how can we effectively address clinical inertia to improve ... · melanie davies: so, we need to...

How can we effectively address clinical inertia to improve glycaemic control in patients with type 2 diabetes?Transcript from a touchPANEL DISCUSSION

0.5 AMA PRA Category 1 Credits™

Funded by an independent medical education request from Merck Sharp & Dohme Corp. This activity is provided by touchIME.

PROF. DEL PRATOProfessor of Endocrinology and Metabolism, School of Medicine,

University of Pisa, Pisa, Italy

PROF. DAVIES (Chair)Honorary Consultant

Diabetologist, University Hospitals of Leicester

NHS Trust, Leicester, UK

PROF. DAGOGO‑JACKChief of Endocrinology, Diabetes

and Metabolism, University of Tennessee Health Science Center,

Memphis, TN, USA

www.touchendocrinology.com/education-zone/ 2

touchPANEL DISCUSSION

A panel of internationally renowned diabetes experts discuss the impact of clinical inertia in the treatment of type 2 diabetes, and how it can be addressed in clinical practice.

Professor Melanie Davies chairs a discussion with Professors Samuel Dagogo ‑Jack and Stefano Del Prato to review current knowledge of clinical inertia in type 2 diabetes, and how and why clinicians must tackle this important issue.

This activity is intended for diabetologists, cardiologists and primary care physicians who treat patients with type 2 diabetes.

This touchPANEL DISCUSSION was recorded in January 2020.

INTRODUCTION

• Define the potential impact of clinical inertia on their patients with type 2 diabetes

• Identify the patient subgroups who will benefit most from early intensification of antihyperglycaemic treatment

• Describe which of their patients will benefit from early treatment intensification and how changes can be implemented into clinical practice

LEARNING OBJECTIVES:

TOPICS DISCUSSED:

After watching this touchPANEL DISCUSSION, participants should be better able to:

• What is clinical inertia in type 2 diabetes and what is its impact on patients?

• How can early treatment intensification improve glycaemic control?

• Are there specific patient subgroups who could benefit from early antihyperglycaemic treatment intensification?

touchIME ENDOCRINOLOGY3

Clinical inertia in type 2 diabetes

HOW CAN WE EFFECTIVELY ADDRESS CLINICAL INERTIA TO IMPROVE GLYCAEMIC CONTROL IN PATIENTS WITH TYPE 2 DIABETES?

Melanie Davies: Hello. My name’s Melanie Davies, and I’m a Professor of Diabetes Medicine and honorary Consultant Diabetologist at the University Hospitals of Leicester NHS Trust in the UK.It’s my great pleasure to welcome you to this discussion about tackling clinical inertia to improve glycemic control in people with type 2 diabetes, and I’m joined by a fantastic faculty. I’m really pleased to welcome Professor Sam Dagogo‑Jack, Chief of Endocrinology, Diabetes, and Metabolism at the University of Tennessee in the U.S. Welcome, Sam. Sam Dagogo‑Jack: Thank you, Melanie.Melanie Davies: And also Professor Stefano Del Prato, who’s Professor of Endocrinology and Metabolism at the School of Medicine, University of Pisa, in Italy. Welcome, Stefano. Stefano Del Prato: Thank you, Melanie.Melanie Davies: So, over the next 30 minutes or so we’re going to discuss this very important issue of clinical inertia. We are going to look in three areas.

Agenda

Firstly, why it’s important to identify and address clinical inertia in our patients with type 2 diabetes; how early treatment intensification can improve glycemic control and how we might go about addressing that; and finally to think about particular groups of patients or groups of people with type 2 diabetes who would benefit particularly from earlier treatment intensification.So firstly I want to tackle this first area, what is clinical inertia, why it’s important, and how it can lead to adverse outcomes for our patients, and to just very briefly touch on some of the factors that lead to clinical inertia. And just to start, I just want to refresh our viewers’ memory about the recent ADA EASD consensus, which really reminded us that we need to put the patient at the heart of their treatment, really think about patient‑centered care, and that really what we’re trying to do is to address interventions that really improve the quality of life of our patients and reduce complications, and how it’s really important to think about that particular patient and address their key characteristics to really optimize treatment.

Why is it important to identify and address clinical inertia in patients with type 2 diabetes?

