Conference Highlights That Shouldn't Stay in Vegas

American College of Gastroenterology (ACG) 2016 Annual Scientific Meeting

David A. Johnson, MD


November 04, 2016

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

I am back from the 2016 American College of Gastroenterology annual meeting in Las Vegas. There was a tremendous number of posters and presentations on new science. I want to highlight my top 10 presentations for you. There are a lot more, and I leave it to you to go review the abstracts and see what piques your interest. For this discussion, I tried to cultivate what I learned that might change practice in the near future. These are the highlights and are not ranked in any particular order.

Edible Colon Preps

We all have angst for our patients who do not want to take their colon preparation. There is a mitigation risk for patients who will not accept colonoscopy that we could obviate if we had some alternative. There are a number of new alternatives out there.

Dr Doug Rex[1] discussed a new formulation of edible colon preparations in which pegylated products were put into a variety of food preparations ranging from bars to shakes. Patients consumed these over the course of the day before their procedure. The researchers conducted a test with six formulations in different variations and compared it with active comparators. The overall limit of volume in the edible preparation was around 1.8 L. The standard (MoviPrep and those types of comparators) low-volume limit was around 2 L. Using an Ottawa scale, 93% [of patients] rated the lead formulation as good or excellent. And with an Aronchick scale for the comparators, 86% rated the lead formulation as good or excellent. The trial was not designed to find statistical difference between the two, but the new preparations did not appear to be inferior to the standard preps.

This research is clearly in the beginning. It was a phase 2, dual-center, randomized, single-blind study, so more needs to be established on this. What does it cost, and how does this play out in real life? I cannot tell you, but it is exciting to have an alternative for our patients taking colon preps.

Gastric Peroral Endoscopic Pyloromyotomy (G-POEM)

Dealing with gastroparesis is a trouble spot for clinical care and something we do not really have a lot of good medications for, if any.

We have heard a lot about the peroral endoscopic myotomy for achalasia, which has really become a very exciting area and incredibly safe in expert hands. This study was a single-center retrospective review[2] from Emory looking at 10 patients treated with G-POEM as an emerging option for treatment of refractory gastroparesis—diabetic in four patients (40%), idiopathic in four patients (40%), one post-infectious (10%), and one post-surgical (10%). The duration of the procedure was around a mean of 47 minutes. The length of the myotomy was fairly short, around 3 cm. The mean length of stay in the hospital of 2.5 days was remarkable. No adverse events were found to be significant. The procedure was clinically successful in eight of the 10 patients. There was normalization of gastric emptying in five patients and improvement in two patients.

This may be an emerging option for those types of refractory patients.

Ayurvedic Medicines and Lead Toxicity

This interesting study[3] comes from an area that I was very unfamiliar with. An aspect of Indian medicine, called Ayurveda, goes back hundreds of thousands of years. It uses a variety of interventions with herbs and some harmful metals in pharmaceutical-type ways and preparations to promote or maintain health or to remediate disease. These medicines can be obtained over the Internet. Toxicity of these heavy metals is thought to be muted by a variety of pharmaceutical techniques. One of the techniques also involves prayer, so you can figure out how this may be a real issue.

[The investigators] were concerned about the heavy metals. When they looked at studies of these formulated medicines, one study found that 41% [of formulations] had arsenic, and another study found that 64% contained lead and mercury. They [performed] a retrospective analysis in New York over an 8-year time span. They looked at patients who had presented with or had been diagnosed with lead toxicity. The majority of these were patients presenting with abdominal pain. Many of these patients had other symptoms, particularly constipation, motor weakness, acute kidney disease, and even acute pancreatitis.

Interestingly, the majority [of the patients] were males. Basophilic stippling, a parameter on the hematologic peripheral smear for lead toxicity, was pretty rare and observed in only seven patients. These patients were diagnosed with lead toxicity only when they were asked about their medications. They were treated with penicillamine and virtually all had symptomatic and therapeutic results.

It caught my eye that physicians in gastroenterology and surgeons alike really need to be aware of the clinical features of lead toxicity, such as abdominal pain. A variety of these patients come in with a microcytic pattern. It is not just found in kids eating paint or clay. We need to ask about lead toxicity risk [associated with all] medications. Herbal products [have been associated with] liver injuries. Take a good history, particularly if you have an ethnic group that may be more [prone to] taking these types of medications. Lead levels need to be done. Again, you need to ask the right questions, but you cannot ask the right questions if you do not think about it.

