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Time Stamps

• 02:34 Can we give metformin in the hospital?
• 10:50 Incretin-based therapies
• 14:27 Sodium Glucose Cotransporter-2 Inhibitors
• 16:27 Sulfonylurea & Thiazolidinediones
• 18:00 Basal Insulin Inpatient

Show Notes

Note: This applies specifically to Type 2 Diabetes Mellitus. 

Where does the dogma of stopping metformin come from?

• Metformin (of the biguanide class) is often held on admission due to concern for development of lactic acidosis
• Biguanides increase insulin sensitivity, but also inhibit pyruvate dehydrogenase, potentially leading to lactic acidosis
• Phenformin, an older biguanide, was found to cause lactic acidosis because
  1. Phenformin has a large lipophilic side chain, leading to increased binding to mitochondrial membrane and therefore more anaerobic metabolism
  2. Phenformin has a long half-life (11 hours) compared to metformin (4-8 hours)
  3. Up to 10% of patients have defects in phenformin metabolism, leading to prolonged circulate in the bloodstream
• Phenformin was pulled off the market in the 1970s due to high rates of lactic acidosis
• Phenformin made everyone skeptical of the safety of all biguanides and case reports of metformin leading to lactic acidosis appeared. Almost all of these case reports were in patients either who
  1. Took high doses of metformin (>20 grams), with renal dysfunction, or 
  2. Had a lactate-predisposing conditions (e.g., sepsis, decompensated heart failure, etc.)
• The lactic acid generated by metformin is typically handled by the kidneys and liver quite easily

Can metformin be used in patients receiving contrast?

• The 2021 American College of Radiology (ACR) Manual on Contrast Media has a statement about metformin and iodinated contrast use
  1. Patients taking metformin are NOT at higher risk than other patients for post-contrast acute kidney injury.
  2. There have been NO reports of lactic acidosis following intravenous iodinated contrast medium administration in patients properly selected for metformin administration. 

Can we continue incretin-based therapies (GLP-1s and DPP-4) in hospitalized patients?

Incretin-based therapies:

• Mechanism: stimulates insulin secretion in response to elevated blood glucose levels
  • They are relatively safe to use (see considerations below) inpatient without concern for PO intake since they act only in response to a glucose load.
• GLP-1 (glucagon-like peptide) receptor agonists
  • Examples: meds that end in “-tide” (e.g, liraglutide, exenatide)
  • Avoid in patients with:
    • Pancreatic disease
    • Nausea and vomiting on admission because GLP-1s can slow down gastric emptying, leading to nausea and vomiting
      • One study found about 10% of patients on GLP-1s became nauseous 
    • Concern for gastric dysmotility
• DPP-4 (dipeptidyl peptidase 4) inhibitors
  • Examples: things that end in “-gliptins” (e.g., sitagliptin, alogliptin)
  • Avoid in patients with:
    • Pancreatic disease
    • Heart failure (only saxagliptin)

What about the other oral diabetes medications? What should we consider when resuming or stopping outpatient diabetes upon admission?

Note: Meglitinides and alpha glucosidase inhibitors will not be discussed

• SGLT-2 (sodium-glucose transport protein 2) inhibitors
  • Examples: meds that end in “-flozin” (e.g., empagliflozin, canagliflozin)
  • Mechanism: Inhibits SGLT-2 receptor in nephrons, reducing reabsorption of glucose, thereby decreasing serum glucose levels
  • Avoid in patients with:
    • Hypovolemia
    • Poor (or variable) oral intake (such as being made NPO)
• Sulfonylureas
  • Examples: glipizide, glyburide
  • Mechanism: increase insulin release from pancreas (independent of oral intake!)
  • Avoid in patients with:
    • Poor (or variable) oral intake (such as being made NPO)
• Thiazolidinediones (PPAR-gamma agonists)
  • Examples: meds that end in “-zone” (e.g., rosiglitazone, pioglitazone)
  • Mechanism: reduce insulin resistance
  • Avoid continuing in all patients due to their increased risk of heart failure and rosiglitazone’s risk of MI

How do we appropriately use insulin in hospitalized patients with type 2 diabetes?

