NHS Camden – How to Manage the Poorly Controlled Type 2 Diabetic
Speaker key
MV Mark Vanderpump
UM Unidentified Male
UF Unidentified Female
MV I’ve been asked to do poorly controlled diabetes. If you’re telling someone what a HbA1c means, I say, look, if you take two away and double it, that’s been your average blood sugar, and people always think, because my HbA1c is nine, my average sugar is nine.
If you start telling them that it actually means your average sugar is 14, and they look at you with some horror. It’s also quiet interesting how good diabetics actually think their sugar is six, but when you say, actually it means your average sugar is eight, and your HbA1c is seven, your average sugar is about ten, and they’re quite surprised that so-called good control, how high your average blood sugar is, and there’s quite variable rates of glycation.
This is my way that I now work it out, because I stay on the old units, just to say, it’s quite a neat system. Minus 2, minus 2, so 6, take 2 from 6, becomes 4, take 2 from 4, becomes 42, 5 becomes and then 3, 6 from 8, 2 from 8 is 6, then 2 from 6 is 4, so I just write that down on the pad in front of me. So, when someone comes in with a 79, I know that’s going to be 9.4. It’s quite neat, isn’t it?
Someone else came up with that, not me, by the way, but it also fits quite nicely with the take two away and double it, so it’s got a nice symmetry, I found.
This is quite… this is now how that relationship I was talking about was created, when you’ve got this HbA1c and your average blood sugar. So, these are the individual patients that created that take two away and double it, so there’s a 10%, there’s the straight line that means your sugar is 16.
Okay, but what’s quite neat to show is that this guy here has an HbA1c of 11.5, and his sugar is only about eight average. This person here has got a HbA1c of about seven, and an average sugar of about 16, so if you start introducing insulin to this person, they’re going to go hypo with their first two units. This guy, you’re going to keep telling, because he’s not monitoring, that he’s doing brilliantly. He keeps exactly where he is.
Everyone happy with that? In terms of what you’re going to do? Do you think this guy could be reassured, that his sugar is 20 and his HbA1c is only seven?
Would you treat his HbA1c if you knew he was in that group? Well the reason why may not is that it’s all about glycation and those varying rates of glycation and all the long term outcomes are according to HbA1c, so if you are lucky enough to glycate at quite high levels, then maybe you’re protected against long term complications. And, maybe this person is going to get complications at much lower sugars, if you like, because they’re glycating so abnormally, maybe that reflects.
Anyway, it’s just an interesting approach. The key thing, we always have that concept that people made up, in the old days, when, I don't know if anyone remembers when diabetics used to check their blood sugars, do you remember those days?
And, people who’d come to you with a HbA1c of 10% and they’ve all got a sugar of five, six or seven, you go yes, right, and they have this concept that they made it up on the bus on the way in, but of course, this poor guy may actually be telling the truth, so you’ve just got to be a bit careful, believe the patients and actually, now and again, doing the odd blood sugar, like we used to in the old days, actually can help you.
So, just in terms of the natural history, the key concept then is this insulin resistance, where many, many years, and this could be up to 20 years before you get diabetes, that by the time your sugar starts to go up, you’ve still got a higher insulin level than your non-diabetic. But basically you just can’t keep your foot flat on the floor of the car anymore, and gradually you get this beta-cell exhaustion, and that’s when your sugar starts to rise. And this could be four to seven years before you get frank diabetes symptoms, and that was always the epidemiological projection, but of course, now you’re screening everyone, you’re finding all this undiagnosed, asymptomatic disease, you’re trying to catch people in that very early phase, when the HbA1c has gone up, and they haven’t got hyperosmolar symptoms.
