Author Archives: gutsandgrowth

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About gutsandgrowth

I am a pediatric gastroenterologist at GI Care for Kids (previously called CCDHC) in Atlanta, Georgia. The goal of my blog is to share some of my reading in my field more broadly. In addition, I wanted to provide my voice to a wide range of topics that often have inaccurate or incomplete information. Before starting this blog in 2011, I would tear out articles from journals and/or keep notes in a palm pilot. This blog helps provide an updated source of information that is easy to access and search, along with links to useful multimedia sources. I was born and raised in Chattanooga. After graduating from the University of Virginia, I attended Baylor College of Medicine. I completed residency and fellowship training at the University of Cincinnati at the Children’s Hospital Medical Center. I received funding from the National Institutes of Health for molecular biology research of the gastrointestinal tract. During my fellowship, I had the opportunity to work with some of the most amazing pediatric gastroenterologists and mentors. Some of these individuals included Mitchell Cohen, William Balistreri, James Heubi, Jorge Bezerra, Colin Rudolph, John Bucuvalas, and Michael Farrell. I am grateful for their teaching and their friendship. During my training with their help, I received a nationwide award for the best research by a GI fellow. I have authored numerous publications/presentations including original research, case reports, review articles, and textbook chapters on various pediatric gastrointestinal problems. In addition, I have been recognized by Atlanta Magazine as a "Top Doctor" in my field multiple times. Currently, I am the vice chair of the section of nutrition for the Georgia Chapter of the American Academy of Pediatrics. In addition, I am an adjunct Associate Clinical Professor of Pediatrics at Emory University School of Medicine. Other society memberships have included the North American Society for Pediatric Gastroenterology Hepatology and Nutrition (NASPGHAN), American Academy of Pediatrics, the Food Allergy Network, the American Gastroenterology Association, the American Association for the Study of Liver Diseases, and the Crohn’s and Colitis Foundation. As part of a national pediatric GI organization called NASPGHAN (and its affiliated website GIKids), I have helped develop educational materials on a wide-range of gastrointestinal and liver diseases which are used across the country. Also, I have been an invited speaker for national campaigns to improve the evaluation and treatment of gastroesophageal reflux disease, celiac disease, eosinophilic esophagitis, hepatitis C, and inflammatory bowel disease (IBD). Some information on these topics has been posted at my work website, www.gicareforkids.com, which has links to multiple other useful resources. I am fortunate to work at GI Care For Kids. Our group has 17 terrific physicians with a wide range of subspecialization, including liver diseases, feeding disorders, eosinophilic diseases, inflammatory bowel disease, cystic fibrosis, DiGeorge/22q, celiac disease, and motility disorders. Many of our physicians are recognized nationally for their achievements. Our group of physicians have worked closely together for many years. None of the physicians in our group have ever left to join other groups. I have also worked with the same nurse (Bernadette) since I moved to Atlanta in 1997. For many families, more practical matters about our office include the following: – 14 office/satellite locations – physicians who speak Spanish – cutting edge research – on-site nutritionists – on-site psychology support for abdominal pain and feeding disorders – participation in ImproveCareNow to better the outcomes for children with inflammatory bowel disease – office endoscopy suite (lower costs and easier scheduling) – office infusion center (lower costs and easier for families) – easy access to nursing advice (each physician has at least one nurse) I am married and have two sons (both adults). I like to read, walk/hike, bike, swim, and play tennis with my free time. I do not have any financial relationships with pharmaceutical companies or other financial relationships to disclose. I have helped enroll patients in industry-sponsored research studies.

Do We Still Need PPI-REE?

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“It is on shaky ground that one defines a disease by a response to therapy rather than by its clinical and mechanistic characteristics.” This is noted in a recent editorial (Clin Gastroenterol Hepatol 2014; 12: 2023-25, study: 2015-22).

The editorial makes this comment because the related study finds that the esophageal tissue from eosinophilic esophagitis (EoE) patients with proton-pump responsive EoE (PPI-REE) was indistinguishable from patients with EoE who do not respond to PPIs.

The study examined 196 consecutive patients and performed immunohistochemistry to examine major basic protein (MP), eotaxin-3, and tryptase.  Key finding: none of these markers were able to distinguish EoE from PPI-REE; however, these 3 assays did identify EoE with 100% accuracy compared with controls.

From the editorial: “We can approach EoE as a disease in which use of PPIs is the first step in treatment, and diet and steroids represent step-up therapy…We may not understand why some patients with EoE respond to PPIs yet others do not.”  It is possible that genetic testing in the future will allow us to distinguish which patients will benefit from PPIs, topical steroids or diets.

Bottomline: Now that it is well-recognized that a substantial portion of EoE patients benefit from PPIs, is it necessary to try to use a separate label for this subset? Probably not.

