So, Dr. Martin, we have gotten quite a few questions about celiac antibiotics. So should we just kind of generalize them and say, can the panelists just address the conundrums related to antibiotic management of SIBO? I agree, Eden, that's a great way to handle it. I also want to add, those were some absolutely epic talks from Vivek and Jill. There's tremendous detail in there, and they absolutely exude knowledge. And that's why we have so many really great and detailed questions. And I applaud the members of the audience for submitting such really detailed and erudite real-life clinical questions. We have a lot of questions, Eden, as you said, that relate to antimicrobial therapy for small intestinal bacterial overgrowth, or SIBO. Many of them center around the fact that it is really difficult to get third-party payers to foot the bill for rifaximin for this particular indication. And so clinicians want to know if there are some workarounds that can be suggested to help get this expensive antimicrobial agent for their patients. They try other agents like neomycin, but now that's in short supply and really hard to get. And so they'd like to know, well, if they can't afford rifaximin, is there a way that I can get it? If I can't get it for my patient, I've tried neomycin, and I can't get that either. Is there something else you can suggest? And I'd say that we've got at least a dozen questions that basically are about that issue. So if the faculty can comment, much appreciated. Hi. I'm going to go ahead and jump right in there. So rifaximin is indicated for IBSD and for hepatic encephalopathy. So it does not have an indication at this time for small bowel intestinal bacteria overgrowth. It is utilized in studies, and it's studied for, and it's used nationwide. So the challenge with coverage is that you have to have a diagnosis of IBSD to get covered for SIBO. So when you're submitting that prescription, you want to make sure that the patient has some type of overlap, and there is a diarrhea component. The challenge is that it is one of the recommendations for IMO, or intestinal methane overgrowth. And that's where the challenge of the coverage is mostly. Sometimes insurance, the pharmaceutical companies will give us samples, but that's been far and few between recently. I haven't had samples for the medication for probably over a year. Um, the other option for IMO is neomycin. So it's a, it's a different pathway. So you would want to use specifically for IMO a course of neomycin and that's backlog. So we go back to using metronidazole, which is what we originally used for treating for, for SIBO. So in years ago, we never tested for IMO. It wasn't a condition that we even were aware of, although we knew that constipation may have been associated with this symptom. There was one attendee I did put in the chat. Go back to the reference that I added in my, in my list, American College of Gastroenterology, their clinical guidelines on SIBO. And it's authored by Dr. Pimentel, who's a thought leader and researcher in SIBO. And on page 172, it gives a list of suggested antibiotics for treatment for both conditions. And it gives the efficacy rate. And this is where you really have to have a conversation with your patients. Because in my mind, SIBO is after I've ruled everything out. I want to make sure, you know, I'm treating their functional bowel disorder. I've, I've ruled out celiac disease. They don't have Crohn's disease. They don't have pancreatic insufficiency, because these patients have very high anxiety to the bloat and the visceral hypersensitivity too. Maybe they have non-ulcer dyspepsia. Maybe they really need to be on a small dose of a tricyclic, you know, to help with that, mitigate that, that visceral hypersensitivity. Because then you get into the cycle of antibiotics, antibiotics, antibiotics. And I, and I feel bad for my patients because they just want another course of antibiotics. There's a good literature on herbal products, and I didn't give you that information today, but there's a series of, of herbal products that you can purchase that also help with SIBO. And I've had some of my patients do their own research because that's not on our radar, but he had such an amazing response to it that I'm, I'm going to be more open to giving that as an option to patient. Because this is, when it comes down to taking care of patients with SIBO, this really is shared decision-making. Okay, do you want me to give you an antibiotic for 14 days that has a 50% efficacy rate, or do we really work on mitigating your symptoms? And what are those symptoms? If someone's having one bowel movement twice a week, then I'm going to work on moving their, getting their motility moving before focusing on SIBO if there was a positive methane test. So there's still some things that we can help them clinically with their symptoms before going down this, okay, what is the antibiotic I need to give you, and how often I need to give that to you. Hope that makes sense. That's my philosophy. Okay. Jonathan, I just want to commend you. That was really an outstanding review. And I think she brings up two points. One, in her discussion, she's being the patient advocate. She's clearly explaining to the patient that we have this particular best treatment, but we don't have access to it. Here, for lack of a better description, second-tier antibiotics, maybe some side effects, maybe not as effective. And although we should all be evidence-based and evidence-driven providers, you know, her comments on some alternative therapies that may not have the science there, as long as they don't hurt anyone, I think that's a little bit of the practice of the art of the medicine. Work with the patient, be honest, mostly review