[IMJ On-Air] Hyperglycaemia and COVID-19

[IMJ On-Air] Hyperglycaemia and COVID-19
Date:
18 January 2023
Category:

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In the first year of the COVID-19 pandemic, a handful of international studies showed that there was increased risk of adverse outcomes in hospitalised patients comorbid for diabetes. Odds ratios for mortality conferred by pre-existing diabetes ranged from 1.5 to 3.6. What this relationship might be in Australia was not known until researchers in Melbourne retrospectively examined electronic medical records from the two waves of COVID-19 in that city.  

The prevalence of diabetes among Melbourne inpatients is around 35% and in 2020 over 70% of all Australia’s case load was in Victoria. This presented an opportunity to observe the relationship between the conditions with substantial statistical power. But while ICU admission and mortality were more common in those with diabetes than those without, neither diabetes nor hyperglycaemia were independently associated with in-hospital mortality. In this podcast the authors speculate as to why there was this deviation from patterns observed internationally. A possible explanation involves the receipt of dexamethasone therapy in patients with hyperglycaemia, which was found by other researchers to be preventative for COVID-19-associated mortality. 

Credits

Guests
Associate Professor John Wentworth FRACP (Royal Melbourne Hospital, Walter and Eliza Hall Institute)
Dr Rahul Barmanray FRACP (Royal Melbourne Hospital; the University of Melbourne)
Dr Dev Kevat FRACP (Western Health; Monash University)
Dr Mohammad Ashraful Islam (Goulburn Valley Health) 

Production
Produced by Mic Cavazzini DPhil. Music licenced from Epidemic Sound includes ‘Repurposed’ by Cody Francis and ‘’Til All That is Left is Ash’ by Ludlow. Image by skynesher licenced from Getty Images.

Feedback on this on this episode was kindly provided by Dr Amy Hughes and Dr Joseph Lee.


References

Transcript

MIC CAVAZZINI:               Welcome to IMJ On-Air, podcast of the Internal Medicine Journal. I’m Mic Cavazzini for the Royal Australasian College of Physicians. Today’s episode shows off some Australian research from the January edition of the journal. The study looked at outcomes of patients hospitalised for COVID-19 who also had underlying diabetes or hyperglycaemia. Even if you’re not an endocrinologist or respiratory physician, I think this story presents an important message about population research. In particular how you go about untangling the confounds introduced by co-morbidity, healthcare setting and interventions.

Starting in 2020, a handful of studies from the USA, France, Italy, Belgium and China had consistently shown increased risk of adverse outcomes of COVID-19 in patients with diabetes. Odds ratios for mortality conferred by pre-existing diabetes ranged from 1.5 to 3.6.

Well, 5% of the Australian population is known to have diabetes, but among inpatients at Melbourne hospitals that figure is more like 35%. And in 2020 there were over 20 300 confirmed cases of COVID-19 in Victoria, representing 72% of all Australia’s case load.

This presented researchers in Melbourne an opportunity to retrospectively examine the importance of the risk relationship in an Australian setting, and hopefully to provide insights into protective factors too. This resulted in a large collaboration called Diabetes IN hospital – Glucose and Outcomes in the COVID-19 pandemic. To guide this journal club had the IMJ endocrinology editor, Associate Professor John Wentworth.

JOHN WENTWORTH:     Yeah, I work at Royal Melbourne and the adjoining modern Eliza Hall Institute and I work in general endocrinology.  But the research interest is in type 1 diabetes, immunology, and screening and prevention of the disease with immunotherapy.

MIC CAVAZZINI:               And you had the pleasure of reviewing this paper about the DINGO COVID-19 study. The lead author is Rahul Barmanray, an endocrinologist at Royal Melbourne Hospital and lecturer at Uni of Melbourne. Rahul, how were you sitting in front of the scrabble board before you come up with a study title with a catchy acronym?

RAHUL BARMANRAY:    Yeah, we do like our abbreviations in clinical research.

MIC CAVAZZINI:               Is there anything else you want to add about your CV?

RAHUL BARMANRAY:    Not at all, except that I had the pleasure of working by the Royal Melbourne and Western, two of the sites hardest hit by COVID.