• Patients on sliding scale insulin monotherapy can have a higher average blood glucose than patients on basal-bolus insulin (per RABBIT-2 trial)
• Hyperglycemia can lead to more infections due to neutrophil impairment
• Target blood sugar in hospitalized patients is 140-180 mg/dL (per NICE-SUGAR trial conducted in critically ill patients)
• Factors to consider when starting weight-based insulin regimens
  • GFR <60
  • Older age
• If starting new insulin, consider basal dose of 0.2- 0.3 units/kg/day
• If blood glucose is low- to mid-200s, can use basal insulin + DPP-4 inhibitor + sliding scale insulin

Transcript

Shreya: For first time listeners of this CORE IM segment, Mind the Gap is a series all about challenging dogma in medical practice by examining the existing evidence. Today I will leave you in the trusted hands of  two new hosts who I’ll let introduce themselves.

TL: Welcome to Mind the Gap, I’m Tyler Larsen, a hospitalist at the Los Angeles VA.

SP: And I’m Satya Patel, also a hospitalist at the Los Angeles VA.

TL: Today on Mind the Gap we’re talking about everyone’s favorite topic: inpatient diabetes management.

SP: This is Mind the Gap, so we’re talking about DKA, right?

TL: Not exactly the gap I wanted to focus on today Satya. I actually want to talk about what the heck to do when managing type 2 diabetes in the hospital.

SP: Oh, this is such a great topic. As a resident, I feel like I was taught to just hold all oral diabetes meds on admission.

Dr. Umpierrez: I will tell you that if you go to Israel, 60% of patients are managed with oral agents. If you go to the United Kingdom, about 40% are treated with oral agents and they continue to use the oral agents and you are not a goal, they add insulin.

SP: That’s Dr. Guillermo Umpierrez, an endocrinologist at Emory, who has authored almost all the papers on the use of diabetes meds in the hospital. I’m really appreciative of his work because, before we looked into it for this episode, I didn’t have a good grasp on what I should actually do with all those diabetes meds. Did you?

TL: What are you talking about, it’s simple. You just stop the oral meds and start insulin sliding scale. Done. That’s all there is to it, right?

SP: I don’t know Tyler, I think it’s more nuanced than that. Sliding scale can totally feel like a “set it and forget it” intervention for us, but for our patients, it means getting poked anywhere from 4- 6 times a day.

TL: It’s easy to forget how uncomfortable sliding scale can be for patients and how much time is needed for nurses to do that many fingersticks. To get some clarity on how to approach this, let’s explore some of the evidence – (SP: or lack thereof) – behind the inpatient management of type 2 diabetes. 

SP: So on today’s episode, we are going to tackle three questions: 

• To start – where does the dogma of stopping metformin come from?
• Next up – do we need to stop all other oral diabetes medications on admission?
• Finally – how can we use insulin in hospitalized patients with type 2 diabetes?

TL: Satya, did you want to start us off with a case?

SP: Absolutely! Mrs. Sita G Lipton is a 74 year old female with Type 2 Diabetes Mellitus and HTN, who is admitted for intermittent chest pain and dyspnea. Her blood glucose in the ER is 210. You do a medication reconciliation and she’s on the following meds for her type 2 Diabetes: metformin, glyburide, sitagliptin, and empagliflozin.

TL: Oof!

SP: I had a similar reaction. Let’s say that we decide to make her NPO for a stress test in the morning. What should we do with Mrs. Lipton’s diabetes meds?

TL: I feel like everybody does something different. There are so many options! We have oral meds, sliding scale and basal insulin.

SP: Totally agree! It’s really confusing. Let’s tackle metformin first – I feel like this fear of lactic acidosis has just been burned into my brain. Where does the concern for metformin-associated lactic acidosis, or what some affectionately call MALA, come from? 

TL: To truly understand where this comes from, we have to take a quick pathophys detour (Satya – oh noooo here we goooooo). Hear me out, it’s actually pretty interesting – a lot of the concerns about MALA largely come from phenformin, a sibling of metformin.

SP: Metformin’s got a sibling?! This is like a soap opera where suddenly we discover that MALA’s friend is more than just a PALA.

TL:  Yep, both metformin and phenformin are part of the big happy biguanide family.

SP: Tyler, can you remind me what a biguanide does? 

TL: Well, like so many things, it’s not completely understood. But what we do know is that biguanides inhibit pyruvate dehydrogenase, forcing cells into anaerobic metabolism.

SP: And increased anaerobic metabolism will ramp up lactate production, right?

TL: Yep. 

SP: Wow. The biguanides accomplish what most medical students only dream about – DESTROYING THE KREB’S CYCLE.

TL: Exactly. So, yes, technically metformin increases lactate production, but the key thing to know is that the liver and kidneys can easily able to handle this increased lactate load, so we don’t even see a change in serum lactate levels clinically.

