I have a few thoughts. I'm not seeing any questions on the chat and we have about 15 minutes. So I thought I would maybe start the discussion. I think you did a fantastic job in terms of dispelling maybe some of these, I still like to call them myths of the association of PPIs and several of these conditions. But regardless, patients come to our clinic with a number of concerns. So maybe a question I have for you is, number one, what approach do you use to dispel some of those concerns, number one? And number two, are there any tests that you get at baseline or you're monitoring some of these things, whether it be calcium, magnesium, vitamin B12? Are you doing any testing to maybe allay some of these concerns? I think that might be a helpful issue to discuss for our audience. So for patients, I sometimes see patients with grade C esophagitis or grade D esophagitis, who are worried about the risk for dementia or osteoporosis, and then they don't want to take the PPIs. So for them, I shared these two studies, the Paul Moyaddy studies, and then the Jankowski study, the ASPECT trial and the COMPASS trial, about these are the randomized control trials. I explained to them what randomized control trials are. So there is no placebo effect, and then one group is blinded, they don't know what they're getting. So that seems to help. And then the number of patients in those trials, there is the BADIS ASPECT trial, there are like 2,200 patients. And then in that other trial, there are approximately 12,000 patients or so. So discussing that seems to help. And then I give them, and that seems to allay their fears. And the other thing is not only with the quality of life, uncontrolled reflux also increases the risk of, especially in BADIS patients or so, as you know, it increases the risk of progression to neoplasia. And that seems to help with these patients too. That is one thing. That is one thing. And then the other thing is eventually we may be having this new, the potassium acid blockers, which are more effective than those. So something to look at that aspect too. In terms of monitoring patients, usually it is not recommended for monitoring, but I personally, I do monitor patients for annual magnesium levels and then creatinine levels. I do not do CBCs to look for anemia or so. Okay, so you are doing annual, you said magnesium levels? Magnesium and creatinine levels. Okay, okay. There are a couple of questions. So one says, do you propose anti-reflux surgery after successful endoscopic BADIS eradication? I do not. And I would, if there is, if it is unsuccessful BADIS eradication, and then the reason for that is there are two aspects to BADIS eradication. One is ablation therapy. And then the second one is maximal acid suppression. So if the ablation is not being effective, that tells me that there is some degree of acid exposure going down. So that is the reason I would do a anti-reflux surgery if I'm unsuccessful with BADIS eradication. What is more important, is it the repair of crura or the LES augmentation? It is, if in a patient with hiatal hernia, with a large hiatal hernia or so, so the diaphragmatic crura are quite separated. So just taking care of the LES would not fix the problem or so. Correct. So the larger the hiatal hernia, the more important the crural repair becomes. And then they are also talking about what kind of anti-reflux surgery for patients who have, I think they mean ineffective esophageal motility. Yeah, so in patients with ineffective esophageal motility, studies have shown that there is no difference between nascent fundoplication and tupae or the partial fundoplication in terms of the post-op dysphagia. However, most surgeons do not want to do a nascent fundoplication on a patient with ineffective esophageal motility. So they would usually go for a tupae fundoplication or so. And in patients with absent contractility, very guarded about sending them for anti-reflux surgery, two options are either doing the tupae procedure or if a patient has a decent enough BMI to go for a gastric bypass surgery or so. Excellent points. There is another question actually on the chat. I would request attendees to put their questions in the Q&A section, please. But basically I'm gonna read this out. What to do for ongoing bloating in spite of PPI therapy with history of positive acid reflux testing. So it tells us that this patient needs treatment, neuromodulator or other therapies like relaxation techniques. So for a patient with bloating with PPI therapy, so two things I would think about is bacterial overgrowth. And then the second one is gastroparesis. So if the patient does not have bacterial overgrowth or gastroparesis, then I will treat it as functional dyspepsia or so. So probably I'd be using Buspirone, which relaxes the gastric fundus and it seems to help with that aspect. And also relieves the anxiety too. So that is one or FDGARD. These are all the possible options. I think that's a great question. I would completely agree with you. You know, sometimes we also teach patients a few things like avoiding atrophagia, avoiding drinking with a straw, reducing their intake of carbonated beverages. You know, and if you're seeing a lot of atrophagia, cognitive behavioral therapies that you can offer these patients. Prashanthi, another question. Do you recommend stopping PPI therapy in patients with PPI responsive GERD who have low magnesium or advise them to continue with magnesium supplements? So there is a reason for having the patients on PPI therapy. So probably these are on long-term PPI therapy. So it may be because the patients have erosive reflux disease or they may have bad esophagus. So in those patients, there is a reason for continuing the PPI therapy. So we'll continue with the PPI therapy and then give magnesium supplements. Yeah, so I think the point you are making is stay with the treatment that is indicated. And as long as you are able to keep the magnesium levels up with supplementation, it should be safe enough to do that. Another question that came up was, I think they mean duodenal gastric reflux post-cholestectomy and PPI is not working. When is anti-reflux surgery indicated? So I'm wondering if they mean this is mostly bile reflux, if I'm not mistaken. I'm not mistaken. So, yeah. So we go through the same algorithm as before. So doing like an impedance test and then the impedance test does show increase in the non-reflux, non-acid or weakly acidic reflux episodes or so. If there are more than 80 total reflux episodes, then anti-reflux