MIC CAVAZZINI:               And from your 20 co-authors, we also have with us Dev Kevat and Ashraf Islam. Can you both introduce yourselves briefly before John hits you with his questions.

DEV KEVAT:        Certainly. Yeah, my name is Dev, I'm the lead for diabetes at Western Health. And it's been a pleasure to contribute. We fortunately or unfortunately had a large number of people to contribute to this very interesting study.

ASHRAF ISLAM: Yeah I’m Ashraf, I’m currently working as an advanced trainee in Shepparton. But during the study, I was doing my master's thesis with Professor Elif Ekinci in Austin health. So I have got the opportunity to collect the data for this collaboration.

JOHN WENTWORTH:     Yeah, well, terrific to have you all here today. Thanks for joining us. I wanted to start, I guess, by acknowledging that we're speaking to you from the lands of the Wurundjeri people. At least I am, and others of us may be elsewhere. But I did want to acknowledge that to start. Now. This was an unusual study in that it got a lot of different sites working together, I wonder if you could tell us how it all came together.

RAHUL BARMANRAY:    Thanks, John, perhaps I'll start with a brief summary of the inception of this study. So as endocrinologist we’re familiar with working in the inpatient- outpatient space. And we're increasingly cognizant of the fact that inpatient diabetes is a greater proportion of those individuals admitted to hospital, as well as having significant implications for morbidity and mortality in hospital. This has been known about for at least the last two decades, and, and the field is really maturing. So of course, when COVID-19 came along, and these initial studies from elsewhere in the world was showing that diabetes, and indeed high blood glucose, in hospital in patients with COVID, was associated with increased morbidity and mortality, well, it was really incumbent upon us as impatient diabetologists to see if that was the case in a local context, as well. And so the study aimed to give clinicians much more information about the implications of COVID-19, its treatments, and any other sort of surrounding issues regarding comorbidities on their patients’ diabetes, hyperglycaemia and eventual outcomes. At the time, when, if you remember back then, we really didn't know all that much about COVID-19, and what implications it had acutely or even chronically.

JOHN WENTWORTH:     Thanks Rahul.

DEV KEVAT:        I could just build on what Rahul said—it's Dev here—Now, I think, John, your question about working together as a really important one. We work all in different health systems and as we all have experienced, and many of the listeners will experience, there's some fractures in record-keeping between different hospitals, particularly in some states. And you know, it was really wonderful to be able to work with clinicians across all of the sites across northern and western Melbourne to contribute data. And I think that was due to the personal connections and the supervisory connections that we all had. I think that obviously gave us numbers in a way that would be otherwise very hard to do, and that gave the study some power and validity and the ability to really explore things in some depth.

JOHN WENTWORTH:     Great. And, Rahul, what are essentially what did the study show you in a nutshell?

RAHUL BARMANRAY:    Yeah, in a nutshell, the results were somewhat surprising in light of those international associations that were found in the early part of the pandemic. And perhaps we’ll talk about the reasons for that somewhat later. But essentially, in our Victorian cohort in 2020, in the first two waves of the COVID-19 pandemic, in patients with COVID with diabetes and hyperglycaemia, were no more likely to have adverse outcomes than those without diabetes or without hyperglycaemia, particularly for mortality. Now, ICU length of stay was slightly longer for those with hyperglycaemia, and there was some biasing by indication based on therapy. But unlike international experiences, diabetes, at least in our cohort, was not independently associated with increased mortality.

JOHN WENTWORTH:     And that's obviously a fairly hard outcome. And can you just give me a sense as to what the odds ratio of death with diabetes as a risk factor was, and how well-powered your study was to identify a similar effect. You might need to remind us how many patients were included.

