It's a Wrap: A Look Back at the Highlights of Digestive Disease Week 2016

David A. Johnson, MD


June 17, 2016

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Hello. I am Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.

I'm back from Digestive Disease Week (DDW) 2016. As any of you who have been there know, it is very much an array of confusion trying to figure out where to go, when to go, and what to see. Those of you who weren't there probably had a much calmer week! I wanted to identify what I thought were some of the most meaningful presentations, whether you were there or not, and give you some highlights to pay attention to in the forthcoming literature as these abstract presentations evolve into articles.

Let's get right to it.

Resuming Aspirin After Endoscopic Therapy for Peptic Ulcer Bleeding

The first study was from Francis Chan and Joseph Sung's group from Hong Kong, who are very well-established researchers in the area of peptic ulcer bleeding and certainly in the area of nonsteroidal anti-inflammatory drug (NSAID)-related complications.[1] They looked at the early and late complications following resumption of aspirin in Helicobacter pylori–negative patients after endoscopic therapy for bleeding peptic ulcers. There is a significant risk for neurovascular and cardiovascular complications in these patients who are on aspirin for those indications. The risk profile doubled if the patients had their aspirin withheld for more than a week.

The bottom line is that when you have a patient come in with a peptic ulcer bleed, get them back on their aspirin as quickly as possible if they are taking it for primary or secondary prophylaxis for cardiovascular and neurovascular disease. There was no increased bleeding risk in these patients following therapeutic intervention.

More Data on the Low-FODMAP Diet

There was a lot of data presented about the low fermentable oligo-, di-, and mono-saccharides and polyols (FODMAP) diet. This has become the new trend, if you will, for irritable bowel syndrome (IBS).

Bill Chey and his group from the University of Michigan presented a number of great studies; two in particular caught my eye.

The first study looked at the low-FODMAP diet and regulation of visceral nociception by changing the gut microbiome and the related intestinal permeability in IBS.[2] We're looking at this low-FODMAP diet because these fermentable sugars can influence the gut microbiome, leading to upregulation of visceral nociception, cytokines, and intestinal permeability.

The second study was a randomized controlled trial that compared the low-FODMAP diet versus a control diet based on modified National Institute for Health and Care Excellence (NICE) guidelines, among participants with diarrhea-predominant IBS.[3] They involved a dietician, but the low-FODMAP diet was the winner when looking at a composite symptom endpoint, and it was particularly effective for abdominal pain.

The point here is to get a dietician involved. Most of us, I think, when we talk to our patients about a low-FODMAP diet, we might give them a sheet of paper and say, "Avoid this and avoid that," but it's really not possible for the patients to get their head around that. Talking to Bill very specifically about this, he's very wed to the idea that we need to get a dietician actively involved when we start to look at our intervention strategies for IBS in general.

Preprocedural Indomethacin for ERCP

Another study that caught my eye came from Joseph Leung's group.[4] I don't know if you do endoscopic retrograde cholangiopancreatography (ERCP), but clearly the use of rectal indomethacin has become a standard of care particularly after the procedure, when patients are high-risk following a therapeutic ERCP. In this multicenter, randomized controlled trial, they evaluated the use of preprocedural rectal indomethacin (100 mg as a suppository).They found that the risk for post-ERCP pancreatitis was nearly two times lower for the group receiving preprocedural indomethacin compared with the group receiving postprocedural indomethacin.

This comes right on the heels of a recent article in the Lancet looking at a group of 2600 patients from China where they evaluated postprocedural rectal indomethacin in high-risk patients among participants who universally received preprocedural rectal indomethacin.[5] Whether the patients were high-risk or not, they all did better with preprocedural indomethacin in terms of post-ERCP pancreatitis.

This has changed my practice and this is certainly something that I do routinely now in preprocedural ERCP. This should be a rapidly emerging standard of care.

Vedolizumab Safety

We've all used vedolizumab, which is an alpha-4 beta-7 integrin inhibitor that has been tremendous as a non–tumor necrosis factor (TNF) alpha treatment for use in our patients with inflammatory bowel disease (IBD). Nevertheless, there have been a couple of safety concerns.

One concern is about increased cardiovascular and neurovascular risk. There was at least a safety signal that was evident, and this was presented in a study collaborated on by AbbVie, which produces the competitor drug adalimumab.[6] The data they presented suggested that there was a slight increased risk for these outcomes with vedolizumab. This is something to have on your radar.

Vedolizumab was also associated with improvement in sleep quality.[7] This is something that in IBD is very significant, because with sleep fragmentation, you upregulate cytokines that are very much associated with upregulation of activity in IBD. The effect of vedolizumab on sleep quality improvement is a significant effect, but I think this is probably similar with other drugs. Nevertheless, discussing sleep with your patients who have IBD should be part of your routine.

Caffeine and Risk for Advanced Hepatic Fibrosis

Moving to liver disease, a systematic review and meta-analysis showed a beneficial effect of caffeine on the risk for advanced hepatic fibrosis.[8] This study suggested that regardless of the etiology of liver disease, be it viral hepatitis, alcohol-related disease, or even nonalcoholic fatty liver disease (NAFLD), these patients could benefit from an incremental exposure to three more brewed cups of coffee per day.

So I now tell my patients that if they like coffee, go ahead and have it. It's one of those few feel-good moments, because most of the time when you ask if they like something, they start to cringe as if you're going to take it away.

Outcomes With Higher Infliximab Trough Levels

For infliximab and the anti-TNF alpha drugs in general, there seems to be a significant advantage of higher trough levels. Dr Abreu and her group from Miami presented a study that looked at higher trough levels of infliximab and found that they resulted in higher perianal fistula healing in patients with Crohn disease.[9]

We often standardize our therapy to a 5-mg/kg or 10-mg/kg infusion, but we may want to be looking at trough levels instead, in particular for complicated disease.

