COMMENTARY

New Technologies and Surprising Discoveries Take Center Stage at ACG 2018

David A. Johnson, MD

Disclosures

October 25, 2018

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

I am back from the American College of Gastroenterology (ACG) 2018 Annual Scientific Meeting, which was held this year in Philadelphia, Pennsylvania, and have a lot of exciting highlights to share with you. There will certainly be lots more to follow up on as these studies mature, but there is some information that you will find potentially impactful to your practice right now.

New Imaging Sheds Light on Crypt Dysplasia's Impact

Dr Nick Shaheen and colleagues[1] looked at a biopsy technique using wide-area transepithelial sampling (WATS) with computer-assisted 3D analysis. For those who have not used this technique, it is a stiff brush that you rake up and down the wall of the esophagus. It covers about a 6-cm portion and moves around the circumference back and forth in a saw-like technique. It allows us to get a wide range of sampling, which is then sent for computer analysis using transepithelial sampling. With the assistance of computer-generated learning, we can potentially pick up more dysplasia or even crypt abnormalities.

Researchers looked at 151,224 WATS biopsies, 4049 of which had no evidence of dysplastic Barrett's esophagus on baseline. After following these for an average of 1.4 years between assays, 19 progressed to high-grade dysplasia or early esophageal adenocarcinoma. This equaled a mean rate of 0.33% per patient per year, much higher than what we have seen in the incidence of progression in nondysplastic Barrett's esophagus. An additional 380 patients had crypt deformities or crypt abnormalities. After following these patients for a mean of 1.25 years, researchers observed that 10 progressed to high-grade dysplasia or early esophageal adenocarcinoma, for a rate of 2.1% per patient per year. This is notable, because the rate at which patients with any crypt abnormalities progressed to any neoplasia or dysplasia (low-grade dysplasia, high-grade dysplasia, or adenocarcinoma) was 9.9% per patient per year.

What does this mean? Certainly, this newer technique of sampling for tissue in Barrett's esophagus patients has been shown to be very promising in its ability to pick up lesions at high risk for progression early. This allows us to then potentially intervene earlier, which obviously with dysplasia would mean ablation. It is a technique you should consider, because it is easy and a lot less tedious than having to do the biopsies, especially on long-segment Barrett's esophagus. But I was concerned about the progressive risks in patients who had nondysplastic Barrett's esophagus and the crypt abnormalities that were defined and picked up by this computer-generated evaluation.

Colonoscopy Screening Time in Adenoma Detection

The next abstract[2] shows us that time matters when it comes to performing colonoscopies. We know that when it comes to screening, withdrawal time correlates with adenoma detection. However, this group looked specifically at withdrawal time in patients undergoing colon cancer screening of the right colon. They randomized 179 patients to undergo screening of the right colon at thresholds of ≥ 3 minutes and 197 at thresholds of < 3 minutes.

Lo and behold, they found that there was increased benefit with additional time, with an adenoma detection rate in the right colon of 35% in the ≥ 3 minutes cohort versus 12% in the < 3 minutes cohort (P < .0001). This significant advantage of ≥ 3 minutes over < 3 minutes was also observed for the total adenoma detection rate (59% vs 36%, respectively; P < .0001). The odds ratio (OR) for finding adenomas was increased by over fourfold if you spent more time in the right colon.

This alerts us to the fact that we should look at the right colon twice and make sure we spend lots of time doing so. I look forward to seeing what the serrated lesion detection difference was here. I expect it would also be higher.

Cancer Rates in Obese Patients

The third abstract[3] dealt with the effects of obesity on associated gastrointestinal cancers, including colon, gastric, esophageal, and pancreatic cancer. Researchers looked at two large databases collectively offering information on millions of patients: the Surveillance, Epidemiology and End Results (SEER) database, and the National Inpatient Sample (NIS) database.

They found that the cancer incidence increased in young adults (age < 50 years), in particular for colorectal cancer. This correlates with increasing evidence in other reports that prompted the American Cancer Society to recommend screening beginning at age 45 now.[4] The US Multi-Society Task Force on Colorectal Cancer has still set this recommendation at age 50 but has long endorsed age 45 for African Americans.[5] Nonetheless, this particular analysis recognizes this increasing risk for colon cancer.

Compared with nonobese patients, the steepest rise in obese patients undergoing resection for colorectal cancer was in the 18-to-49 age group (+13.1%) and for gastric cancer in those 75 years or older (+15.3%). Esophageal and pancreatic cancer resections also increased incrementally in those younger than 75 years of age.

This means that our obese patients need to be screened, and certainly evaluated, should there be any signs or symptoms warranting that—more so, perhaps, than some of our nonobese patients.

Are Gluten-Free Products What They Say They Are?

The next abstract[6] asks whether we are really getting what we pay for when it comes to gluten-free products. This is a study from Dr Peter H.R. Green and colleagues at Columbia University in New York City, who are very much the leaders in looking at gluten-related diseases. This is the same team that earlier brought to light that many probiotics contain gluten, even if they say they do not.

In the new study, the team used a handheld portable gluten detection device (Nima; Nima Labs) to analyze data collected over a period of approximately 18 months and shared from 804 users. Researchers were able to see where users lived, what they ate, and where they ate it. They found that 84% of the tested foods were labeled gluten free, but 32% of these actually contained gluten. The presence of mislabeled foods differed by meal, with gluten detected in 27% of breakfast and 34% of dinner foods that claimed not to contain it. Gluten-free foods were more likely to have gluten in the Northeast as opposed to the West. It would be worth knowing if this correlates with different gluten-free diet interests in those regions. The findings were particularly resonant because the cross-contamination rates were most notable in pizza (53.2%) and pasta (50.8%).