the side effects that could be significant, potentially harmful, because they do exist. But it's okay to practice the art of medicine in 2023. The art of medicine at one time was very common. We should be data-driven, but be the patient advocate, and don't be afraid to use the art of medicine and be the patient advocate. And so our next question is, Dr. Martin, is continued surveillance recommended if patient has non-dysplastic Barrett's, but repeat EGD one year later is negative? Vivek, can you advise us on the proper management there? Yes, so that's a fun question, because Barrett's in this country comes in two varieties. One that is the biopsy of the irregular Z-line, which is probably the more common Barrett's that we diagnose. And then there is the real Barrett's, which is the short or long segment length of esophagus. And by the way, both are being followed right now. And I don't mean to say that you can really get away from it, but the GE junction conundrum is a controversial topic that we can discuss another time. But the question that is posed is that you had Barrett's today, but no Barrett's next year. There are two possibilities for that outcome. Number one, that the Barrett's was diagnosed at some point at the GE junction at a biopsy that described intestinal metaplasia. And then at the follow-up biopsy, that target area was not hit. And or there really wasn't intestinal metaplasia. It was an overhaul last time. And or that the current pathologist is not really interpreting it as intestinal metaplasia. So that's the one outcome where there was Barrett's positive last year, but not positive this year. That's the GE junction situation. When you have a non-GE junction segmental Barrett's, then the likelihood of having a positivity last year and negativity this year is basically the sampling error. And that the biopsies were likely not performed from the Barrett's segment. And or the pathologist has failed to interpret it as specialized intestinal metaplasia. So complex topic. I tried to present it simply. But the answer is once you have diagnosed the Barrett's, unfortunately, if it's a bona fide diagnosis, you are committed to the recommended surveillance intervals, unfortunately. Dr. Cole, just to build on that, there was a question that also had asked if you have a diagnosis of short segment Barrett's in the setting of esophagitis and then several subsequent endoscopies are negative, do you continue on that PPI and that surveillance regimen? Yeah. So there is a couple of ideas on this. One is that, you know, if somebody, so esophagitis, erosive esophagitis is probably endoscopically proven. Erosive esophagitis is probably the best diagnostic test for good. You know, you really don't, unless you're ingesting lye or, you know, some formality added daily basis, you know, that is the most likely reason that that's the most confirmatory test for the presence of acid reflux. Now, in patients who, in the real world, in patients who have developed erosive esophagitis, it would probably make sense that they continue on some form of PPI therapy, especially if they are overweight, they smoke or they're non-adherent to dietary and lifestyle recommendations, which majority of patients find it difficult to do. So that's the reality of the situation. Now, every so often you'll have a biopsy done in esophagitis because it looks ugly and people think it might be cancer and it does pick up the esophagitis, but it also raises a question, as I mentioned in my talk, whether there is indefinite for dysplasia pathology or low grade dysplasia pathology. So these patients will typically get a repeat endoscopy and at the repeat endoscopy, one of two outcomes is possible, or three outcomes, actually. Number one, erosive esophagitis has not healed. So you're back to the square one. Number two, erosive esophagitis has healed and there is no Barrett's. And then the number three is erosive esophagitis has healed and there is Barrett's. So then whichever pathway you find, that is the one that you have to take. Our next question is, how do you go about educating patients when they fear taking PPIs on a long-term basis? So this was an issue created by New York Times many years ago. And as it does every so often, New York Times pops up and we have a situation. After that, the investigators, very thoughtful and very well-known folks, including consensus meetings, and they looked at the data that created this problem, which is that PPI use creates bone loss and hair loss and magnesium and this and that, dementia. And they found that these were basically associations. These are association-based risks and not high-quality, randomized controlled trial type of events. So based on that, several years ago, the American Gastroenterology Association came out with a very firm guideline that for those patients who need, that for those patients who need, who have a clinical need to be on a PPI, they should absolutely be placed on that agent. And at this point, there was no firm evidence that they really create or contribute to dementia. So basically, one of the Australian studies looked at, is it 20,000 patients on PPI, 20,000 patients on no PPI and they measured the dementia rates. What does that tell you? So that's the kind of data that there was. So at this point, it's safe to take PPIs for those patients who need it. Indiscriminate use of PPI should be avoided. And I do believe that there is some guidance to maybe check a magnesium annually, because that may be the strongest association in terms of, you know, and that may be also in certain select number of patients. But I know Joe and John or Aaron, you have any other comments on that? Yeah, I can definitely add to that, Vivek. I mean, you know, that's the data that you