M. Brian Fennerty, MD, is the editor of Journal Watch Gastroenterology and Professor of Medicine and Section Chief of Gastroenterology in the Department of Internal Medicine at Oregon Health & Science University.
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(2 votes, average: 3.50 out of 5)The effectiveness of endoscopic ablation of neoplastic (dysplastic) Barrett esophagus (BE) has made it the new standard of care in many communities; referrals to surgeons have largely disappeared. However, the procedure is still evolving — from thermal ablation by laser in the 1980s and early 1990s to BICAP probes and Argon Plasma Catheter (APC) in the mid-to-late 1990s to specific radiofreqency catheters (Barrx Halo 360 and 90 systems) in the current decade. Cryoablation catheters are also now available.
At the same time, endoscopic mucosal resection (EMR) technique has also evolved with the Duette and other systems. EMR now allows “wide area” resection of flat BE as well as the original approach of targeted resection of mucosal nodules and depressions.
So, with such a large variety of effective techniques available for treating limited flat BE mucosa, let me present a case study and ask what you would do.
A patient has 2 cm of circumferential BE with a single 1-cm tongue extension. Biopsies demonstrate focal high-grade dysplasia and widespread low-grade dysplasia. Careful inspection with high-definition, white-light and narrow-band imaging reveals no surface irregularity and minimal vascular heterogeneity.
I look forward to the discussion.
(8 votes, average: 3.38 out of 5)In treating patients with constipation, we have several options for first-line agents: bulking agents/fiber, osmotic laxatives, or stimulant laxatives. When a patient has a suboptimal result, we commonly add or move to another class of laxative agents. Fortunately, most patients respond to these interventions, but we all have patients whose condition is “refractory” to these commonly used treatments. In the last few years, newer agents to manage constipation such as lubiprostone and linaclotide have also become available. But how best to manage these patients remains unclear, at least to me. So, here’s what I would like to know from you.
What do you use as first-line treatment in a patient with constipation?
What is your add-on treatment when your first-line treatment fails?
Do you use the newer agents, and if so, when? Do you use them to substitute for another agent or add them on?
In what circumstances do you consider surgery to treat constipation?
If a colonoscopy is negative, do you routinely use other diagnostic tests in a patient with constipation?
Looking forward to hearing your management strategies.
(3 votes, average: 2.00 out of 5)Colonoscopy prevents most colorectal cancers, but only when it is performed as part of a high-quality examination. The quality measures most often discussed include cecal intubation rate, cecal withdrawal time, documentation of bowel prep quality in endoscopy reports, adenoma detection rate (ADR), and appropriate recommendation of subsequent screening or surveillance intervals after colonoscopy. While third-party payers are increasingly considering using some of the above as pay-for-performance measures, I have also noticed many more patients asking about some of these measures when they are being consented for a colonoscopy. This leads me to ask you the following.
1) Do you routinely inform your patients of your ADR, cecal intubation rate, and/or withdrawal time?
2) Do you follow guidelines regarding repeat colonoscopy intervals (i.e., 10 years for normal-risk patients with a normal exam, 5-10 years for 1-2 small adenomas, etc.)?
3) Do you document bowel prep quality on your reports, and if so, do you use a validated method such as the Boston Bowel prep score?
4) Are these above measures available on your website or posted in your office?
5) For those of you who do not do some or all of the above, why don’t you?
6) Do you think patients care about these facts?
I am looking forward to an interesting conversation.
(2 votes, average: 4.50 out of 5)The diagnosis of this increasing and now epidemic infection has been evolving as well. When I first started testing for this infection, a cytotoxin assay was used that delayed the diagnosis and was very operator-dependent. Enzyme immunoassays came next, and more recently PCR testing of stool has become available. Despite the increased accuracy and more rapid results available today with PCR testing, it seems that we have not yet altered our testing pattern. It used to be that we recommended 3 separate stool samples be tested before excluding the diagnosis of C. diff infection. I know that practice remains prevalent today.
So, what I would like to find out from you are the following…
1) Do you know what C. diff test is used where you practice?
2) How quickly do you get the results back?
3) How many stool samples do you routinely test?
4) If testing is negative and symptoms persist, how long do you wait before “retesting?”
Looking forward to the dialogue.
(1 votes, average: 5.00 out of 5)I am amazed at the variation I have seen in the use of endoscopic ultrasound (EUS) in staging Barrett esophagus (BE). Some of us use EUS universally, and others (myself included) never use it to stage intramucosal carcinoma or high-grade dysplasia.
So, let me propose a case and ask what you would do: The patient is a healthy 58-year-old man with 3 cm of BE with a 0.5 cm nodule in the distal segment. There is no ulceration or other surface irregularity found upon inspection with high-definition white-light and narrow-band imaging.
Would you:
1) Stage with EUS and resect the nodule?
2) Resect the nodule and stage with EUS only if intramucosal carcinoma or greater neoplasia is seen?
3) Resect the nodule and stage with EUS for invasive adenocarcinoma only?
4) Perform radiofrequency ablation (RFA) of the nodule after staging EUS?
5) Perform RFA of the nodule without staging EUS?
I look forward to your comments.