Gallstone Pancreatitis

Gallstone pancreatitis is a problem we have all the time. Our surgeons potentially say, "They have gallstone pancreatitis. Bring them back in a month or two when their pancreas calms down."

This presentation[4] was an analysis of the well-validated Nationwide Readmissions Database. It was a Healthcare Cost and Utilization Project. They looked at the 30-day [outcomes] in patients once they had initial presentation for gallstone-related pancreatitis. The investigators separated [the results] based on [the severity of] pancreatitis. As predicted, if discharged after having severe pancreatitis, patients were more likely to be readmitted. An index admission cholecystectomy reduced risk for readmission by 60%. Nearly 1 in 10 patients were readmitted after gallstone pancreatitis within 30 days. A majority of these were related to acute pancreatitis-related complications.

Pressing on with an early cholecystectomy before that patient goes home is a very significant modifiable factor. I think your hospital systems will like that a lot when you start to look at readmission rates after initial diagnosis of gallstone pancreatitis.

Readmission Following Clostridium difficile Infection

The next study[5] was also a retrospective analysis of the Nationwide Readmissions Database. These investigators looked at the readmission rate of 38,000 patients admitted to the hospital with C difficile infection; 21% were readmitted within 30 days, and 27% were readmitted with a primary diagnosis of C difficile infection. The top three causes of readmission were C difficile reinfection, septicemia, and heart failure. C difficile [was associated] with the highest risk for readmission within 30 days; 1 in 5 patients with a C difficile infection was readmitted to the hospital within 30 days.

The investigators found that patients were less likely [to be readmitted] if they were sent to a nursing home or a managed facility as opposed to being sent home. Think about what happens if patients are sent to a managed facility: They get some type of relative precautions [to help prevent] reinfection.

When they go back to their home, however, they go back to the same environment where they had C difficile before they were admitted. I think what is reflected [in this study] is that these patients went back to their environment. A seed of spores can live in a viable fashion for weeks or months after they have been spread on a surface. Every time you flush the toilet, they become aerosolized. [For my patients like this], I do a timeout with what I call "bathroom hygiene." I do a very specific analysis with my patients and say, "You are going back home, but before you get there, I want the toilet and its handle, along with everything in the bathroom, including the sinks, to have a Clorox-level bleach disinfection. I also want you to throw away your toothbrush."

Again, I think that [going home] was likely a cause for this high rate of readmission. Think about that when your patients are going home because it is clearly a predictor.

Coffee and Acute Alcoholic Hepatitis

We recognize that acute alcoholic hepatitis has an incredibly high mortality rate, approaching 30%. We need to be doing something for patients with alcoholic hepatitis. Not all of them qualify for steroids, and steroids do not really change mortality.

The study from the Translational Research and Evolving Alcoholic Treatment, or the TREAT group consortium, which was presented by Naga Chalasani[6] from Indiana University, looked at a PNPLA3 gene as it relates to coffee drinking and fatty liver disease. This gene is particularly responsible for a balance of energy usage and storage in adipocytes.

This has been well looked at in the nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis arena, but now they are looking at it as it relates to acute alcoholic hepatitis. The study patients were looked at from the standpoint of acute alcoholic hepatitis and were then balanced against patients who were heavy alcohol consumers on a regular basis. [The investigators] looked at their outcomes over the course of follow-up.

This particular gene was a relative predictor. Patients with a PNPLA3 genotype polymorphism were more likely to develop alcoholic hepatitis. But coffee [intake] was a decelerator of the risk for alcoholic hepatitis in a profound way: Reduction approached nearly 80%.

I would not tell heavy alcohol consumers to just drink more coffee as a stand-alone recommendation, or have them think that this obviates the need to be aware of the health implications of heavy alcohol use and the need for an appropriate reduction in consumption, or, in the case of alcoholic hepatitis, abstinence from alcohol. In patients with a higher alcohol consumption, it may be an appropriate discussion to at least say that coffee is potentially beneficial and should be encouraged in those who enjoy its consumption.

Studies have found [that benefits occur with] caffeinated coffee, filtered coffee, and brewed coffee—not instant or decaf coffee, and not from caffeine in other drinks. The threshold seems to be three or more cups a day. We do think that caffeine alters the liver-signaling pathways and inflammatory pathways, and there are a lot of emerging data. It is not quite clear how this works, but it does.

If you are interested in this topic, I will refer you to my most recent review as it relates to the value of coffee for mitigating the risk for severe liver disease in hepatitis C and some fibrotic liver diseases. This is something that you really need to be aware of, and it is a really easy thing. As I said in my first review, your patients are going to like it "a latte" when you tell them they can drink more coffee.