RAHUL BARMANRAY:    So we had 840 admissions that met our inclusion criteria. There were a few more people admitted with COVID-19 during that period around Victoria, but some of those people were admitted with other issues and happened to incidentally have COVID. So we really included those people who were admitted for COVID, who needed inpatient treatment of their COVID-19. And we found that the multivariate-adjusted odds ratio for diabetes for in-hospital mortality was 1.3. But the confidence interval very much crossed 1, so there was no association there. And so with almost all of the inpatient admissions with COVID-19 for that period, and we have a we have a figure that shows our, the patients admitted in our study, compared with the case rate in the community in Victoria, and the two overlap quite well. So we can be pretty confident that we're reflecting the true relationship, and the true incidence of COVID-19 the community. And so the fact that we have most of those patients, purely by dint of our hospitals being around the epicenter of the Victorian COVID-19 epidemic, which many will be people remember, particularly in the second wave, was that inner north west of Melbourne, and then spreading out into the western and northern suburbs from there.

JOHN WENTWORTH:     And so, I mean, what effect size might you have thought you might see, and, did you have enough numbers to assure yourselves that you indeed could be confident that there wasn't an increased risk?

RAHUL BARMANRAY:    So the effect seen in other studies, the odds ratio with diabetes and mortality, has ranged between 1.5 up to 3.6, with marked variability between location. So some studies, particularly in China, or around the epicentr3 of the pandemic, showed relatively low odds ratios, but had much higher numbers. And other experiences, for example, the Italian and Spanish experiences, showed much higher odds ratios of mortality. So those were the effect sizes were expecting. We saw a lower effect size around 1.3. But given our numbers, 800, and half of whom had either diabetes or hyperglycaemia, we expect them to have been adequately powered or detected a true difference if there was one.

JOHN WENTWORTH:     Great. And obviously the definition of diabetes was, I guess, not an exact science in this study. And I'd like to bring Dev and Ashrafin to really see if they could comment on whether there might have been population differences across the different health services. I know, for instance, that Royal Melbourne does a lot of its diabetes through remote glucose monitoring, that gets reviewed centrally and similar systems aren't yet established, or I don't think were established in other places. But I wonder if you could comment, where we all looking at the same sorts of patients at these different hospitals? Were there differences between hospitals, either anecdotally, or even scientifically? Do you have a comment?

DEV KEVAT:        Yeah John, I think that's a really excellent question. And one of the things we always have to be concerned about when we're collaborating across sites is getting the definitions right, and correctly applied across all the sites. And we spent quite a lot of time doing that in terms of the search criteria. I think you're correct to say that the way in terms of finding the glucose results may have varied a bit from site to site. But in terms of the actual numbers, I think there was, you know, good consistency between the different sites. So at Western health, we didn't have the same sorts of systems at other sites. So we did a lot of manual reviews but we had a team of people working hard around the clock to gather the hundreds and look through those charts. Although the information isn't automated, we do get glucose metric readings of down to the point one decimal place. So we're pretty confident because our search strategy originally involves looking at all the patients who are had a COVID positive diagnosis as defined at the time, and then manually searching those records. And we had a pretty comprehensive way to look at that. And we also had a crosscheck mechanism to check our own accuracy at our own site. So that was our approach at Western.

JOHN WENTWORTH:     Thanks. So at Austin health, which is in the in the northeast of Melbourne, I know that there's a an HbA1cwas routinely done for anyone who set foot in the hospital as a screening mechanism. Was it still in place? And again, was your ascertainment similar in approach, or how did you go about finding the patients with diabetes out there?

ASHRAF ISLAM: Yeah, so I have searched the data, according a diagnosis of COVID at that time. And all the patients admitted in Austin health who has age more than 45 had got this HbA1c. So I have checked all the HbA1cmanually. And I also checked all the blood glucose has done on the patients who admitted for with the diagnosis of COVID. From there, I have curated at more than 100 data for this study. And we use the REDCap. So Rahul has come up with a form that what other data he wanted to know. So we entered all those data according to that.

JOHN WENTWORTH:     Great. And tell me, you've had a look across three categories of people; those who didn't have diabetes or any high glucose in hospital; those who came in with a pre-existing diagnosis of diabetes, or those who showed, I guess, stress hyperglycaemia in response to critical illness probably caused by COVID. And you didn't find increased mortality, after correcting for a number of common and expected factors. So why was that when, you know, there was clearly an effect only a matter of six previously observed in other studies. Why was there no mortality risk associated with type 2 or type 2 diabetes.