(2 votes, average: 5.00 out of 5)Our hospital used to provide hydrogen breath testing for the community but recently discontinued this practice. I was asked to comment on whether it should be discontinued and how often I used the test. It surprised me that I had not ordered a hydrogen breath test in the 2 decades I have been here but that many docs did. Although all of us are aware that small intestinal bacterial overgrowth can occur (e.g., scleroderma-type bowel motility disorders, post-operative blind loops, etc.), it seems that this diagnosis is being made more often in otherwise normal people without an obvious etiology.
So the conversation I want to generate is the following:
1) How often do you entertain a diagnosis of SIBO, and what symptoms/settings make you consider the diagnosis?
2) Do you think SIBO is being overdiagnosed or underdiagnosed?
3) If you consider SIBO, do you do a diagnostic test, and, if so, which one?
4) Given that no test for SIBO is validated against a gold-standard diagnosis, how do you chose the test you are using?
5) If you do not test for bacterial overgrowth, do you treat empirically, and, if so, with what?
6) What test characteristics do you want to see before you would use a test for bacterial overgrowth?
I look forward to the conversation!
(3 votes, average: 3.00 out of 5)I have been using PPIs to manage GERD and acid-sensitive dyspepsia since omeprazole first became available in 1989. Although no drug class is absolutely safe, there is, as yet, not a single case report of a death related to this drug class, despite hundreds of millions of patient-years of exposure. Despite this remarkable safety profile, much attention has focused recently on the overall safety of PPIs, as they have been associated with enteric infections (e.g., c. difficile), decreased bone density, electrolyte abnormalities (e.g., low magnesium), etc. However, most of these risks have been described in epidemiological studies that can establish association but not causation, and we learned an important lesson about interpreting such results with caution after authors and the FDA sent a message about the so-called interaction between PPIs and clopidogrel that turned out to be clinically irrelevant.
Despite the benefits of PPIs, increased scrutiny of the safety of this drug class has led a number of my patients to question recommendations about trying or continuing PPI therapy. I think that patients are wise to ask about the relevant side effects of any drug, but I have had trouble giving much in the way of advice or information about PPI risks, given the lack of credible evidence of cause and effect.
So, what do you tell your patients about risks when you start them on a PPI therapy?
What do you tell patients on long-term PPI therapy?
Do you use drug holidays?
Do you do bone-density studies earlier or more often in patients on PPIs?
Do you monitor magnesium levels?
Do you have patients stop therapy if they at risk for enteric infections (e.g., from hospital antibiotic exposure, travel to developing nations, etc.)?
I am looking forward to your insightful comments.
(1 votes, average: 5.00 out of 5)All gastroenterologists are very familiar with celiac disease, including its characteristic findings on small bowel biopsy and the treatment with a gluten-free diet. But I have noticed that we as gastroenterologists approach the possibility of sprue, or those suspected of having gluten sensitivity without sprue, with extraordinary variability. For instance, a negative screening tissue transglutaminase (TTG) has greater than a 99% negative predictive value (essentially excluding celiac disease), but a positive TTG has only a 25% to 35% positive predictive value, meaning that most patients who test positive do not have celiac disease.
So, first, here are some questions:
1) Do you still take biopsies in some patients with a negative TTG, and, if so, how do you decide which patients should undergo biopsy?
2) Do you take biopsies in all patients with positive TTG screens? If not, do you put these patients on a gluten-free diet as a trial?
3) Where and how many biopsies do you take to diagnose sprue? Do you always take biopsies in the duodenal bulb?
4) If you take duodenal biopsies, how long do you want the patient on gluten prior to the exam?
Now, let’s talk about gluten sensitivity:
1) If you take biopsies in patients with symptoms suggestive of sprue, and the biopsies are normal, but the patiens are improved on a gluten-free diet, what do you tell these patients? That they are sprue-variant? That they do not have sprue, but they are gluten sensitive?
2) Do you prescribe the same diet to these patients?
Please weigh in. I look forward to seeing your responses.
(6 votes, average: 3.83 out of 5)We all are seeing this disease more often than in the past. Whereas the diagnostic criteria now seem firmly entrenched, the optimal treatment strategy remains to be determined. Treatments have included food avoidance, anti-secretory drugs, topical steroids, immunomodulators, and combinations of these approaches.
So I am interested in how you treat eosinophilic esophagitis.
What is your first line therapy?
Do you put every patient on a PPI?
Do you use food avoidance, and, if so, is it directed empirically or by allergy testing?
Which topical steroid do you use?
Do you treat before dilating?
How long do you treat, or do you maintain patients on therapy?
Let’s get the conversation rolling!
(5 votes, average: 4.40 out of 5)Most gastroenterologists are aware of the increasing incidence of hepatocellular cancer (HCC) in patients with cirrhosis. Most are also aware of the updated 2011 guidelines from the American Association for Study of Liver Diseases that recommend screening many patients with cirrhosis for HCC with every 6-month ultrasound examinations. These guidelines are based largely on a cost-effectiveness analysis showing that, at a certain threshold, incidence of HCC screening would be cost-effective in various cirrhotic states. However, there is a lack of data from prospective trials showing that screening is effective in preventing death from HCC and almost no data on the efficacy of such an intervention in the U.S.
1. Do you think we should screen patients with cirrhosis for HCC?
2. How effective do you think such screening is?
3. How would you screen (ultrasound, CT, MRI, alpha fetoprotein)?
4. What frequency intervals should be used?
5. If you do not screen, what data would compel you to begin screening?
I look forward to the discussion.