Risk Factors for Progression of Barrett Esophagus

As far as risk factors in Barrett esophagus, Joel Rubenstein and his group from the University of Michigan presented some interesting data on identifying risk factors for progression of Barrett esophagus in patients with low-grade dysplasia.[10] This was a single-center evaluation that found that 54.6% of the patients with Barrett esophagus who had low-grade dysplasia confirmed by an expert pathologist regressed to nondysplastic Barrett epithelium. The results of this study indicated that patients who had unifocal dysplasia, were female, or had higher body mass index were more likely to regress.

When you find this low-grade dysplasia, in particular, you need to really evaluate these patients more cautiously before resorting to an ablation strategy.

Outlook With Short-Segment Barrett Esophagus

Another question is, what happens when you have Barrett esophagus with short segment?

There was a nice presentation that came from a multicenter consortium led by Prateek Sharma, looking at a cohort of over 4200 patients with Barrett esophagus.[11] They found 167 patients who had short-segment Barrett esophagus and were followed for a mean of about 6 years. None of the 167 patients in this cohort progressed to any more worrisome conditions. When you find these patients with short-segment Barrett esophagus, you really need to strategize. Maybe we can extend the interval and, at some point, remove the need for continued surveillance. Certainly there is also support for the notion that patients with an irregular z-line should not be enrolled in a surveillance program.

Use caution around short-segment Barrett esophagus and be careful for what you wish for when you start doing these biopsies. It changes lots of things, including insurance costs.

Staff Radiation Exposure During ERCP

Another study that caught my eye, as somebody who does ERCP, was related to radiation exposure to personnel involved in ERCP.[12]

One of the things that the researchers looked at was the position of the patient. The patient in the left lateral decubitus position posed a higher risk for radiation exposure to the individuals in the room. The prone position was associated with lower risk for radiation exposure—basically half of that of the patients who were in the left lower lateral decubitus position.

For those of us who do ERCP and have radiation exposure, we need to be particularly sensitive to eye exposure for radiation. The current maximum exposure to the lens of the eye is 20 mSv per year, and this is really a standard. So if you're looking at trying to monitor yourself and your radiation exposure, you need to be thinking about eye exposure and protection. We can also minimize this by positioning the patient more often in the prone position.

Surveillance After Barrett Esophagus Ablation

The surveillance interval following Barrett esophagus ablation is something that continues to be a question. When you send patients to an ablation, it would be great if we could say that they don't need further surveillance.

Nicholas Shaheen and his group looked at their consortium and follow-up consisting of about 3000 radiofrequency ablations in the United States and about 400 from the United Kingdom, for whom they achieved complete endothelium remission of the intestinal metaplasia.[13] They've developed a model following this, which basically looked at a variety of predictors, including worse pathologic grade, baseline age, and whether or not the patient had long-segment versus short-segment Barrett esophagus. They were able to identify a cohort of patients that could have extended surveillance intervals far from their current recommendations, suggesting that there may be at least a 50% reduction in surveillance endoscopies.

Stayed tuned to Dr Shaheen's group, as we really need to do better as far as what we're doing with some of the postablation patients.

Topical Budesonide for Eosinophilic Esophagitis

Another study that caught my eye was from Dr Hirano's group, which has unquestionable expertise in esophageal diseases. This study was a consortium with Dave Katzka's group at the Mayo Clinic, evaluating the safety and efficacy of oral budesonide for maintenance therapy for eosinophilic esophagitis.[14] This was a prospective, open-label study of adolescents and adults. In fact, it was the first prospective cohort using topical steroids to date.

Basically, what they've showed us is that oral budesonide was very effective in maintaining endoscopic and histologic remission up to 24 weeks, and there were no unexpected safety signals. Importantly, in the nonhistologic responders, a longer duration of topical steroids didn't seem to lead to any type of continued improvement.

Sleep Fragmentation, the Gut Microbiome, and Lymph Node Signaling

The final study that I want to mention, which my group was involved in, explored the effect of sleep fragmentation on the composition of the gut microbiome and mesenteric lymph node signaling.[15]

What was found in this study was that during sleep, there is a circadian effect in the gut microbiome. In the course of a normal day, through a clock mechanism that the body generates, there is a variation in the circadian rhythm of the microbiome. In this study, sleep fragmentation in mice inverted the microbiome, leading to total dysbiosis. We know that sleep fragmentation changes intestinal permeability and, hence, gut translocation risk, so we looked at 60 gene arrays from mesenteric lymph nodes that encoded for cytokine and chemokine upregulation to promote gut integrity. All 60 of these went down as a response to sleep fragmentation and were associated with the gut dysbiosis. We then looked at the brain gene arrays, which was not discussed in this presentation, but we found that in the same gene arrays in the brain, 60 out of 60 all had disruption.

So, sleep has a tremendous effect on the gut microbiome but also on gut integrity and the gut immune system. This is another reason to get a good night's sleep. More to follow on this, and certainly we need to stay tuned to the implications of sleep on the gut. Sleep is something that I discuss with all of my patients. Patients with IBD, NAFLD, and other diseases really need to focus on better sleep.

That's my wrap-up, if you will, on the presentations that caught my eye at DDW 2016. There were lots more. I'm sure that a lot of media coverage will extrapolate some of these findings, but I just want to give you a little snapshot of what I thought was important. Hopefully this was helpful, and we'll look forward to these studies being published as articles, which will give us a better idea of the true science around them.

I'm Dr David Johnson. Thanks again for listening.


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