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Rodman & Renshaw and Close Concerns hosted a call with noted endocrinologists Dr. Jay Skyler and Dr. Irl Hirsch on February 7, 2008, to discuss the NIH announcement that the intensively controlled trial of ACCORD had been halted. Our quick take is below, followed by the full transcript of the call
Quick Take on Rodman & Renshaw and Close Concerns conversation with diabetes experts Dr. Irl Hirsch and Dr. Jay Skyler:
Mike King: The NIH announced on Feb 6 that it had halted the intensive arm of the ACCORD trial because of an increase in mortality. What does this mean in terms of current patient care?
Dr. Irl Hirsch: There are patients around the country who work really hard to bring their A1cs to normal, and theyre not going to stop doing that just because they are hearing they should bring their A1cs up. However, the people who are very motivated and almost obsessed with their diabetes are the minority of diabetes patients. Im getting email messages from all over the country from PCPs and what we have is mass confusion. People dont know what they should be telling patients and unfortunately we still need more data and it needs to be published in a peer-reviewed journal. Its hard to give recommendations until we see the data in more detail. Im particularly interested in how many of these patients, who all have had high risks for coronary disease, had known history of stroke or myocardial infarction or stent placement or CABG, and how these patients did compared to patients who had high risk but no known disease because it is possible that there are differences between these groups. Its premature to come up with definitive conclusions that lead to recommendations for PCPs and patients until we see those sub-analyses. Its reassuring that we were told that this was not due to rosiglitazone (Avandia), which was used in the study. Im a bit relieved about that, not because Im a TZD supporter, but because its good for patients. There are so many potential mechanisms that we can speculate about why, and if nothing else this study is hypothesis generating about this topic. One hypothesis that was quoted in the New York Times this morning about hypoxia and retinopathy in the 1980s but the bottom line on that particular topic is that it deserves study and it will take time to figure it out.
Mike: Is it possible that there was a knee-jerk reaction to this or were the right steps taken? Dr. Jay Skyler: Data safety monitoring boards (DSMBs) deal with this issue all the time. This was a very small increased risk. It was statistically significant and there was a large patient population. Its a tough call but it probably was reasonable to stop the study then. The issue is not so much stopping but how to put it in perspective. One thing is that there were fewer non-fatal MIs in the good-control group. A second point is that it is my understanding that most of the deaths occurred in the hospital, often following procedures or surgery, and the cause of death in those cases was clear and adjudicated. What it suggests is that theres something that makes these people more vulnerable when theyre having a procedure or in the hospital for something. Perhaps its subtle hypoglycemia that is going undetected or hypoglycemia affecting autonomic nervous system function. This was not ordinary treatment but extraordinary effort with sometimes four or five medications, which is beyond the realm of usual clinical practice. This could have induced an exacerbation of fatty liver, something that insulin mediates, which is in turn associated with hepatic insulin resistance, and just this week in Cell Metabolism there was an editorial by Brown and Goldstein about an article by Dr. Ronald Kahn at Joslin Diabetes Center about total hepatic insulin resistance vs. selective hepatic insulin resistance and the conclusion was that hepatic insulin resistance may be the primary mediator of atherosclerosis, which explains why people with diabetes are more prone to atherosclerosis. Perhaps there was more weight gain in the rigorously treated group since they were using a combo of TZDs, SFUs, and insulin, which all cause weight gain. Weight may have been a crucial factor in leading to increased mortality the patients faced when they had an event and were in the hospital. This may turn out to be a mixed study in the long run. We dont know what the impact on microvascular disease will be. Non-fatal MIs are reduced. It may be that if you had an event in that group and you had surgery you were more likely to die from the procedure. Im not going to change my clinical practice one iota. I am for an A1c of 7% and if I can get it safely to less than 6.5% or 6% without significant hypoglycemia then thats what Im going to do. I dont think this should change practice. Its one bit of evidence in a whole pool and theres no reason to throw strict A1c goals out.
Mike: The WSJ wrote about the fact that the investigators did not believe that Avandia played a role in the mortality but there was more rosiglitazone used in the intensively treated group.