Decision cycle for management of type 2 diabetes1

1. Davies MJ, et al. Diabetes Care. 2018;41:2669–2701. American Diabetes Association. Management of hyperglycemia in type 2 diabetes, 2018. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD), American Diabetes Association, [2018]. Copyright and all rights reserved. Material from this publication has been used with the permission of American Diabetes Association.

We highlighted this problem of clinical inertia and how important it is for us as clinicians to think about that very early, and to take into account all of the factors within an individual patient that may impact on outcomes, things like mental health, depression, their social circumstances, and to really work with patients to overcome some of these issues. And this is important because we know that clinical inertia, which is this failure to properly intensify treatment and reach good glycemic control, leads to poor outcomes for our patients.

Consequences of clinical inertia and lack of early treatment intensification1,2

HbA1c, haemoglobin A1c; CV, cardiovascular.1. Khunti K and Millar‑Jones D. Prim Care Diabetes. 2017;11:3–12. 2. Paul SK, et al. Cardiovasc Diabetol. 2015;14:100.

It impacts on their long‑term risk of cardiovascular disease. It increases their risk, for example, of MI, stroke, heart failure if we don’t achieve good glycemic control, particularly early in treatment, particularly early on. And we’re starting to understand that this is a complex problem that involves factors within the clinicians themselves, concerns about some of the treatments we have and the side effects that they may cause, lack of knowledge sometimes, and training of healthcare professionals.



Barriers generating clinical inertia1,2

CV, cardiovascular. 1. Khunti S, et al. Br J Diabetes Vascular Dis. 2015;15:65–69.2. Okemah J, et al. Adv Ther. 2018;35:1735–1745.

And I think it’s true to say it’s becoming a very complex area, lots of choices for clinicians to choose from, and difficult to keep up to date with all the recent guidelines. There are undoubtedly particular factors within people with diabetes themselves that may lead to clinical inertia. And we’ll talk about this, but also there may be issues in the health system itself that may impact on access and other factors. So, Stefano, can I come to you first in terms of how big is this problem of clinical inertia, and what’s your experience and your view? Stefano Del Prato: Melanie, clinical inertia is a big problem because, if you just look at the data available in terms of what is the rate of success in terms of achieving a given value for glycogen/hemoglobin ‑ maybe we can come back a later on in term of visualization also for the target ‑ but if you look in general in a user, there the classical goal of 7% HbA1c, and you look at the number of people achieving that goal, this is very low. And actually, there are very interesting data coming from the U.S., from your country, Sam, showing that in the past 20 years, there was not very much of a change in terms of the percentage of people achieving that goal. This is particularly striking in light of the increased number of drugs that have been made available. So, I do tend to account for this difference in more available drugs, drugs that are supposed to be even more effective, and the fact that the percentage of people achieving the goal is not increasing due to clinical inertia. We maybe are not using [new drugs] in the best

manner, or we are not sufficiently able to implement the potential of the new drug in order to increase the number achieving earlier and better glycemic control. Metformin is the front‑line treatment for diabetes. And if you look at the data available, you can calculate that there is an average failure of between 15–20% of people failing on metformin treatment. And you have been part of the ADA EASD consensus. The recommendation is you fix your target, but you have to be controlling if you are achieving that target at an interval of three months. And you are supposed to move on that on a three‑monthly basis, which is not what’s happening for a number of reasons. And you have mentioned some of those reasons. Melanie Davies: So, Sam, can I come to you, because Stefano’s agreed that this is a common problem and we’ve talked about some of the factors that may contribute. In your view, what are some of those important factors that are really leading to this clinical inertia? Sam Dagogo‑Jack: Thank you, Melanie. The opening comment you made regarding the multifactorial origin of inertia is spot on. We do have the physician or provider‑based constraints, and the contributions from the patient himself or herself and, of course, the healthcare system. And perhaps by far the most worrisome physician factor is the inverse relationship between a plethora of new agents for controlling diabetes and lack of progress in the numbers at goal, and therein lies an opportunity for education. I think a lack of specific education on the part of the generalist who basically handles 80–90% of the diabetes burden