The only other thing I have apart from a stethoscope, which I occasionally forget is a tape measure, and it’s always around the belly button, but it’s a really nice tool to demonstrate. What I do, I draw a circle, I say, look, the fat you can feel, the love handles between 25 and 35 BMI is only an inch. That’s why liposuction doesn’t work. Not only that, it reappears within a year. The fat you’re getting is all intra-abdominal fat, and that’s inside the gut, inside the liver and that’s collecting because your insulin doesn’t work anymore, so what you’re doing is you’re catching this phase here of your fat starting to represent this sign of insulin resistance. Catch them 20 years before they get it.
And, the other interesting thing, I think, you know, the South Asian men actually have a much higher insulin resistance at a much thinner abdomen, so actually their risk of diabetes is kicking off much earlier in that waist circumference, so you’ve got to take a couple of inches off for the South Asian men in terms of their risk, so actually their risk is starting to go up at 35, rather than 37.
Now, the other key thing, I think, in this area is the patient’s self blame attitude, where you’ve got to really get across this fact that they come in, and they say, it’s a bit like going to the headmaster, they think they’ve failed, they’re on their tablets, they’ve not behaved themselves, or they may not have done, but they do have to be told that, after a while, everybody gets worse. It’s not their fault as such, and as I said, I usually say to them, look, if I was seeing you 10 to 15 years ago, I would have told you, you’ve got a one in two chance of seeing me today for injectable therapy.
Remove that blame from them, so it’s one of those hurdles that you’ve got. So, there’s lots of hurdles that have been shown to stop people getting injectable therapy, a lot of it actually interestingly is from the doctor, rather than the patient, but from the patient, this sort of blame culture is actually quite important, so try and remove that. And again, I often just draw out what happens to people over the years, and no matter what the intervention, you can keep pulling the line down, with more and more tablets, but eventually you lose.
If you’ve not got any, I say, at the time you’re diagnosed, you may be down to 20% of your beta-cell function, by the time you get down to 5%, no matter how many tablets you take, it isn’t going to work, so just tell them that 15%, and some people are going to drift off. If you’re a young, thin type II, you may need insulin within a couple of years. If you’re a very overweight type II, a bit older, it may be 30 years, so there’s clearly a wide variation. So you’ve got to really look at your type II’s, particularly the younger ones. How quickly do you think they’re going to fail and in terms of their beta-cell function?
So, this is the traditional model that we had, where you started dieting and exercise, you gave them one tablet, they were fat, you gave them Metformin. If they were thin, you gave them Gliclazide. When either of those failed, you added the other one, when those failed, you just added insulin, so that is the very traditional model, and of course, life has become slightly more complicated than that now, and it’s also interesting, just to the point that’s been given to primary care, that actually the choice of agents has really expanded and made it quite a tricky choice sometimes.
One of the key things I try and get across to people who are managing. Often you might have 2-300 patients with type II. A lot of them may have poor control, who do you focus on? And, I think one of the things we’re not very good at is realising how little glucose lowering does to improve your life expectancy, and so what you’ve got to remember is actually, before you intervene with the glucose lowering intervention, is what are you actually offering that patient?
Who are the 20% maybe of your group of patients who you really need to be focused on, who really need their glucose lowering? And, I was just reading, sorry, I didn’t have a chance to do a slide, I only saw it today.
This is just the numbers needed to treat for five years, to prevent an event, and I’ll read it out, but the top line is, cholesterol reduced by 1 mmol/l, blood pressure reduced by 10 mmHg, HbA1c by 1%, so you’ve got to treat 60 patients for five years, and reduce their cholesterol, to stop one heart attack, but actually the glucose, that’s 140, so it’s a lot of people to reduce their blood glucose by 1%, for five years. If you add that up, that’s 30 quid a month, with some of the new tablets.
How many people are you actually stopping getting an event when you’ve only got 140 there? So, it’s 139 would not have had an event, and the other, there’s an NNH down here, which is the number needed to harm, and that’s 21.