Dr. Skyler: They did a statistical analysis to see if there was a correlation of this with any of the drugs and they said they didnt find one. I will accept that. I never believed in the Nissen meta-analysis in the first place. I have never written a prescription for Avandia in my life and I dont think that analysis was correct. I think Avandia has been falsely accused.
Kelly Close: What does the DSMB look for in these analyses?
Dr. Skyler: The thing that annoys me about this is that we dont have all the data in front of us. The NEJM is probably where theyll send it because itll likely be accepted and they like this kind of thing. The NEJM publishes things like this within a week to ten days. But here were sitting in a vacuum. We have the media scaring patients but we dont have the data.
Kelly: Gina Kolatas article in the New York Times has lines like And there are troubling questions about what the study means for people who are younger and who do not have cardiovascular disease. Should they forgo the low blood sugar targets? No one knows.
Dr. Hirsch: Thats interesting because what I said to her was: If you go back and look at last year in JAMA, we have the SEARCH data with an explosion of diabetes in non-Caucasian young teenagers and its very difficult if not impossible to extrapolate the data in ACCORD to that population or to people in their twenties, especially women with type 2 diabetes of child-bearing age. And that turned into what you read in the NYT last night. We have to wait for the data to come out, take a deep breath, and come up with specific recommendations for different populations of patients. Even with the younger patients Im still quite concerned about the microvascular morbidity that will come out over decades. No one is talking about microvascular complications because it wasnt presented. Its not on anybodys radar.
Mike: PROactive missed its primary endpoint when it had a population with underlying comorbidities. Are companies getting into trouble with this patient population? Are we not going to look at drugs in more fragile populations in the future?
Dr. Hirsch: People with diabetes werent even let into the original statin studies. People were afraid of looking at a more fragile population. Over time we learned that the statins were a good thing. We have all learned over the years that hypertension and dyslipidemia and hypercholesterolemia are bigger risk factors for macrovascular disease than hyperglycemia, so when you do a hyperglycemia study and look at macrovascular outcomes, we only have one study (EDIC) that has looked at that, and it took 15 years after the end of the study to get an endpoint. We are going to become more careful about doing hyperglycemia studies with macrovascular outcomes. In the UKPDS there was a much earlier group of patients without the same macrovascular risk factors at baseline, and there was a 15% reduction in myocardial infarction, but the p-value was 0.052 and because of that we dont have a type 2 diabetes study that shows a reduction in macrovascular endpoints. Thats true, but thats why I say its really going to depend on the population.
Dr. Skyler: We do have the UKPDS and the EDIC study and both took a long period of time. Funny things happen in all of these studies. It could have been chance or maybe if wed stretched the study five or seven years the curves may have crossed again. However, the job of the DSMB is to protect the participants.
Dr. Hirsch: When I was in training, the exact same conversations were taking place in Miami about glucose control and retinopathy in the DCCT. When the increased retinopathy occurred in the secondary intervention group, they had to make the decision whether to go on. But they gritted their teeth and moved on, and here we are with 76% less retinopathy because they waited longer. This was an important signal, but whether they stopped too early is a fair question to ask.
Kelly: What are the implications for PCPs regarding treatment? How is a PCP going to characterize high risk to a patient?
Dr. Skyler: We still need to exercise clinical judgment. It will be up to the doctors to do that.
Kelly: Does that mean easier or simpler therapies are more likely to be used? Theres a lot of discussion about being overwhelmed by the complexity as it is and this adds to the confusion, right?
Dr. Skyler: It adds confusion but I dont think theres enough here for me to change my practice.
Dr. Hirsch: We talk about insulin resistance. I think the PCP is developing study resistance because every week there is a major study that goes against the traditional grain of thinking. With all of these major studies coming out monthly if not weekly in all areas of medicine, the PCPs now more than five or ten years ago are really saying lets see where the dust settles on this. Theyre not going to know that only 18% of people reached A1c target in STENO-2, nor are they going to care. Whats going to drive this is what AACE and IDF and ADA say. People look to medical schools and academia and societies for guidance. The average physician or even specialist is not sophisticated enough to come up with their own recommendations for patients. They look to thought leaders. They used to look to industry more for this but over the last few years, industry has gotten a little bit of a bad name, so theyve lost some of their respect.
