Diabetes type 1.5

AKA Flatbush diabetes, atypical diabetes, diabetes type 1B and more recently ketosis prone type 2 diabetes. This increasingly recognized but still under appreciated condition was reviewed in the March 7 2006 issue of Annals of Internal Medicine.

With the emergence of this relatively new profile of diabetes the traditional classification has been challenged. Older concepts, though useful and largely true, must now be nuanced. For the past 20 years the defining characteristic of type 1 DM has been that when deprived of exogenous insulin the patient invariably develops ketoacidosis (DKA) in the basal state. In contrast, while type 2 diabetics may develop ketosis under stress (e.g. with myocardial infarction, sepsis, etc.) they never develop DKA in the basal state.

For classic types 1 and 2 these principles remain valid. They were a welcome replacement to the outmoded notion of “adult versus juvenile onset” types and the more recent (and extant but nevertheless confusing) terms “insulin dependent” and “non-insulin dependent” diabetes.

Enter now the new profile which might be described as the occasional but not invariable development of DKA during exogenous insulin deprivation in the basal state. These are the patients who come in with DKA (often with no apparent precipitating stress) but who, weeks or months later, discontinue insulin and do just fine. At times they behave like DM-1; at other times they look for all the world like DM-2.

What’s going on? Since these folks were first noticed in 1987 they tended to be regarded as a fuzzy overlap syndrome, poorly understood. Research in the ensuing years has improved our understanding of the condition and it’s all nicely summarized in the Annals review. Take home points follow.

1) It tends to be seen in African American and Hispanic persons, though not exclusively so. 25% to 50% of African American and Hispanic patients who present with DKA (not to be extrapolated to all African Americans and Hispanics with diabetes) have been reported to exhibit this profile.
2) Unlike classic DM-1, patients tend to be obese at presentation with DKA.
3) It does not appear to be an autoimmune disorder, in contrast to the well documented autoimmune beta cell destruction of classic DM-1. Instead it’s an intermittent reversible beta cell failure.
4) The beta cell failure appears to be, at least in part, an exaggerated form of glucose toxicity. Thus, presentation with DKA may follow a prolonged period of uncontrolled hyperglycemia, with recovery of beta cell function following a period of glycemic control with insulin.
5) More than 80% of patients have a family history of DM-2.
6) This profile of diabetes is to be distinguished from other atypical forms of diabetes including MODY and LADA.

Note---to confuse things, LADA in some writings has been given the designation DM-1.5. One of these days maybe the experts who sit down at meetings and talk about such things will deliver a clarification, written in stone.