So, the same reduction in HbA1c harms one in 21 patients, and only protects in terms of heart attacks, one in 140, the stroke is one in 767, and cardiovascular disease in total, it’s 118, so you’re treating in sugar terms your whole population of practice, if we say roughly what you’ve got, in terms of most practices may be 2-300, if you gave all of them an agent to reduce their HbA1c by 1%, you stop one heart attack. It’s actually amazingly few, so you’ve got to think about who is going to benefit from the glucose lowering.
So, you tend to think about the younger people, because the UK PDS suggested you needed to live for ten to 15 years with your lower sugar, to actually get a benefit in mortality, therefore if you are a 75-year-old man in Camden, with an expected life, maybe five years or so, you are not going to live long to demonstrate that benefit, if it’s just sugar lowering you’re offering them.
If he’s got retinopathy, or a microvascular complication, which is clearly sugar dependent, then you have an obligation to get their sugars down, but it’s amazing how many people I see with type 2 diabetes who have had it for years, terrible blood sugars and they’ve still not got a single dot at the back of their eye.
In some ways, some of them still seem to be protected, no matter what they do. They don't seem to get any microvascular complications, so it’s really thinking about the younger people who are going to live for a long time, plus the group, who are getting progression of their microvascular complications as the key people to lower sugars.
The rest of them, you could probably be quite relaxed about your HbA1c targets, and start to individualise the care of each patient, rather than just following an algorithm, that all 150 patients need their HbA1c down by 1%.
The other thing to remember, and I know it’s not on this slide, it’s on this slide, is you know, there’s been quite a lot of studies now that have shown in this aggressively treated 65-year-old group roughly, getting their HbA1c nearer to 6.5% increased mortality in the first three to five years, and that increase in mortality persisted for five years from the end of the trials, which were stopped, because the interventions were actually killing people.
So, I think you’ve just got to be concerned about what patients you’re really targeting, with your glucose lowering, poorly controlled type 2 diabetes, as the umbrella type.
Anyone seen Sky Four? I think this is probably the lizards in the casino basin that he throws the baddy into. And, this is quite a cool guy, who only eats twice a year, obviously if James Bond is around, it’s a bit more often, and he’s got a saliva packed full of GLP-1, which is a newish agent now in type 2 diabetes, the first real one to start people losing weight as well as benefiting their control.
And, you can potentiate that effect in two ways. One is, you can inject direct, or secondly, you can stop the breakdown of a slightly reduced amount of GLP-1 in type 2 diabetes, and leave it hanging around longer, so it actually exerts a sugar lowering effect.
So, I just thought I’d mention that there’s been a new agent, some of you may have heard of, which is quite a novel way of lowering sugar, by increasing the amount of glucose excreted in the urine, it’s a specific receptor within the sodium glucose transport in the kidney. It’s a very glucose dependent effect, so basically it doesn’t cause hypoglycaemia. It reduces your HbA1c by 1%, which is what you’d expect of any good diabetic drug.
It’s gone through the NICE process, it’s got a bit of a negative review, but I think probably this is a concept that we’re going to hear a bit more of. It’s also weight losing.
The problems with it are that one, is that it increases the sugar obviously in the urine, which is why you’re getting rid of sugar from the blood, so there’s a higher risk of urogenital infections. There have been one or two issues about bladder cancer, which clearly, given the controversy with pioglitazone is a bit sensitive, but I just think it’s quite a neat way, and of course, we’ve got bariatric surgery that we don't normally talk about in this country very often, but it can be a very effective way of curing type 2 diabetes.
This is a 52-year-old Asian, quite a nice case, he’s Kenyan Asian origin, and he was...this is a guy now and in terms of who you worry about, this is somebody who I would worry about.
He had a heart attack when he was 32, no family history of diabetes or heart disease, interestingly. Ten years later, he got diabetes, and hadn’t really been doing much with it. He’d been seen elsewhere, and was on these gliclazide and metformin, and elsewhere recognised that he’d got poor control and started NovoMix 30, but he described quite significant bruising and lipohypertrophy at the site of injections, and then had just given up with taking it.