SP: Well, if the liver and kidneys can handle the lactate produced by metformin, what exactly did phenformin do to get such a bad rap for the entire biguanide family?

TL: It’s a good question. Phenformin had a good run for about 20 years, but then people started noticing phenformin’s association with severe lactic acidosis and ultimately it was pulled from the market in the 1970s.

SP: Leave it to a big sibling to ruin absolutely everything. 

TL: As an older brother, I completely understand that. There are a few major reasons why phenformin causes such severe lactic acidosis. The first has to do with its size. Phenformin has a huge side chain which has more affinity for binding to mitochondrial membranes than metformin does.

SP: So, if I’m following along correctly, that means phenformin causes more lactate production than metformin does, right?

TL: Bingo. The second reason is that phenformin also has a longer half life than metformin. And to make matters worse, 10% of people have defects in phenformin metabolism and so those folks will have even more phenformin lingering around in their bodies.

SP: Sounds like phenformin, the older sibling, might be hanging around in their parent’s basement (or in this case, the bloodstream) a lot longer than expected. I can kinda see why everyone became terrified of continuing any biguanide during hospitalization.

TL: Yep, but the teaching point is that not all biguanides are the same! Even though there is a clear association between phenformin use and lactic acidosis, there isn’t great evidence linking metformin use with lactic acidosis when prescribed appropriately. 

SP: Yeah, and I’ve heard some folks question whether metformin causes lactic acidosis at all!

TL: Yeah, so  bringing in some more pathophys, metformin probably won’t cause lactic acidosis because it has a relatively short half-life, so it won’t linger for long periods of time to cause trouble.

SP: When prepping for this episode, a recurring theme that I noticed is that MALA was mostly seen in patients that already had lactate-predisposing conditions. The literature about MALA comes mostly from case reports in patients with kidney failure, liver failure or metformin overdoses. The metformin kind of just feels like a bystander here.

TL: Yep aside from metformin overdoses greater than 20 grams, almost every case of MALA is in patients who have other reasons or risk factors for lactic acidosis, like decompensated heart failure. And if the case reports don’t do it for ya, a 2010 Cochrane review of metformin and lactic acidosis evaluated over 300  studies and found 0 cases of lactic acidosis, despite over 70,000 patient-years of metformin use.

SP: Wow, zero?! That’s an impressive stat. One thing about that Cochrane review that I wanted to point out is that it excluded patients with a Cr greater than 1.5, which is super relevant since metformin is renally cleared.

 TL: That’s a really important point, Satya! From reviewing all this literature the biggest thing that I’m taking away is that it sounds like we can continue metformin in patients without renal dysfunction.

SP: Yeah, as long as they don’t have a lactate-producing condition, we should continue metformin. To make sure we weren’t going too rogue while thinking this through, we asked Dr. Umpierrez to weigh in.  

Dr. Umpierrez: If you’re going to use Metformin, you should check your creatinine levels, the GFR level, and don’t take any chances. If the GFR is below 45, 30 hold it. When it’s between 30 to 45, you should use half dose. So no more than one gram per day. So somebody has acute kidney injury and creatine is rising, stay out of trouble and hold the medications. And then you can restart whenever the patient is volume repleted and creatine is stable. And that, that will be safe.

SP: After talking to Dr. Umpierrez, I feel a lot more confident about continuing metformin for my patients without renal dysfunction or lactic acidosis. And in the spirit of challenging the norm a little more, let’s actually pit two dogmas against each other.

TL: Who let the dogmas out, am I right?

SP: Haha, I love it! The other dogma I am referring to is the concern for contrast-induced nephropathy. Whenever I order a CT scan with IV contrast, a little pop-up shows up that asks “is this patient taking metformin?” And it ends up making me really nervous and I sit there agonizing over what to do. I know that the true rate of contrast-induced nephropathy is hotly debated these days, but, should we be holding metformin when patients are getting IV contrast studies?

TL: Well whether or not contrast-induced nephropathy exists is a topic for a whole other episode. Fortunately for us, the American College of Radiology (the ACR) actually has a statement about metformin and iodinated contrast studies. The ACR states that patients taking metformin are NOT at higher risk than other patients for contrast-induced nephropathy or lactic acidosis.

SP: Ok, so it’s probably fine to give IV contrast and get that CT scan for patients taking metformin, as long as their kidney function is okay. But what about Mrs. Lipton? She’s not getting a CT scan or anything, but is there a good reason to hold her metformin on admission?