RAHUL BARMANRAY:    Yeah I think you really cut to the heart of the matter, John. And it really reflects the rapidly changing nature of COVID, particularly in that first year, even now. And in this particular case, it really comes down to the use of dexamethasone as standard of care in patients with hypoxia. It just so happened that the RECOVERY trial—a large trial published in the New England Journal of Medicine which really established dexamethasone as standard of care in those patients with COVID-19, admitted who experienced hypoxia—that the preprint publication of that occurred around the same time as the second wave and Victoria was ramping up. And so Victoria was really the first place in Australia that had significant numbers of COVID-19 where people were being treated with dexamethasone. Dexamethasone, as many listeners will know, of course, causes hyperglycaemia. And associated with the stress hyperglycaemia of the inflammation with COVID-19, many many patients were receiving often very high doses of insulin in order to maintain their glycaemia.

Certainly that was the Royal Melbourne experience. And I believe there's a there's a case series from Sydney showing a similar experience. And so the fact that these people who were developing hyperglycaemia, much of which, as you say, John, was stress hyperglycaemia, because of their dexamethasone and because of their COVID-19. But dexamethasone is a mortality-reducing therapy. We're certain that after our multivariate adjustment, there is going to be some confounding relationship between dexamethasone, hyperglycaemia, and in hospital mortality, where it's hyperglycaemia itself no longer comes down as increasing mortality. Because dexamethasone is reducing the mortality and those patients who are biased by indication to receive it, because those are the sickest patients who would have had the highest mortality had there not received dexamethasone in the first place.

JOHN WENTWORTH:     But what about the people who definitely had diabetes before they turned up to hospital? You had a fair cohort of those, didn't you? Are you less certain that they truly had type 2 diabetes before they came in? I thought, half of the diabetes cohort, or hyperglycaemia cohort, were people with a pre-existing or fairly good case for a pre existing diagnosis of type 2 diabetes.

RAHUL BARMANRAY:    That's right. So 300 patients had diabetes, about 100 patients had hyperglycaemia without diabetes, and the remaining 400 had no diabetes and didn't experience hyperglycaemia in hospital. And so those 300 patients with diabetes, some of them experienced hyperglycaemia. But some didn't. And in factm some of the people with a pre-existing diagnosis of diabetes received dexamethasone and didn't become hyperglycemic, which is consistent with the non-COVID experience uncommon experience. And so when we were able to look at each of those risk factors and the outcomes independently, that was when we saw there wasn't an association.

JOHN WENTWORTH:     But what you're saying essentially is the dexamethasone is such an effective treatment, that mortality is really, really low. And therefore the risk of diabetes is mitigated. It's somewhat counterintuitive to me at least. And I'm just wondering what other factors might be out there to explain what is quite an unusual finding, in the context of the world literature, I presume we were dealing with similar types of COVID, we were dealing with Delta. I guess some of the previous papers may have also been dealing with other strains. And so maybe that's a difference. But, you know, maybe the people with diabetes in this study were not very similar to those in the rest of the world. I don't know if you could comment on that at all.

RAHUL BARMANRAY:    Yeah, one of the key differences between the Victorian COVID-19 2020 experience was the demographics of people who got COVID. So those in Victoria will remember that our first wave was really returned travellers; a few people who've contracted it on cruise ships returning to Victoria that tended to be quite young international travellers who’ve returned, or backpackers who are on their way back overseas. Whereas the second wave was very much a nursing home-predominant disease, there were obviously many school-based outbreaks. But younger people tended not to get as unwell. The people who ended up in hospital tended to be older and more comorbid and so therefore diabetes in the elderly, people who are nursing home-resident is probably a different condition, on average, to a general working age population—as tended to be the people who got COVID in some of the international cohorts, particularly in China and Spain. And so that probably explains much of the difference. And it really is one of the key points of this paper; that the contextual relationship in which a particular association is being studied is key, and can really change the outcomes that we see. And so we wouldn't have known these results had we not performed the study in our context. We would have, perhaps, tried to extrapolate from the international experience to the Victorian experience. But as our study shows, maybe that wouldn't have been appropriate.