Mike: The A1c endpoint was called into question with Avandia first. Are we impugning UKPDS/DCCT A1c or is A1c just part of the answer and we need better clinical surrogates?
Dr. Skyler: We may need more than A1c but its the best we have right now. It correlates extraordinarily well with microvascular endpoints. In the EDIC follow-up, although it took 18 years, it did have an impact on coronary disease and death. I think its a good outcome measure. The fact that we have one study that goes against conventional wisdom doesnt change the whole dynamic. This is a special group of people who had severe risk and who had most of their other factors (lipids etc.) taken care of extraordinarily well, and the control group had darn good glucose control. The first group went a little farther and something happened that we dont completely understand. We need to mine the data to understand further why this happened. I am unwilling to throw out A1c or change my clinical practice. No single study in a special group of people treated in a special way should change the whole way we treat everyone with diabetes. It would fundamentally be a mistake, it would be a big step backwards, and I would loudly say, no, no, lets not do that.
Dr. Hirsch: It would be premature to do anything at this point, especially until the study has been published. All were doing right now is speculating.
Kelly: What does this mean for drug development?
Dr. Skyler: Just as we saw with the ENHANCE study, where the FDA was much more sensible about it than the hysteria in the media, I suspect that the Agency will be more sensible about this as well. I dont think well see a change in the way they behave. When we think about what we do clinically, we think about the last trial we saw, but we often forget all the myriad of data that have been published going back decades. I view this as the same hysteria that occurred with the Womens Health Initiative, and this was a group of women who went on estrogen twelve years after menopause, exposing them to estrogen when they had been deficient for all of that time. That is not the way estrogens have generally been used in practice over the years. There are myriad of analyses showing that estrogens are useful in heart disease, breast cancer, osteopenia, etc. We should avoid hysteria in all things.
Kelly: About your quote that moving people from poor control to good control could be quite damaging, could you talk more about that?
Dr. Hirsch: Im using that retinopathy story in the DCCT as a historical example, but the idea is that if you bring someone with preexisting disease down very quickly it could have adverse effects. With retinopathy, if you take someone without retinopathy you dont have to worry about worsening their disease. The speculation here is that if you already have coronary disease and you bring it down to normal, something else may be going on. In the retinopathy situation it was hypoxia. Well, maybe this is microvascular hypoxia in a macrovascular setting. Or maybe its autonomic neuropathy. Or maybe its hypoglycemia itself, or glycemic variability. From a drug development point of view, it might require industry to select populations of patients who are safe from these outcomes.
Mike: It was a big study. Why would this skew towards the intensive group?
Dr. Hirsch: We dont know. We dont know how many of these people were like UKPDS people vs. fragile people like the PROactive population.
Kelly: I had understood there was a small arm looking at glycemic variability.
Dr. Hirsch: At one point they talked about using CGM to look at that but I dont know if it happened. Dr. Michael Brownlee presented some fabulous data at ADA Postgrad showing that one spike in glucose turns off an anti-atherogenic enzyme and causes oxidative stress. Variability was not part of the protocol in ACCORD. Whether you got basal or prandial insulin was all up to the investigator because the only treatment surrogate they were using was A1c. It will take complicated and long data analysis looking at the type of therapy to figure that out. Hopefully the investigators will do this. Email Question: What proportion of your patients is reflected in the ACCORD study?
Dr. Hirsch: About 80% of my patients have type 1 diabetes. This did not get into my conversation with Gina Kolata. You cannot extrapolate between populations. At the university, of my type 2 patients, at least half of them meet the ACCORD criteria. So maybe 10-15% of my patients meet the ACCORD criteria.
Dr. Skyler: I see primarily type 1s. Amongst my type 2s, these are an important subgroup, but theyre a minority.