TL: Like everything in medicine, it depends. We don’t know what her kidney function is yet. Once that’s clarified, we can consider continuing the metformin.

SP: Now that we’ve got a tentative plan for the metformin, what should we do with Mrs. Lipton’s other diabetes meds? As a refresher – in addition to metformin, Mrs. Lipton is also on glyburide, sitagliptin, and empagliflozin. What are we doing with the rest of these meds? To wrap our heads around this stuff, I think it would be really helpful to go over the major categories of diabetes meds. 

Dr. Umpierrez: So in 2012, when we wrote the guidelines for independent society… then, we have very little data at all on the use of oral agents. So therefore, we recommended to stay away or not usually recommend to use oral agents in the hospital. Since then there have been large number of observational status and a few randomized control studies suggesting that perhaps oral agents are acceptable in some circumstances.

TL: Let’s start with a broad class – incretin-based therapies. Satya, what exactly is an incretin?

SP: So Tyler – there are two main classes of incretin-based meds – glucagon-like peptide 1 receptor agonists and dipeptidyl peptidase 4 inhibitors. Let’s just call them GLP-1s and DPP-4s from here on out.

TL: I’m cool with that. And for those of you who need a refresher, the GLP-1s are your -tides, (SP: like liraglutide and exenatide) and the DPP-4s are your -gliptins (SP: like sitagliptin and alogliptin). But how do the GLP-1s and DPP-4s actually work?

SP: Well, GLP-1s and DDP-4s stimulate the pancreas to secrete insulin, but only in response to elevated glucose levels. So the good thing is that if your patient is NPO, incretins WON’T make them hypoglycemic.

TL: Uhhh, that sounds like exactly what we are looking for in our hospitalized patients.

SP: I know, right? Since Mrs. Lipton is NPO for that stress test, we don’t have to worry that her sugars will just drop if we continue her sitagliptin. It basically does the same thing that the bolus part of a basal-bolus insulin regimen does by taking care of those high sugars after eating a meal.

Dr. Umpierrez: DPP-4 worked for postprandial correction because it increased insulin and suppress glucagon. So it is about the same if you do basal plus a DPP-4 versus basal bolus because the bolus and the sitagliptin works on correction of postprandial. 

TL: DPP-4s and GLP-1s really seem like an underutilized class of medications. Kind of too good to be true! Are there any drawbacks?!

SP: Well, if your patient has pancreatic disease, we really should pump the brakes on using DPP-4s and GLP-1s. The thinking is that these meds excite the GLP-1 receptors in the pancreas, leading to hyperplasia, which can block pancreatic ducts. This can then lead to pancreatitis.

TL: We also asked Dr. Umpierrez what he’s seen, especially when it comes to GLP-1 downsides

Dr. Umpierrez: We use Exenatide given twice daily and it shows that it’s safe and effective in improving glycemic control, but it’s associated with nausea and vomiting and decreased appetite. And I think there was 9% or 10% of patient who has significant nausea who discontinued the medication. 

SP: So the takeaway for me is that if a patient is admitted with nausea or vomiting, don’t add a GLP-1 because it can add fuel to the fire.

TL: And if they were taking a GLP-1 before admission, hold it since it can cloud the picture.

SP: So the GLP-1s cause nausea and vomiting because they slow down gastric motility. That’s why in patients with diabetic gastroparesis, I would also avoid GLP-1s.

TL: I’m with ya on that.. But what if our patient is already on a GLP-1 as an outpatient and they come in for something totally unrelated to gastric discomfort, is it safe to continue it on admission?

Dr. Umpierrez: If somebody is taking a GLP-1, let’s say before admission.. at discharge, I would definitely continue with Liraglutide or Dulaglutide or one of the semaglutides without any question. I would prefer that to insulin therapy. 

SP: That’s great to know! Switching gears to DPP-4s, do I need to worry about anything else besides pancreatic disease?

TL: For whatever reason, one of the DPP-4’s, Saxagliptin, actually has an FDA warning due to increased rates of heart failure hospitalizations, so I tend to hold Saxagliptin in patients with heart failure. 

SP: Ok to recap, DPP-4s and GLP-1s seem pretty well tolerated in the hospital especially because they promote insulin release only after our patients are eating that delicious pudding.

TL: But we should hold both GLP-1s and DPP-4  in pancreatic disease, especially in pancreatitis.

