulin: understanding its action in health and disease. Br J Anaesthesia 2000;85:67-79. 3. Gerich J, Martin M, Recant L. Clinical and metabolic characteristics of hyperosmolar nonketotic coma. Diabetes 1971;20:228-38. 4. Madison LL. Low-Dose Insulin: A Plea for Caution. N Engl J Med 1976;294:393-4. 5. American Diabetes Association. Hyperglycemic Crises in Patiens With Diabetes Mellitus. Diabetes Care 2003;26 (Suppl 1):Sl09-17. 6. Alberti KGMM, Zimmet P, DeFronzo RA, Keen; H. International Textbook of Diabetes Mellitus, second ed 1997, p 1218. 7. Lever E, Jaspan JB. Sodium bicarbonate therapy in severe diabetic ketoacidosis. Am J Med 1983;75: 263-8.

Thank you very much 3 April 2003
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Antonio P. Ligot,
general surgeon/Hospital Director
Good News Clinic &Hospital

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Re: Thank you very much

goodnch{at}hotmail.com Antonio P. Ligot

Dear CMAJ.JAMC,

Thank you very much for the article on Diagnosis and Treatment of Diabetic Ketoacidodis and Hyperglycemic Hyperosmolar state. Much more so thank you for not requiring subscription membership to download the article. We, in the Philippines can not avail of subscription membership through email for reason beyond our control.

Respectfully,

Antonio P. Ligot, M.D.