is at the level of the GP, and the endocrinologist is rarely involved. I get referred the complex cases that have defied control at the community level, often already having some complications. And they come to the academic center and visit with a professor of diabetes, and we do crisis control. But more proximally, maybe a decade or so earlier intensification of care appropriately directed could have averted some of the complications we see. So, physician inertia, largely due to perhaps educational barriers or other systems‑based barriers that negate the deliberate intensification of care in a timely fashion. Many physicians are actually sitting too long on elevated HbA1c levels, hoping for some kind of miracle, that the medications that are currently failing somehow would grow muscle and become more efficacious with time. That is warped logic that really needs to be rebutted. There is no physiological basis for anticipating improvement in glycemic control on a drug that has failed in three months, that waiting three more months or one year in some of the studies; people sitting on HbA1c levels of 8% for one and a half years before adding firepower to the regimen. Melanie Davies: So, we need to get it right early.Sam Dagogo‑Jack: Right.Melanie Davies: Stefano, you’ve done a lot of work in this area. What, in terms of the message to the team and the primary care team and the team, the multidisciplinary team in terms of how we should be addressing those newly diagnosed patients and getting it right, any tips there?Stefano Del Prato: You know, I’d just like to follow up what Sam said. You know, I think this is a multifactorial problem. So, we really need to try to approach this on a different level. And on that level, I also use the patient level. I do have the impression that awareness about the severity and how serious diabetes can be in the general population, not just for the patient with diabetes, is not sufficient. I do remember an ADA survey in the American population suggesting that people in America were more concerned about shark bites than diabetes. So, I think that is the first thing. People need to understand that diabetes can be a serious condition. That has to be understood by the general population, by the patient at the time of the diagnosis, by the people at risk of developing diabetes, and by the healthcare providers, of course. And if that is the case, then I think that we have more opportunity to really achieve better outcomes. Now, in a more pragmatic manner, what I think is important is that we need to have the entire team aware of the fact how important it is to achieve good glycemic control. And one way to favor that is to go away from the word of intensive treatment, because intensification, intensive may sound aggressive. I think that we should talk about appropriate treatment.

And appropriate treatment is what we need to go for, is a treatment that tries to achieve good glycemic control while reducing as much as possible side effects, because in that way we may also hope of winning in terms of adherence to the treatment. So, early identification of patients at the time of the diagnosis, starting a treatment that may provide good efficacy with as low as possible side effects because that can reduce the need for a patient to go back to the physician and also increase their adherence, and because of that could also help in reducing inertia.Melanie Davies: So, those are really important points, Stefano. And Sam, we’ve talked a lot about healthcare professionals. We’re talked about the patients. The other factor is the barriers within the system themselves and sometimes access to not only education but also new therapies. Sam Dagogo‑Jack: Right. Melanie Davies: Any sort of considerations? I know that things vary in different healthcare systems. Any comment on that?Sam Dagogo‑Jack: Yes, it’s an important area. Research has shown that, wherever there is some obstacle to accessing care, the results have been less than spectacular. So, in the case of diabetes, the newer medications are efficacious and better tolerated than the older generation drugs, yet in specific markets and territories they may not be on the hospital formulary or the insurance companies’ formulary of preferred agents. They sometimes are relegated to third‑tier or fourth‑tier agents, only to be mobilized after older, less well‑tolerated drugs have failed. And that sometimes can lead to years of exposure to inefficacious and potentially harmful agents before optimizing care by deploying the newer agents. So, a systemic change in the thinking process of those who enact policies about formulary placement of agents is needed. If an efficacious and well‑tolerated drug is permitted to be used early in a healthcare system, the downstream savings from avoidance of complications need to be captured upfront, instead of being discounted and only focusing on the immediate cost of the medications. So, cost, economic thought, sometimes is shortsighted by limiting access to agents that, because of their newness and still being patent protected, may be a little bit pricier than 50‑year‑old agents that are now largely generic and less expensive. But that expense that is driving short‑term decision‑making is indeed shortsighted, because over the lifespan of the patient, the cost can become very effective in preventing greater costs in caring for unnecessary complications.Melanie Davies: So, a really important point. Now we’re going to talk a little bit around how we can try and address clinical inertia and how earlier treatment can improve glycemic control.



How can early treatment intensification improve glycaemic control?

Different strategies to treat hyperglycaemia

OAD, oral anti‑diabetes drug. Adapted from: Del Prato S et al. Int J Clin Pract. 2005;59:1345–55.

And I think, Stefano, you’ve done a huge amount of work in this area, which reminds us that often the traditional approach is to wait to fail, so that we have this stepwise wait until things are not going well before we start something else. And that traditionally has compounded clinical inertia and led to patients really being left with poor control for a long time. And you’ve done a lot of work, and you too, Sam, in terms of reminding us that there should be perhaps a different approach in terms of how we can really try and address clinical inertia, something that we addressed in the ADA EASD consensus, to really think and get people thinking about how they can get in earlier, with treatment really supporting patients early on to try and get better long‑term glycemic control.