SP: And pump the breaks on GLP-1s if the patient is coming in with nausea or vomiting or has gastroparesis.

TL: And finally, for DPP-4s, we need to be careful with Saxagliptin and heart failure.

Let’s move on to the Sodium Glucose Cotransporter 2 inhibitors, a.k.a. SGLT-2s. These prevent glucose reabsorption in the nephron, so you end up peeing out more sugar.

SP: So these are your empagliflozins and canagliflozins. Tyler, do you have a way of keeping the names straight?

TL: The way I remember the SGLT-2s is that they all end in -flozin because when you take them, your glucose starts “flowzin” all over the place.

SP:  Hahaha, I like it! SGLT-2s act as diuretics (TL: #Flozinators) We really need to think about a patient’s volume status before deciding what to do with the SGLT-2.

TL: Right. So if my patient comes in with volume overload, I usually continue the SGLT-2 to help with the diuresis. But if my patient is hypovolemic or isn’t eating much, I’m usually more cautious and hold the SGLT-2.

Dr. Umpierrez: The SGLT-2, we have no data. There was a one small studies published a few months ago from Germany… didn’t improve much glycemic control, but it was tolerated. But the problem with SGLT-2 is you have poor oral intake. There is a small, but a significant risk of ketoacidosis. So we all have seen the SGLT-2 associated diabetic ketoacidosis. So because of the volume depletion, we need more data on an SGLT-2’s.

SP: Ok, so let’s apply this to Mrs. Lipton – she’s NPO for that stress test, so I think it would be a good idea to stop the empagliflozin, at least until we have more studies.

TL: That’s not unreasonable. Why don’t we move on to sulfonylureas?

SP: That sounds great. As a refresher, sulfonylureas are your glipizides and glyburides. They increase insulin release from the pancreas regardless of oral intake.

TL:  And that’s exactly why sulfonylureas are notorious for having a higher risk for hypoglycemia. They aren’t forgiving like GLP-1s and DPP-4s that will wait till there is food in the system to release insulin. The sulfonylureas are merciless and are releasing insulin regardless of your patient’s PO intake.

SP: Savage! Since Mrs. Lipton is NPO for that stress test, let’s hold her glyburide to avoid low sugars.

TL: Agreed – let’s move onto another class of medications – thiazolidinediones (so glad that we call them TZDs). Examples of TZDs include pioglitazone and rosiglitazone. 

SP: Tyler, isn’t there a SmashMouth song with the lyrics “and all that glitazone’s gold?”

TL: I feel like every time we talk, the puns start coming and they don’t stop coming, but let’s get back on track here. Because TZDs reduce insulin resistance, we don’t have to worry about hypoglycemia.

SP: The downside is that rosiglitazone actually increases risk of MI and all TZDs have a black box warning because they can cause or worsen heart failure.

TL: Aaaand that’s probably why we never see anyone on these.

SP: Exactly.

TL: Ok, so to close the loop on Mrs. Lipton’s med rec, we are going to wait for that Cr to come back before we know what to do with the metformin. We’re going to continue her sitagliptin, since it acts like bolus insulin. And we’re going to hold her glyburide and empagliflozin because she is NPO.

SP: If I am counting correctly, that means we’re holding at least half of her medications. That’s a lot. We better talk some contingency-planning here. What the heck are we going to do if her sugars go up while she’s in the hospital?

So let’s talk about how we can use insulin to fill in the gap we created by stopping half of Mrs. Lipton’s home meds.

TL: Speaking of not opening any more gaps, what should our target sugars be in the hospital?

SP: We’ve been taught to aim for a sweet spot of blood sugars between 140 and 180, but that’s extrapolated from studies in critically ill patients.

TL: 140-180? Shoot, as a resident I was happy if the average glucose was under 300. 

SP: Me too! Turns out, ADA guidelines actually have a Grade A recommendation to use insulin in all hospitalized patients with blood sugars consistently over 180.

TL: 180? That number is way lower than I expected. Most people don’t usually use sliding scale insulin until the sugar is in the mid-200s. We asked Dr. Umpierrez about his practice and he has some pretty strong feelings about sliding scale. 

Dr. Umpierrez: I just think that correction doses are useless for most people in the hand. The problem is when you start using sliding scale and the glucose remains in the 200 or more and you just continue to use sliding scales I mean that is wrong. 