Vitamin D Deficiency and NAFLD

We know that vitamin D deficiency is associated with a host of different diseases. It is very prevalent; an estimated one third of patients are vitamin D deficient. Nonetheless, the increasing evidence that vitamin D [deficiency] may increase the risk for metabolic syndrome ties into why it may play into NAFLD.

This analysis[7] of the National Health and Nutrition Examination Survey (NHANES) suggested that vitamin D deficiency might predispose patients to increased severity of and mortality from NAFLD. The investigators not only correlated the degree of steatosis based on grading the ultrasound report, but they also looked at a NAFLD fibrosis score. There was an inverse relationship between the vitamin D level and the degree of steatosis and degree of fibrosis. They also tracked this out, and follow-up extended out to 19 years. They demonstrated that this played out with an increased association with diabetes and Alzheimer disease–related mortality. The hazard ratio was around three times greater for those two related mortalities, based on vitamin D deficiency.

I tell my patients all the time, particularly those with inflammatory bowel disease or liver disease, to take 2000 IU daily. I check them after 6 months just to make sure that we are in the right ballpark. Taking a little more vitamin D becomes almost a value-added [activity] to me. Maybe take it with coffee; it may be a reasonable thing for everyone to do.

Obeticholic Acid for Primary Biliary Cholangitis

The next presentation[8] is a follow-up on some very interesting data on obeticholic acid (OCA) [a farsenoid X receptor agonist], which was approved by the US Food and Drug Administration in late May. A farnesoid X receptor is basically a nuclear receptor expressed in the liver and the intestine. It is a key regulator of bile acid and inflammatory, fibrotic, and metabolic pathways.

Dr Paul Pockros from the Scripps Clinic and colleagues combined [results of] three randomized, double-blind, placebo-controlled trials, used a composite endpoint, and presented the pooled analysis. The [results] were highly statistically significant for [efficacy of OCA in] patients who had not responded entirely or favorably to, or who were intolerant to, chenodeoxycholic acid. OCA seemed to be very well tolerated. Starting with 5 mg and titrating it up over 6 months to 10 mg seems to mitigate against the risk for pruritus, a side effect of this drug that is also an effect of the primary disease.

It is very reassuring that we now have something new that can be of value for primary biliary cholangitis patients.

Rapid-Infusion Infliximab

I thought the next study, on infliximab, was pragmatic.

Many of our patients are getting kicked out of the hospital infusion centers. Many of you may do [infliximab infusions] in your office or your ambulatory infusion center. We tend to drag [infusions] out over a 2-hour period, and patients [may receive] premedication according to dosing information. This study[9] looked at changing the infusion time to 90 minutes or to 60 minutes. The investigators had remarkable results. They looked at infusions of 88 patients receiving infliximab. [Infusions were reduced] to 90 minutes, and if that was tolerated, they went down to 60 minutes. Patients had remarkable infusion tolerance. Virtually everybody was able to tolerate this. Over the total 151 infusions at their center, 121 hours were saved by these accelerated infusions.

This may be something for you to look at. It is easy to change as it relates to time in your center, and it may dramatically increase your throughput as it relates to utilization of infusion centers.

Certolizumab and Breastfeeding

The last study[10] I wanted to mention is about the use of certolizumab (Cimzia®) as it relates to breastfeeding. Many of us have been concerned to some degree about placental transfer of adalimumab and infliximab, particularly in the later trimesters. These drugs have been shown to have some transmission to breast milk, and all of these drugs are category B. Some experts suggest that certolizumab may be a safer drug in patients who are pregnant. This has led some to say to their patients anticipating pregnancy, "Why don't we start you or switch you to this drug?"

This study looked at the transfer of certolizumab into breast milk. The investigators looked at a number of breastfeeding mothers; 17 were entered into the sampling cycle. The assays registered virtually no or minimal drug levels that were not statistically different from the threshold. Their conclusion was that the continuation of certolizumab is compatible with breastfeeding.

If you have a patient who is breastfeeding and wants to know what should be done while she is on this medication, I think this is reassuring.

Lots of things went on in Vegas, and many things were too good to stay in Vegas. If you were there, hopefully you can take them out of Vegas. If you were not, I can bring them out of Vegas for you, and you can have some interesting dialogue and discussion. Be on the lookout for things coming in the near future relating to the exciting presentations at the American College of Gastroenterology meeting.

I will see you next time. Thank you again for listening. I am Dr David Johnson.


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