DCCT/EDIC: 30‑year effects of early intensive therapy in type 1 diabetes1

DCCT, Diabetes Control and Complications Trial; EDIC, Epidemiology of Diabetes Interventions and Complications; HbA1c, haemoglobin A1c.

1. Nathan DM, et al. Diabetes Care. 2014;37:9–16.

We’ve got examples in the area of type 1, work such as the DCCT trial, which showed us that early intensive treatment with insulin therapy can really lead to good long‑term outcomes. And we’re starting to see some evidence in type 2 around early combination treatment leading to better outcomes, and the VERIFY study of early combination with metformin and DPP‑4 showed that.

VERIFY study: time to first and second treatment failure1

* HbA1c of at least 7% at two consecutive scheduled visits, 13 weeks apart from randomization through period

CI, confidence interval; DPP‑4i, dipeptidyl peptidase‑4 inhibitor; HbA1c, haemoglobin A1c; HR, hazard ratio.

1. Matthews DR, et al. Lancet. 2019;394:1519–1529.

So, Stefano, do you want to comment, because you’ve written a lot of work in this area, in terms of the broad principles of how we can address clinical inertia and what we should be thinking about to really tackle earlier, better control?Stefano Del Prato: Of course, you know, education is important, but I think that also we need to understand



that type 2 diabetes is a complex condition. You know, it may sound simple enough. You know, we tend to blame the habits of the people, they eat too much, they don’t exercise, which is totally true. However, all this impacts on a very complex pathophysiologic background, and we need to understand that that is the case. We started off thinking ‑ and proving ‑ that type 2 diabetes is the result of an impairment of insulin secretion and insulin action. But now we have realized there are multiple other factors contributing to that. And now we have better way to address those factors because we have more specific drugs hitting on each one of those pathophysiological mechanisms.So, if you do appreciate that type 2 diabetes is a complex condition, I think that it is sort of natural to consider that starting with one treatment and hoping that one treatment is able to ensure sustained glycemic control is very unlikely. And there is a number of evidence for that, starting from the UKPDS. The UKPDS was the first one to show that over the time any treatment ‑ although those were traditional old drugs ‑ any of them were sort of failing sooner or later.So, one way to consider is to tackle more than one of the pathophysiological factors at the time of the diagnosis. And I think that nowadays it’s more feasible, because we have drugs that are associated with less side effects and can be better tolerated. And that’s exactly what has been done, for instance, in the trial that we have performed and recently published, which is called VERIFY that you are referring to, were people with a very mild hyperglycemia to start with, because people that have been recruited to the study were people with an HbA1c between 6.5% and 7.5% to start with, and they have been randomized to treatment with a monotherapy with metformin or a combination of metformin and a DPP‑4 inhibitor. What has been shown is that the early combination was associated with 50% less failure over time, providing the people starting on the combination therapy with two more years of good glycemic control as compared to the monotherapy initiated patients. So, I think that there are different ways that we can consider, and I think that more data are going to build up to give us more information on what is the potential for a more complex, but more effective treatment that provides more sustained glycemic control and remains tolerated by the patients. So, I think those things can build up in terms of helping to reduce clinical inertia and increasing the number of patients in the early stages of the disease remaining under good glycemic control. Melanie Davies: Excellent. So, Sam, what lessons can we learn from the DCCT in type 1 diabetes in terms of clinical inertia? Sam Dagogo‑Jack: The DCCT results confirm what Stefano just mentioned about the VERIFY study on the value of early optimization of glycemic control. And for members of the audience who may not recall the details of the DCCT, it was a type 1 diabetes‑based study, and randomized 1,441 patients equally into intensive insulin therapy, since