TL: If we are reacting to high blood sugars with just sliding scale, we never get good glycemic control. We actually have good data showing that patients on sliding scale alone have a higher average blood glucose than patients on basal-bolus insulin.

SP: So? What’s wrong with that? What’s wrong with a little bit of permissive hyperglycemia? 

TL: Well, hyperglycemia isn’t all that benign. When up against basal-bolus regimens, sliding scale has been shown to have higher rates of badness, like wound infections, pneumonia, and bacteremia.

SP: Wait what? What does hyperglycemia have to do with more infections?

TL: We don’t know for sure, but we think that hyperglycemia can mess with neutrophil function, leading to more infections.

SP: Soooo letting sugars ride in the 200s is more dangerous than I thought, good to know! The bottom line seems to be that a reactive strategy alone never gets good control, and bad control can lead to bad outcomes.

TL: Yeah, and as we’ve already covered, there are multiple ways to achieve good control and everyone does something a little different. What does Dr. Umpierrez say about how he uses insulin?

Dr. Umpierrez: You have to individualize care. 70% of our surgical patients at Emory are with base alone and they do very well. If you just tell every surgeon to give 0.2 units per kilo, before surgery, the blood sugar cruise, very little hypoglycemia, very little hypoglycemia, because it’s only poor basal and then you titrate and sliding scale may work and it worked, but there was a 20, 30% failure rates and the basal the Rabbit 2 trials showed that with sliding scales, you get more complications, more AKI, more infections. 

TL: I feel like we are pretty bad at starting basal right off the bat. Any good ways to come up with a starting dose?

Dr. Umpierrez: We recommend the initial dose based on the risk of hypoglycemia. And that two factors are quite important. One is kidney function. So if the GFR less than 60, the risk of hypoglycemia is much higher. The other is age. Older guys in the hospital don’t need they very little, very little so. So in those patients, we recommend the total daily dose of 0.3 units per kilo. 

SP: So now that we have an estimate of the total daily dose, we should talk about how we are going to write the insulin orders in the patient’s chart.

TL: I like to take half of the total daily dose of correction and make it basal and then I turn the other half into a TID bolus regimen, usually adding about 10% to the TDT as I make that calculation. I’ll also add sliding scale on top, just to make sure I stay on top. 

SP: I do something really similar.

TL: I think lots of us do it this way. Interestingly, it turns out that if your patient’s sugars are in the low to mid 200s, there’s another way to do this as well.

Dr. Umpierrez: Now, if you do basal plus other agents, like basal plus DPP-4. We did that study in 280 patients, and we call it the Sita-Hospital trial. It was a basal plus sitagliptin, one injection of basal one injection of sitagliptin versus basal bolus approach. And we saw no difference in glycemic control in 300 patients, medicine and surgical patients in general ward. So, so if you asked me, I mean, my favorite approach for most people in the low 200 mid 200s, I’d use the  basal plus approach… because people don’t need too much and you do basal plus corrections.

TL:  That makes so much sense. Remember how we talked about how DPP-4s are basically our bolus insulin?

SP: Yeah, and that’s exactly how he’s using the DPP-4 in this case!

TL: Let’s tee up Mrs. Lipton’s situation. 

SP: Time to put in some insulin orders!

TL: To star, lets add a weight-based basal regimen, continue the DPP-4 that she’s on, and start sliding scale as a contingency.

SP: That sounds good to me. Tyler, we covered a ton of ground in this episode, what are some of your takeaways?

TL: I think the biggest take away, is when it comes to oral meds, we can continue metformin more often than we think, especially if a patient has good kidney function and no lactate-producing conditions. After this episode, I feel a lot more comfortable continuing, or even starting DPP-4s in the hospital, as long as patients don’t have pancreatic disease. What are some of your takeaways?

SP: Metformin was also a really big one for me. GLP-1s also seem pretty good to continue as long as patients don’t have nausea, vomiting, or pancreatitis. And when it comes to insulin, basal is our friend and sliding scale alone is not.

TL: And that’s a wrap! Thanks everyone for tuning in. A huge thank you to Dr. Guillermo Umpierrez (president-elect of the ADA, endocrinologist and professor of medicine at Emory), Dr. Jane Weinreb (Chief of endocrinologist and professor of medicine at UCLA) for peer reviewing. 

SP: Thank you to Dr. Mike Natter for the incredible accompanying graphic and to Max Had for audio editing. Thank you to Dr. Aaron Troy for helping off-air to produce this episode. Our views are our own and do not reflect the views of our affiliated institutions.

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