JOHN WENTWORTH:     What is this meaning for us as we move forward? And I guess I might first step back and ask you to comment—I mean, the previous knowledge that diabetes was a risk factor for COVID-19. Could you comment on how that might have been altering or affecting clinician behaviour or patient behavior? And you know, how this new information might alter any aspects of clinical care?

DEV KEVAT:        I mean, I think it's difficult to be 100% sure, but one thing that has crossed my mind is, we did get a bit more warning compared to some places in the world of what the mortality and the conditions which exacerbated mortality were, with COVID-19 being in Australia, because the borders closed. And our waves were therefore a little bit later. And it did cross my mind, did that mean that we had a heightened awareness of diabetes, and, and the need to pay extra vigilance to these patients? I think Rahul makes a very good point that what this study is actually is showing is that in that context, there were other factors which brought greater risk in a proportionate sense. So for example, age and other sorts of comorbidities were certainly an issue which raised that.

I do think that certainly in my hospital, our ability to make decisions about looking after people with diabetes was increased. We were more proactive with that. And, you now, I think that second factor is really that hyperglycaemia because of the dexamethasone, and that treatment effect was very great. So I guess, looking forward to the future, I think this study was very valuable and it sort of tested—like good science, if you're test things sometimes you find things which are surprising and that certainly provoked a lot of thought in us going forward about how we might approach things.

JOHN WENTWORTH:     And was there good evidence that the mortality rates in Victoria were far lower than those reported in the other studies? Once you account for the increased age of the population in Victoria and other cofactors?

DEV KEVAT:        Well, I think I think it's very difficult to necessarily compare across jurisdictions. But certainly, you're speaking to people and colleagues who have worked with in the UK and the NHS, and I'm not sure if their data is published yet, I don't think we had quite the case mortality rates with that sort of matched population. What's particularly difficult in comparing different jurisdictions is, of course, you know, we had a relatively high testing regime in in Australia compared to some other countries. Not so much now, but certainly back then. But yeah, might get Rahul or Ashraf to comment on that.

ASHRAF ISLAM: Yeah, I totally agree with Dev. Because when I'm looking to the data of the Austin, I can see that we have got a warning shot that the wave is coming. And surveillance on diabetes was increased. And I've gone through the all the medical records for the patients with diabetes, every patient was reviewed by the endocrinologist, and the treatment was according to the patient's need. So I think it was a contributing factor to a deal this situation promptly.

MIC CAVAZZINI:               Can I go back to those preceding international studies. And maybe it's the naive question. That in those international cohorts, is it likely that diabetes was bringing a specific metabolic risk to COVID-19 patients? Or that there's a sort of indirect association of patients who are more overweight, respiratory and cardiovascular difficulties and fatigue, that were then put under pressure during the COVID experience?

RAHUL BARMANRAY:    Yeah, I think it's, it's probably two things. One aspect of it, as I mentioned previously is that diabetes seem to associate with a particular type of patient in  particular cohorts. As we mentioned before, elderly nursing home patients where diabetes may reflect sort of age-related pancreatic dysfunction, more so than, say, metabolic or inflammatory determinants of diabetes.

Whereas in some of those international cohorts—again, particularly the younger working-age, and often predominantly male workers who work in close proximity—abattoir workers was the classic one in Australia, but in say, Spain, greenhouse workers where COVID would spread amongst these populations—that those people where diabetes was present, there probably truly was a difference in their metabolic risk. Diabetes in those individuals who are younger, would truly have likely had greater weight and the diabetes would probably represented something different to what it represented in our cohort.

I think from an inpatient perspective, what we what we know from the literature is that both hyperglycaemia and hypoglycaemia, increase morbidity and mortality post discharge—hypoglycaemia, moreso, than hyper. But so does diabetes and diabetes, probably more so. And so we know from large systematic reviews of patients admitted without COVID, but with community-acquired pneumonia before COVID, that people with diabetes were more likely to die greater than 90 days post discharge. And that probably had nothing to do with their admission, it was probably the fact that they have diabetes. And diabetes, unfortunately, is a risk factor for death through various mechanisms. And if you develop community-acquired pneumonia, then you're probably an older, more vulnerable person. But of course, when people are admitted with COVID, particularly if they're intubated, then there is significant inflammation that occurs and just the recovery from that illness in ICU-related debility means that many of these individuals will, will experience morbidity for some time.