it’s type 1 patients, to achieve and maintain HbA1c around 7% versus the usual care group. They were not neglected. They received what was usual care in the ‘80s, and their HbA1c hovered around 8.5–9%. And over the course of the formal treatment period, a decade‑long treatment, it was observed that the better treated group experienced phenomenal protections from the traditional microvascular complications of diabetes, risk reductions on the order of 60–70%. And when the study’s active intensive intervention ceased and the participants were passively followed in the EDIC phase, the epidemiologic observation phase, what was really extremely surprising was that, despite convergence of the HbA1c between the erstwhile control group and the erstwhile intensive group, the previously better treated group continued to enjoy significant risk reductions, similar to and sometimes even higher in magnitude than what was seen during the study itself, 70–75% reduction in retinopathy, neuropathy and nephropathy. And after 20 years of this observational follow‑up, we observed for the first time in randomized, controlled diabetes studies a 57% reduction in the time to first cardiovascular events. So, microvascular benefits accrued years, decades later. This has led us to hypothesize the phenomenon of metabolic memory or legacy effect, defined loosely as locking in the benefits of future prevention of complications by early intensive optimization of care. Then even if that degree of excellence in control should waiver a little bit and get less excellent, there continues to accrue to the benefit of the patient locked‑in benefits in reduction of long‑term complications in future. I believe secondary analysis of the UKPDS also supported the existence of the legacy effect. And in the diabetes prevention program, a pre‑diabetes study where a lifestyle intervention was applied to one of the groups to prevent future diabetes, after the study ceased and the previous lifestyle group had gained back some of the weight, they continued to develop diabetes at lower rates than the previous placebo group. So, I think there is a generalizable concept here that early optimization of glucose control is the best way to approach the future risks, the clear and present future risks of major complications from diabetes. Melanie Davies: So, you’ve reminded us, really, that there’s a really clear evidence base for this, for early intervention, certainly in both type 1 and type 2 diabetes. Sam Dagogo‑Jack: Right.Melanie Davies: And I think as we move to the last part of our discussion, certainly in the recent update to the ADA EASD consensus, we’ve started to think differently in terms of particular patient subgroups. So, now in type 2 we’ve actually identified groups of patients either with established atherosclerotic cardiovascular disease or those with risk factors that actually, regardless of their HbA1c, should be on some of the newer glucose lowering agents because that confers long‑term benefits.



Are there specific patient subgroups who could benefit from early antihyperglycaemic treatment intensification?

Approach to glucose lowering with medications1

Figure 1—Glucose-lowering medication in type 2 diabetes: overall approach. RA, receptor agonist, SU, sulfonylureas; TZD, thiazolidinediones. Adapted from Davies et al. (1). © American Diabetes Association andEuropean Association for the Study of Diabetes, 2018.

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etesjournals.o

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andAsso

ciates3

ASCVD, atherosclerotic cardiovascular disease; CKD, chronic kidney disease; CV, cardiovascular; CVD, cardiovascular disease; CVOT, cardiovascular outcomes trials; DPP‑4i, dipeptidyl peptidase 4 inhibitor; eGFR, estimated glomerular filtration rate; GLP‑1 RA, glucagon‑like peptide 1 receptor agonist; HbA1c, haemoglobin A1c; HF, heart failure; SGLT2i, sodium‑glucose cotransporter‑ 2 inhibitor; SU, sulphonylurea; TZD, thiazolidinediones.

1. Buse JB, et al. Diabetes Care. 2019 Dec 19. doi: 10.2337/dci19‑0066 [Epub ahead of print]. American Diabetes Association. 2019 Update to: Management of hyperglycemia in type 2 diabetes, 2018. A consensus report by the American Diabetes Association (ADA) and the

European Association for the Study of Diabetes (EASD), American Diabetes Association, [2018]. Copyright and all rights reserved. Material from this publication has been used with the permission of American Diabetes Association.

Melanie Davies: And we’ve now got, I think, really excellent data from the SGLT2s for renal and heart failure benefits, as well as a MACE benefit, but also the GLP‑1 RAs. And so, now our thinking is, rather than wait to failure, that in particular patient subgroups we should be going in much earlier with some of these agents.Sam Dagogo‑Jack: Definitely. Melanie Davies: The other bit of the algorithm talks about getting practitioners to think more clearly around some of the clinical issues where they should be using therapies more quickly, particularly around weight advantage, hypoglycemia. And we’ve talked side effects contributing to clinical inertia on occasions. So, what groups should ‑ or shouldn’t ‑ we be thinking about addressing clinical inertia in across all of our

patients? And what are the big tips, Stefano, that you would give to healthcare professionals around trying to avoid clinical inertia and picking out those subgroups? Stefano Del Prato: Melanie, I think it’s important to try to reduce, as much as possible, clinical inertia at any stage of the disease. There is a very interesting, nice paper which was published a year ago in Diabetes, Obesity and Metabolism by Greg Nichols. And what they did, what they are looking at, the effect of delaying intensification of treatment for people that were on metformin or people who were on a combination therapy, or people on insulin and so on. And they showed that, for any condition, delaying treatment was associated with a worsening of the outcomes, and they also quantified an increase in the cardiovascular events