Dr. Hirsch: An important fact that is often forgotten about is that with patients who already have cardiovascular disease, its the cardiologist whos the PCP and who writes the diabetes prescriptions. This is an important group to talk to about this. Email Question: Can you give your thoughts on the use of exenatide once-weekly in a broad type 2 population? Have your views changed?
Dr. Skyler: No. Im still aiming for as low as I can get easily. Something like exenatide once-weekly could facilitate that without weight gain. Regular exenatide lowers liver enzymes.
Dr. Hirsch: I want to see an ACCORD-like trial in an ACCORD-like population with just exenatide or other GLP-1 agonists or DPP-4 inhibitors. I want to see these drugs in a high-risk population because my guess is that you may do much better than we saw here because of the weight gain issue.
Mike: I know Lillys planning to do that once its approved.
Dr. Skyler: A lot of data suggest that exenatide is beneficial to cardiovascular function.
Dr. Hirsch: In particular, with heart failure. There were no heart failure data in the ACCORD data. This really came onto the radar due to the TZDs. The real question with the GLP-1 is we need human data on heart failure because this may be where you get the most bang for the buck.
Kelly: When will the full ACCORD data be out?
Dr. Hirsch: No idea.
Dr. Skyler: None.
Dr. Hirsch: There will be many papers coming out for years. Email Question: Can A1c drop below 7% safely in non-high-risk patients?
Dr. Skyler: Absolutely. It will continue to be my standard of care.
Dr. Hirsch: I often see type 1 patients whove been on insulin for 50 years and I will continue to not aim for under 7% because theyve already won the microvascular war and its too dangerous because of the hypoglycemia.
Kelly: Which populations would you not recommend for under 7%?
Dr. Hirsch: For the typical ACCORD patient I need more data on primary vs. secondary intervention.
Dr. Skyler: I make individual decisions about each patient.
Dr. Hirsch: In the true geriatric patient with other comorbidities, there is not need to push the A1c down. Another question is, for patients who already have A1c at 6% with minimal therapy, are you going to take their therapy away?
Dr. Skyler: Not at all. People who say this are missing the point.
Dr. Hirsch: I know, but Ive gotten two emails asking this question today. These are the questions that are coming. I would never have expected it. Email Question: Was the problem that A1cs were too low or that insulin was too high?
Dr. Skyler: I want more data.
Dr. Hirsch: We know from CGM studies that theres a lot of sub-detectable hypoglycemia. Audience Question: PCPs read the NYT and WSJ. Im concerned about whether they will say, Im just going to hold off on tight glycemic control for now because its easier to concentrate on blood pressure and lipids.
Dr. Skyler: Thats my fear that people will use this as an excuse not to take care of people as well.
Dr. Hirsch: But thats what were going to see. With P4P, doctors are now going to be stuck. They need to get A1c under 7% but now this study says that if you do that, youre going to die. Follow-up: Can you get a message out to PCPs and payors about this? Payors would be happy to reduce cost. Is there any way to stem this tide?
Dr. Skyler: I think the ADA for a change had a sensible recommendation yesterday: that we should continue to aim for A1cs under 7%. It would be a shame if physicians or payors or anyone else used this single study to change their mindset about clinical practice, reimbursement, etc.
Dr. Hirsch: Its tough without published data. I was asked to write an editorial for JCEM, the journal of the academic endocrinologists. In the spring, the American College of Physicians (ACP) has its meeting. I think the ACP needs a response to this and publish it in the Annals of Internal Medicine, and the same thing for the American Academy of Family Physicians (AAFP) because most PCPs belong to those two organizations. Their take on this will have as much weight as the ADA, whose recommendations dont make it into PCPs mailboxes.
Kelly: What are the implications for inpatient glycemic control?
Dr. Skyler: Its my understanding that most of the deaths were peri-procedure. I cant speculate further.
Dr. Hirsch: If thats the case, I really need to see the details because now we get into issues implicating inpatient and peri-procedure glucose control, which is a topic fraught with controversy itself over the last few years.