And so, again, the context is really important. And in a younger population, you expect individuals to do better but then in a surge setting where a healthcare services overwhelmed, and the care and attention to risk factors like diabetes and hyperglycaemia, can't be given, then of course, mortality rates will be higher. But in Victoria, we were never in a in a surge-overwhelmed setting. I think the nature of the pandemic and the nature of the alert was often called, you know, Code Black and Code Red and so on, I mean, it was certainly serious, but our health service was never overwhelmed. Hospitals were never turning people away, with or without COVID. I'm sure elective surgery was cancelled, but urgent surgery never was. And I think that differs, certainly markedly from the early European experience and probably explained some of these differences.

JOHN WENTWORTH:     Yeah, I was thinking that as well. I mean, although we felt we were in a crisis, I don't think it compared to anything like our northern hemisphere colleagues experienced. Looking ahead, we've got lots of COVID now and then there's talk of another wave about to wash over us would. Would any of you like to comment on the what COVID looks like right now in a tertiary hospital? And what potentially the learnings from this study—how they could be applied to help manage people as they come through the hospital doors? I mean, for a start, how many dedicated COVID wards do we have in the various hospitals now? And how many ICU beds—what proportion of ICU beds are taken up by COVID? Would anyone like to comment on that?

DEV KEVAT:        At Western that certainly changes on a week by week basis. So I was doing around today and in the ICU, I think, probably about 20% of the patients had COVID, or COVID was a significant factor. Most of those patients were unvaccinated. And so, you know, for my mind, I think what this paper adds going forward is sort of a multi-dimensional notion of risk as a clinician as we walk around. COVID, diabetes, obesity, age, are all factors. And it may be that we don't hang our hat so much on one particular comorbid condition as much as we were maybe shaping up to do a year or two ago. And that we in our mind think particularly of how that conglomerate of risk might put a patient at higher risk.

And unfortunately, we do still, certainly at my hospital have a number of people who are not vaccinated or even if they are vaccinated, have not got booster shots. And for my mind, particularly with my pregnant patients who have diabetes, that's something we're always encouraging them to do. So I think, you know, obviously, the mass vaccination of the population has decreased the amount of severe illness, but there are still going to be pockets of illness. And with the condition being so prevalent, we're still going to have a significant component least in the adult population of patients where COVID is playing a factor in their in their admissions. I think it's difficult because obviously, the social aspects and the politics of COVID have really changed and there's a strong push to normalize COVID. But the numbers are so great that we will continue to obviously have a number of patients who we need to manage with this condition, particularly if there are multiple comorbidities.

RAHUL BARMANRAY:    Certainly at the Royal Melbourne, we can recall in 2021, when there'd be three, four, five COVID-dedicated wards in any one time. And now really for the majority of this year, there's been at most one—up to one ICU pod, dedicated to COVID-19. So the face is very much changed from an in-hospital disease to one that's managed for example, in the hospital-in-the-home setting. I happen to work in the Royal Melbourne hospital-in-the-home, and we get a lot of COVID patients that that come under us. But many patients have been incidentally diagnosed with COVID. They've come in for an entirely unrelated issue. They've had a nasopharyngeal swab and COVID has been detected, and they haven't necessarily needed any specific management for that. But then of course, because they've got COVID then we need to manage them as such so that we don't infect others unnecessarily.

And so for those of us who were working last year and the year before, we've very much seen the face change. But we're familiar with how quickly things can change with the advent of new variants. So for example, the Omicron variant last year, and that significantly changed the way in which people were being infected and the number of people who are being infected and requiring hospitalization. And so we're cautiously hopeful that such things don't happen, but well aware that that could happen again. And again, the panoply of risk factors and their interplay with outcomes could again change and these study results themselves specifically may become redundant, but should very much encourage us all to be continuously looking for what are the risk factors that have put our patients at higher risk so that we can mitigate against those so that we can treat them.