risk of 10% for each unit of hemoglobin increase. And that was associated with a 7% increase in the risk of a heart failure hospitalization, and a 7% risk of cardiovascular mortality.So, at any stage, delaying intensification of treatment can increase the overall risk for the diabetic patient. But I think it’s becoming very important earlier on in the stage of the disease, particularly nowadays, because nowadays we have greater opportunities.So, I think, and I usually tend to teach my students, that you can look at your patient, along the suggestion from the ADA as the consensus on individualizing the treatment, in at least three large groups. The first group are the people that come in the office with newly diagnosed diabetes. They have no complications. What do I want to do? I want to avoid complications. How can I do that? Achieving good glycemic control with a low risk of hypoglycemia, a low risk of increasing body weight. Is that possible? Yes, it is possible. But even more, now we may have evidence that some drugs may convey benefits beyond the glycemic effects. And if that is possible, and I can, for instance, reduce the risk of developing or delaying the development of diabetic nephropathy, that would most likely translate into reduced cardiovascular risk, because impaired kidney function is an independent cardiovascular risk factor. And even more, we do know that there is a strong association between glycemic control and microvascular complication. But microvascular complication is another predictor for cardiovascular disease. And we have to remember that in our heart we have coronary arteries. There is an incredible network of microcirculation that can be affected as well. So, it’s important for those individuals to really achieve good glycemic control and increase tolerability, because that will also need the physician to stay on top of it. The second group is people with impaired kidney function. And now we have evidence, as has been suggested to you, that there are opportunities. And then there are the people with already established cardiovascular disease, and already we have evidence now. So, we have better way now to tackle the number of people with diabetes in the different stages of the disease and provide them with better opportunities. Melanie Davies: So, Sam, you talked about the very important area of cost and how actually, from the healthcare provider’s point of view, we need to make the case that a bit of extra cost now may lead to savings in terms of the longer term in terms of reducing complications.Sam Dagogo‑Jack: Right.Melanie Davies: What can be some of the barriers to access to some of these therapies? And how important do you think access to things like SGLT2s and GLP‑1 RAs is important in our healthcare systems?

Sam Dagogo‑Jack: Oh, the access is critical. And I’m thinking of some of the less economically advantaged parts of the world, where kidney disease looms large and people with end‑stage kidney disease do not have state‑provided dialysis centers. It’s almost a death sentence. And these agents that decrease the rate of decline of eGFR and renal function and delay the time to end‑stage kidney disease, time to dialysis, decrease renal death, they are heaven‑sent. And so, when a system has in‑built barriers that preclude access to these drugs, it is my position that the physicians and the patients and other advocates should team up and apply pressure for access to these lifesaving and organ‑protecting therapies. We should not roll over backwards and say, because the economists say they’re expensive, so we use suboptimal care. I think that is almost negligent. And so, in my part of the world, I write and fill out whatever forms are necessary to make sure that they are allowed. So, there are all kind of processes and hoops you jump through if a drug is not on formulary, and I train my fellows and residents as you become the advocate for a diabetic patient. And if you think this is a good drug that will protect kidneys, hearts, myocardium, etc., you should go bat for it so your patient gets it. Melanie Davies: So, I think we’ve had a really good discussion. We’ve reminded people that clinical inertia in terms of diabetes is a real problem. A third to half our patients currently are not being intensified or, we won’t use the term intensified, but not being managed appropriately in terms of glycemic control. We’ve highlighted that there’s a really good evidence base for the importance of avoiding this lack of good control early on. We’ve also talked about that now we have evidence beyond glycemic lowering, that some of these new agents also lead to really important outcomes to protect our patients. And I think we’ve reminded the audience of the complex factors that lead to clinical inertia that we have the ability to address, both at the level of the patient, with better education and support, and healthcare professionals. I think it’s incumbent on us to make the guidelines more simple to follow and be really clear about the advantages, but also discuss some of the complexities of healthcare systems that make this problem difficult to address.So, I’d like to thank both Sam and Stefano for the great discussion. And thank you for joining us.

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Date of original release: January 31, 2020. Date credits expire: January 31, 2021

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