surgery is indicated. So I think that's a great point I wanted to discuss with you. So our recommendations are relatively clear about anti-reflux surgery for acid reflux, predominant symptoms, regurgitation. How do you approach non-acid reflux, which quote unquote is refractory to medical therapy or maximal medical therapy? Our guidelines are relatively silent on that regard. How do you approach those patients or have they sort of come up with a pathway for these patients? So for patients who have this, as long as they have non-acid reflux or weakly acidic reflux in spite of the PPI therapy, not much more we can do. One option is doing the H2 blockers or so. So one thing to remember is, for example, with the PPIs, there is a reduction in the gastric volume secreted too. It is not just the gastric acid. The amount of gastric juice secreted gets lower, lower volume with the PPI therapy. So if you are able to control the, lower the gastric juice secreted, you're also reducing the reflux, which goes from the duodenum to the stomach to the esophagus or stomach. So there have been anecdotal reports about using like Actigol or sodioxycolic acid or cataphate treatments or so. Personally, what I would do is, in addition to the PPI therapy, I would put them on cataphate. If there is symptomatic relief, great. If there is not symptomatic relief, then doing the impedance testing and then depending on the impedance test, refer them for surgery. Okay. Another question is, is LYNX indicated in LPR patients? What are the outcomes? And I think this is taking us into the relatively, I would say controversial topic of LPR. A, do you believe in LPR? And B, what kind of treatments do you offer? The specific question here is about LYNX. So the problem I would worry about, so LPR is a, it does not have specific criteria. So there is always a point of contention between the ENT and the gastroenterologist about what constitutes LPR. So a pH test is, a regular pH test is not useful too, because it may show good, but it may not necessarily show if LPR is coming from that. Going by a PPI trial, mostly in these patients, and if they're not responding, and then there is no other reasons for the throat symptoms. So that is, there is no sinus, chronic sinusitis, there is no asthma or so. So after ENT evaluation, pulmonary evaluation, and if the esophageal evaluation is negative too, then those patients either amitriptyline or gabapentin seem to improve the symptoms. And there is no objective evidence of PPIs. Objective evidence of good. And if PPI, if they're non-responsive to PPI therapy, and if we do the pH testing, do the ENT, pulmonary evaluation, if those are negative too, to treat them either with Elevil or with gabapentin. And the reason I chose, I usually go with amitriptyline is because it's a once a day dose, as opposed to gabapentin, which is three times a day dose. There are trials which showed that they seem to be helpful in these patients with idiopathic symptoms. So that is one thing. In terms of the links or so, even in terms of links or fundoplication too, I would be hesitant to recommend to them because with fundoplication, there is about a 50% response or so in terms of the symptoms. And then I would be hesitant to recommend links for LPR patients. The reason is because they have severe dysphagia. Initially, there is about a 67, 68% of them have dysphagia initially after the procedure. So I would be hesitant to suggest to them. I think those are excellent points. And I think it really depends on, A, what are the symptoms, and B, what is the correlation with physiology, right? So you have to be able to explain that physiology and then discuss the pros and cons of some of these techniques with... While we are on the topic of links, one of the things we run into, at least at Mayo, is that insurance coverage for links is still kind of spotty and patchy. What's your... And so I don't think it is being done very regularly at Mayo. What's your experience at Cleveland Clinic? Our foregut surgeons, as well as thoracic surgeons too, they're not keen on links. They recommend against links. In their patient, if we believe that they're not going to go for a fundoplication, then probably TIF is the next step among all the different procedures available. They're not keen on links procedure. Okay. Another question. Yeah, this is the same thing, sort of what we discussed. We get into an argument with nephrologists regarding elevated creatinine and its relationship with PPI for reflux. How do we respond in those conversations? So it would be like monitoring or so going to the lowest effective dose. A lowest effective dose of the PPI therapy. One thing to be aware of is, again, what is the reason for using PPI therapy? If it is like a grade C or a grade D esophagitis, which is being kept under control with PPIs. Remember 60, 70% of those patients do respond to PPIs. So that is one. And then the second thing is, obviously if a patient has a creatinine of one and then they're rapidly worsening to a creatinine of three or four, well, you're going to stop it. I would repeat the creatinine levels every three months or so. And then if there is a small variation, so we are talking between a creatinine of one and 1.5, I would feel comfortable about continuing with the PPI therapy. And I'm sure so would the nephrologist be. If there is a rapid climbing of creatinine, maybe we should be talking about fundoplication or so. Correct, correct. Yeah, I think you make excellent points. So what is the indication for the PPI? Is it a hard indication or a soft indication? The other thing I've sometimes done in these situations is really dialogue with the nephrologist to get a sense of how convinced are they that this is because of a PPI. Because as far as I know, and I'm happy to hear your thoughts, is that the association rests on this idiosyncratic interstitial nephritis phenomenon that some of these patients have. So I think it is also worth our time to talk to the nephrologist as to are there other etiologies of renal insufficiency that might be operative in this instance? And how convinced are they that this is really from a PPI? So are they seeing higher urinary eosinophils? Was this correlated in time between the initiation of PPI and worsening in creatinine? So I think it's worth having those kinds of discussions with the nephrologist as well. And many of them are very open to those issues as well. So I hope that answers this question.

proton pump inhibitors

GERD

efficacy

safety

reflux complications