JOHN WENTWORTH:     And Ashraf if you're, I believe, up in Shepperton, which has just recovered from devastating floods. What's the what's the lay of the land up there in terms of hospital admissions and how much of a factor COVID is.

ASHRAF ISLAM: I want to add that I have just got an email from our CEO that they have activated Code Yellow, because our capacity of COVID ward is 25 bed and now all the beds are filled up now. So we are in the middle of another wave. But from the experience from the last three years and all the treatment facilities we have got now, and then all the information we get from these studies, I think we can manage those patients more effectively.

JOHN WENTWORTH:     Thank you. And look, a completely different question. You know, this cohort at least in theory would provide an opportunity to see down the track, in years to come. And I guess, looking forward if you had the constitution to go through the process to get permission to follow these people up and to see how they fared, would you like to make some sort of guesses or comments as to how the different cohorts in your study might be in five years time? We're comparing people without diabetes, who came through in that second wave? And I guess a bit in the first wave to those who had diabetes and those who had hyperglycaemia? Would any of you like to comment on that?

RAHUL BARMANRAY:    Absolutely. Perhaps Dev would like to answer first.

DEV KEVAT:        Yeah, look, I think it will be very interesting to see. What we know about the biology of COVID does include knowledge about effects on the pancreas directly. I do think there'll be such a thing as taking a history and understanding whether people had COVID sick enough to get them into hospital. And, you know, we talk about post-transplant diabetes, I wonder if there'll be such a thing as post-COVID diabetes, particularly for the people who are sick enough to be in intensive care or unwell. And so I think comparative cohort studies will certainly show a difference between those two things. I think it's a separate question as to whether there'll be a mortality difference between people had pre-existing diabetes, whether their diabetes indeed is accelerated by such a condition as COVID. And I don't really know the answer to that, but it's certainly something we all need to continue to work out.

RAHUL BARMANRAY:    And I wonder if in the future, we consider COVID-19, as something akin to gestational diabetes, which might sound like an odd metaphor to draw from first glance. But in the same way that in gestational diabetes, I think it’s famous placental lactogen that increases insulin resistance and so that particular stress test, if you develop hyperglycaemia during that particular stressor, even if it disappears following gestational diabetes, then down the track we know that you are at increased risk of developing diabetes proper. And so on the same way, if you experienced COVID-19, and/or are treated with dexamethasone, and you experienced transient hyperglycaemia that goes away at the end of that illness at the end of that course of treatment, that tells us something about your propensity to insulin resistance and your pancreas has ability to withstand a stress or. And tells us that you're probably more likely to go on to develop frank diabetes, type 2 diabetes that is, in future. Whether people are more likely to develop type 3 diabetes, type 3c diabetes that is, because of a direct, toxic inflammatory necrotic effect on the pancreas of COVID-19, is yet to be seen. There have been some case studies suggesting antibody positive diabetes following COVID-19. But these have been so few and far between for the great numbers of people who've been infected with COVID-19 that it's probably not a major factor.

MIC CAVAZZINI:               Many thanks to Rahul Barmanray, John Wentworth, Devaang Kevat and Mohammed Ashraf Islam for taking the time to record this podcast. Members of the RACP have free access to the Internal Medicine Journal, the Journal of Paediatrics and Child Development, and the Occupational Health JournalJust follow the links from racp.edu.au/fellows/resources/journals.

And remember that reading or writing academic articles, even listening to podcasts, can all be counted towards your learning for continuing professional development. There’s a prefilled link to MyCPD at each of the podcast episode pages. And you’ll get an email from the College at the start of the year about many more online resources tailored to all of the CPD categories. Keep an eye out for that and please reach out if you have any questions. The best email for that is mycpd@racp.edu.au.

I’m Mic I’m Cavazzini and this episode was recorded on the lands of the Gadigal people of the Eora nation. I pay respect to their elders past and present, and their ongoing connection to sea and country. Thanks very much for listening.

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