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In a recent issue of the journal McNulty and Hardy published a very interesting case history on the failure to develop diabetic ketoacidosis in a newly presenting type 1 diabetic patient.1 Their third self assessment question was “What may be the explanation for this profoundly unwell patient with type 1 diabetes and hyperglycaemia not to have developed diabetic ketoacidosis?” The authors' explanation is “because her insulinopenia was offset by her hypoadrenalism”.
However, in patients with diabetic hyperglycaemic hyperosmolar syndrome (without ketaocidosis, as in the authors' patient) increased concentrations of adrenal hormones are usually found.2 This makes the authors' explanation very improbable. On the other hand, Schade and Eaton pointed out in 1977 (their p.596) that “insulin deficiency per se may not alone cause ketoacidosis”.3 An illustration of this problem is in the paper by Burge et al4: they compared two groups of diabetic patients, with lower and higher hyperglycaemia. Ketone bodies were higher in the group with lower blood glucose. In decompensated diabetes mellitus, increased amounts of 34 organic acids have been identified5; it is not known whether they are insulin dependent or not. Nevertheless, they can cause severe acidosis, for example, a blood pH of 6.85 was found in the patient of Vernon and Postellon in absence of acetoacetic and β-hydroxybutyric acids.6
Therefore, the authors should also ask: What are the exact mechanisms and details of development of both ketoacidosis and acidosis without ketone bodies in diabetic patients?
Authors' Reply to Letter
Rosival describes our explanation of the case as �very improbable� and implies that our patient may have had hyperglycaemic hyperosmolar syndrome without ketoacidosis ( HONK). HONK occurs in Type 2 diabetic patients, with residual insulin secretion; however, we demonstrated (by glucagon-stimulated c-peptide measurement) that our patient had Type 1 diabetes i.e. insulin deficiency.
We agree adrenal hormones are typically elevated in diabetic metabolic decompensation
(HONK and ketoacidosis) and are indeed implicated in the pathogenesis of both. Our
case illustrated this point: despite the fact that our patient had proven absolute insulin
deficiency (the hallmark of Type 1 diabetes), she did not develop ketoacidosis because
of her co-existent glucocorticoid deficiency (Addison�s disease).
Dr S J McNulty
Dr K J Hardy
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