call out is a great point. Another way, I think, to couch it with the patient, that can make it very understandable for them and show that the choices in their hands is, you know, to point out that the choices aren't unlimited here. And that if they don't want to be on PPIs, the options are to step down to H2RAs. And they can try that, but it's probably not going to be successful. But it's worth a shot. And they'll let you know. Or to step even further, further, further down to antacids. Good luck with that. Or to do nothing. Then they're going to come back asking you for the PPIs. So, you know, we don't have a toolbox that has a thousand sockets in it. There's about four of them. And so we've got to take the one that fits the best. And the patient will usually end up deciding. You'll step them back to an H2RA. But if they truly have GERD, particularly if it's severe, it's not going to cut it. They're going to be unhappy because they've already been on a PPI and been symptom-free. So they're going to end up calling that shot on their own. That's the other way to approach it, is to let the patient make their own decision by explaining the choices. Because they often think that the choices are limitless. And we know that they're not. Good point. So we'll jump back to celiacs for a second here. And Jill, we've got a bit of a case for you. So a patient was tested for celiac disease because they had bloating and some abdominal discomfort, but no other symptoms. And they got the following results. Positive immunoglobulin A, but normal tissue, transglutamase AB, immunoglobulin A. So what would you make of this particular case? So the way the celiac panel serologies are set up, your immunoglobulin level is a level. It's not whether it's positive or negative. So you want to be aware of whether it's, if their level is low. So if they're not mounting enough response to show that you can use an IgA testing. But if it's elevated, then that's not significant to your testing. So first, your serum IgA level, you want to know if it is within normal range or if it's low. If it's low, then you can't depend on your TTG IgA serologies to make a diagnosis. If it's elevated, then you can still use the TTG serum IgA to make a decision on whether they have celiac disease or not. You're looking for an elevated level. Thank you. Our next question is, if a patient had a history of Barrett's esophagus or gastric IM in the past, but the most recent EGD showed negative pathology, would you continue surveillance EGD every three to five years, whether the symptoms were controlled or not? Right. So I think we kind of answered this before, but it sounds like there's two different questions here. So if you have a history of Barrett's, which is bona fide, accurately diagnosed and confirmed by expert pathology, then yes, you are stuck with the surveillance guidance that we have right now. So if the segment is less than three centimeters, you're looking at coming back in five years. If the segment is three centimeters or longer, then you're coming back in three years, at least as per the latest guideline. Gastric intestinal metaplasia is a different box. It's less of a risk issue in the Western world, but in the Japanese and Chinese and Asian populations, gastric intestinal metaplasia has a very different connotation. The AGA has come out with some guidance on this in the last few years, and certain patients with gastric intestinal metaplasia, especially of the incomplete type, and that's a pathological term, with potentially some family history, prior history of stomach adenomas or cancers, some syndromes that they're part of, and so forth, are candidates for routine surveillance every two to three years, but the evidence is very weak in the Western population. I think our policy on gastric intestinal metaplasia is that it certainly serves as a platform for transformation to neoplasia, but we have this discussion with the patient, talk about the pros and cons, and then some of them will end up coming every two to three years based on their risk stratification for what we call mapping biopsies of the stomach. That's a different discussion than the Barrett's, though, in my mind. I think we can sneak in one more before lunch here. When Barrett's is first diagnosed, we do repeat EGD in one year while starting them on a protein pump inhibitor. We do an initial toasting of pantoprazol, four milligrams, two times a day, or 40 milligrams, excuse me, two times a day for two months, and then we titrate down to 20 milligrams until repeat EGD. Is this an adequate dosing of the PPI, and what about an H2 blocker? Once healing is achieved, the minimal dose for PPI that is required for symptom control and for healing is my approach in that. For H2RA, I refer them to Dr. Martin. That means all my patients are unhappy. You know, that's probably why, but I think that, you know, as you know, recently one of the H2RA agents was, you know, taken off and brought back, I believe, in a different way. But, you know, the H2RAs do help. Again, I think, as Dr. Martin mentioned, how much of it is real and how much of it might be a placebo effect. We certainly use it at bedtime to suppress some nighttime reflux, but really speaking, especially for the invoked chemoprevention role of PPIs, I think you're best off with just taking a Barrett's patient and the least amount of PPI that controls inflammation and symptoms long-term. Well, we have come to our break, Dr. Martin. Shall we reconvene at 1 p.m., give a 35-minute lunch here? That sounds great to me, Eden. I think everybody in this course has earned that lunch, so enjoy your breaks. We'll see you at 1.

SIBO management

rifaximin coverage

alternative treatments

celiac disease

proton pump inhibitors