In part 3 of this Exclusive Interview, Kathleen Wyne talks with Diabetes in Control Medical Editor Joy Pape during the AACE 2018 convention in Boston, MA about the insufficiency of DKA as a method of diagnosing diabetes.
Kathleen Wyne MD, PhD, FACE, MACP, FNLA is an endocrinologist and Director of the OSU Adult Type 1 Diabetes Program at The Ohio State University.
Transcript of this video segment:
Pape: So, why is DKA no longer sufficient to make a diagnosis?
Wyne: That’s actually an interesting question too because for many of us when we train, DKA by definition was type 1 or we would say it was pathognomonic of type 1. So, I did part of my training in Texas where some years ago, and I’m not going to say how many, we started seeing certain minority groups coming in with DKA. They required very high doses of insulin – very insulin resistant. They settle out on the insulin infusion at 4 to 6 units an hour, whereas a true type 1 would be at .5 to 1. If you were to do C-peptide at that point, it would be undetectable. You discharge them on insulin, two weeks later, they’re calling in that they’re hypoglycemic. Three months later, their C-peptide is very, very high because they regained their beta cell function; they’re behaving like type 2s. What we’ve learned is that certain people with type 2, if they go untreated long enough, with their high free fatty acids and lipotoxicity and glucotoxicity, the pancreas just stops making insulin. It basically says, forget this I am not going to do this anymore. So, they go into DKA because it’s the absence of insulin that gives you the DKA, not the high sugars. So, once you resolve the glucotoxicity and the lipotoxicity, the pancreas starts making insulin again, and it could keep making it for quite a few years. The best description of this ketosis-prone type 2 diabetes, I think, comes from a cohort from sub-Saharan Africa where they described these lean people who come in, insulin resistant, come in with DKA, and they do beautiful for about five years, and somewhere at about five to seven years, the A1C starts to jump up and then it goes up high. But the key is ketosis-prone type 2 is a very different phenotype than the classic type 1. So, you don’t know what the cause of the DKA is – is it complete loss of beta cells or is it temporary loss of beta cell function? C-peptide doesn’t tell you does it?
Pape: No, and that begs another question: What about the people who are prone to DKA, people who have type 2 diabetes on SGLT2?
Wyne: Oh! So that’s our euglycemic DKA. Euglycemic DKA has been in the literature for many years, we just kind of all forgot about it, but it has always been there. The key there is that with the recognition, the SGLT2s brought it out that we need to remember these exists. We have found a couple of the predictors, but more importantly, we need to rethink and change the way we teach DKA to our medical students, our residents, and this includes internal medicine, family medicine, and emergency medicine. They need to understand that glucose is not required for DKA. If you look at the physiology, the biochemical changes, everything that causes DKA, causes hyperglycemia. But, they are not bidirectional arrows. The glucose is not causing the DKA, it’s the lack of insulin that’s causing the DKA.
So, what are the predictors that we have? One is eating a low-carb diet on one of those agents. The other one, quite simply, is not taking your insulin, which is going to cause DKA anyway, right? But that’s one of the components or just simply taking too little insulin. Something that needs to be kept in mind is that when you’re hyperglycemic, if you’re drinking enough fluids, you can maintain your sugar around 250. So, when my patients come into the ER, and they say, “I have type 1 diabetes, I’m throwing up, my stomach hurts, I think I have DKA,” and the ER says, “Well, your sugar is below 350, go home,” that’s the perfect example of why we need to retrain people to understand it’s not sugar. Just because the sugar is below 350, doesn’t mean they are not in DKA. That’s the lesson we need to learn.