You may want to highlight these findings for your celiac patients.

A Successful Dietary Intervention for Fecal Incontinence

Drs Stacy Menees, and Bill Chey from University of Michigan in Ann Arbor, in collaboration with other colleagues, designed a nice study[7] evaluating intervention with low fermentable oligo-, di-, and mono-saccharides and polyols (FODMAP) diets for the problematic condition of fecal incontinence. They conducted a retrospective chart review of 65 patients with frequent fecal incontinence (35% daily, 21.5% weekly).

Dr Chey has taught us to use a dietitian in instructing patients with fecal incontinence, and that is what they did with these study participants. After applying a low-FODMAP diet, 63% (42 patients) had reported a reduction in their fecal incontinence symptoms.

Although researchers could not determine any demographic or clinical characteristics that predicted response, I think this is a pretty easy intervention to suggest in this indication while we wait for corroboration. I do not think there is a downside to getting a dietitian involved. These patients are frequently house-bound and scared of being outside due to their fecal incontinence. You might want to consider low-FODMAP diets for patients in your practice.

Hospitalization in Cirrhotic Patients

Decompensated cirrhosis is one of the most common causes of hospital readmissions in the United States, accounting for over 150,000 hospitalizations at an annual cost of approximately $4 billion.[8] To better understand this issue, researchers identified 12,599 patients with cirrhosis using ICD-9 codes in the 2014 Healthcare Cost and Utilization Project National Readmission Database, who were then evaluated for readmission. They found that 55% were readmitted within 30 days and 84% within 90 days. If you are a hospital administrator, you cringe at these numbers, in particular readmissions within 30 days, which may prompt a no-pay.

The morbidity implications are also significant here. The most common complications that led to increased rate of readmission were hepatic encephalopathy and hepatorenal syndrome. Interestingly, portal hypertension and variceal bleeding led to a less likely need for readmission.

Consider Albumin

Let's look a little more closely about why hepatic encephalopathy and hepatorenal syndrome are important. Cirrhosis has growing implications and complications directly correlated with elevated prostaglandin E2, which has a dramatic effect on white cell translocation between compartments. You are not able to get the white cells to the ascites, for example, if you are having bacterial peritonitis as well, because you have these elevated PGE2 levels. There are also four receptors for PGE2 on the kidney that downregulate renal perfusion.

As I pointed out in my David Sun Lecture[9] at this year's ACG meeting, albumin provides a simple solution in this scenario. This should be your new golden tool for patients with cirrhosis, because albumin serves as a sink for these elevated PGE2 levels. Again, PGE2 correlates with reduction for translocation and white cells to fight infection, and reduces the renal blood flow. So when it comes to hepatic encephalopathy infections and hepatorenal syndrome, consider albumin.

A prospective, randomized study published this summer in the Lancet[10] compared intervention with IV albumin on a weekly basis to standard care in 440 patients with cirrhosis and uncomplicated ascites. After 18 months of follow-up, patients receiving albumin had significantly higher survival than the standard care group (77% vs 66%; P = .028).

What has it done to my practice? I now monitor albumin levels and supplement my patients weekly or even every other week, aiming for an infusion target of around 3.5 g/dL. The bottom line is, if your hospital argues with you about giving albumin to patients with cirrhosis, you should tell them that saving readmissions is much more important. It is something that is ready for prime time, and you need to consider it.

Avoidant/Restrictive Food Intake Disorder (ARFID)

The last abstract[11] I wanted to share is something that again was brought to my attention by Dr Bill Chey and the group at the University of Michigan. Until then, I really had not heard about ARFID syndrome, which has been recognized in kids and which Dr Chey and colleagues also astutely identified as occurring in adults.

ARFID is a feeding disorder characterized by avoidance or restriction of foods, associated with clinically significant weight loss, nutritional deficiency, and dependence on tube feedings and oral supplements. It is not related to differences in body habitus and body dysmorphic changes, nor is it related specifically to bulimia or anorexia.

Researchers administered a nine-item specific, recently validated questionnaire to 317 adult general gastrointestinal and motility outpatients. They found that approximately 20% of these patients met the criteria for ARFID.

This is important because these patients have significant challenges and problems if we do not identify them correctly. ARFID had demonstrated associations with such things as abdominal pain, constipation, and diarrhea. Multivariate analysis showed significant associations with nausea/vomiting (OR, 3.3; P < .01), dysphagia (OR, 2.24; P = .04), and irritable bowel syndrome (OR, 2.06; P = .04). These patients are at risk of being segregated to treatments for other conditions. If we do not understand that they have a more complex feeding disorder, we risk their falling by the wayside and will be challenged to optimize their outcome.

When treating patients with ARFID, it is recommended to involve a full team of psychomotor or cognitive dysfunctional counseling, dietitians, psychologists, and behavioral-change psychotherapists. This may be what we need to better understand this disease, because it is something we have not thought about in adults.

ARFID is something we now need to add to the menu of potential diagnoses in these complex patients that we frequently are frustrated with, as are they, when it comes to their outcomes. Thank you to Dr Chey and colleagues for bringing this to our attention.

In summary, there were a lot of exciting new studies at this year's ACG meeting. I will look forward to seeing more details as these mature into peer-reviewed manuscript publications. I'm sure there was a lot more at this year's meeting that you'd also be interested in, so I suggest you review the abstracts when you can.

This is Dr David Johnson. Thanks again for listening, and I look forward to seeing you next time.

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