Related blog posts:

Current Mortality from Being Born Premature

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A recent study (Patel RM et al. NEJM 2015; 372: 331-40) provides prospectively collected data on 6075 deaths among 22,248 live births with gestational ages 22-29 weeks from the U.S NICHD Neonatal Research Network. between 2000 thru 2011:

Key findings:

  • Improved death rate in most recent period of study:  number of deaths per 1000 live births was 275  (2000-2003), 285 (2004-2007), 258 (2008-2011)
  • While there were fewer pulmonary deaths with time, the deaths attributed to necrotizing enterocolitis increased: number of deaths per 1000 live births was 23 (2000-2003), 29 (2004-2007), 30 (2008-2011).  Necrotizing enterocolitis was the leading cause of death between 15-60 days of life (Figure 1).
  • Overall, 40.4% of deaths occurred within 12 hours after birth.  Only 17.3% occurred after 28 days of life.
  • For the entire study period, the rate of death (per thousand) was associated with gestational age: 949 (22 weeks), 730 (23 weeks), 427 (24 weeks), 258 (25 weeks), 157 (26 weeks), 115 (27 weeks), 78 (28 weeks)
  • The authors speculate that the overall reduction in death rate is likely related to more aggressive respiratory care (for bronchopulmonary dysplasia); one marker of this was increased usage of high-frequency ventilation.

Bottomline: While there has been improvement, being born premature is associated with high mortality.

Is it Safe to Chew Gum Before Anesthesia?

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According to a recent study highlighted in Gastroenterology & Endoscopy News, gum chewing immediately prior to anesthesia is probably safe.

Here’s an excerpt:

Patients who are fasting before upper endoscopy can safely chew gum up until the time of the procedure, researchers have found…

The prospective randomized controlled study evaluated the effect of gum chewing on volume and pH of gastric contents in 67 patients scheduled to receive IV conscious sedation for upper endoscopy. The night before the procedure, patients were randomly assigned to chew gum until the start of sedation…—or to not chew gum, with no limit on the number of pieces or how long they could chew.

The median volume suctioned from the gum chewers was 13 mL, compared with 6 mL for non-gum chewers. Similarly, gastric fluid also was greater for gum chewers—0.35 versus 0.11 mL/kg for patients who did not chew gum. “The 0.35 mL/kg is still under 0.4 mL/kg, which is where the risk for aspiration comes into effect,” he noted…The pH also did not change.

Take-home message: While this study provides some reassurance, I suspect that asking families to give nothing before an endoscopy will be easier than trying to explain the nuances and risks for aspiration.  For those who have only had gum, though, it may not be necessary to cancel their case.

From Atul Gawande's Twitter Feed

From Atul Gawande’s Twitter Feed

 

 

 

Gut Microbiome, Crohn’s Disease and Effect of Diet

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At this past year’s NASPGHAN conference, Bob Baldassano indicated that a low-residue diet probably does not makes sense for the majority of patients with Crohn’s disease because it would not promote a ‘healthy’ gut microbiome.  Another article (Walter SS, Quiros A, et al. SOJ Microbiol Infect Dis 2014; 2: 1-13) supporting this argument has been published. (Thanks to Ben Gold for giving me this reference.)

In this study, the authors examined the gut microbiome from two healthy volunteers and compared them to six patients with Crohn’s disease (CD) (ages 16-50).  The CD cohort were in clinical remission and were not receiving probiotics.  Subjects were randomized to either a low-residue diet (LRD) or a specific carbohydrate diet (SCD).

Besides having some cool figures to explain their results, the key points:

  • The complexity of the gut microbiome was lower in IBD patients compared to healthy controls
  • Bacteroides fragilis was increased in fecal samples of IBD positive patients
  • There was a temporal response of gut microbiome to SCD with increased microbial diversity while the LRD diet was associated with a reduced diversity of the microbiome in patients with CD

While the number of patients participating in this study are low, the affects of these diets can still be measured due to the trillions of microbes in the gut microbiome.

Also noted: Church PC, Turner D, et al. Aliment Phamacol There 2015; 41: 153-66. “Systematic review with meta-analysis: magnetic resonance enterography for the detection of inflammation and intestinal damage in Crohn’s disease.”

How the gut micro biome may affect other diseases including Multiple Sclerosis: Study Hints Gut Microbiome Plays a Role in Multiple Sclerosis (Link to Gastroenterology & Endoscopy News)

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From NASPGHAN:  Introducing New Website for Teens with Inflammatory Bowel Diseases: JustLikeMeIBD.org  PRESS RELEASE

New York, NY- January 20, 2015 – The number of inflammatory bowel disease (IBD) patients in the U.S. has now increased to an estimated 1.6 million, with approximately 5 percent of that patient population under the age of 18. In response to the growing number of kids with IBD, the Crohn’s & Colitis Foundation of America (CCFA) along with the NASPGHAN Foundation for Children’s Digestive Health and Nutrition, has launched a new website called “Just Like Me” for teenagers with Crohn’s disease and ulcerative colitis.

The interactive site will feature stories and videos from teens with IBD as well as information on school, dating, stress, diet, and research.

 

 

How Bilingual Studies Reflect a Deeper Scientific Flaw

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A recent story on NPR explored the purported advantages of bilingual acquisition.  Previous reports have suggested that individuals with bilingual education attain other advantages in learning and “executive” function.  This may be a bunch of bunk and more related to scientific journals bias of reporting “positive” studies.  If you listen to the report (link below), consider how the problem of reporting bias affects so many fields in medicine and science.

Link: Bilingual Studies Reveal Flaw In How Info Reaches Mainstream

Somewhat related post:

 

The Best Way to Handle Vaccine Skeptics

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According to a recent NY Times editorial, the best way to improve vaccination rates is not to mandate universal vaccination or to label ‘anti-vaxxer’ parents as ignorant.  The best way is to make it more difficult to receive personal exemptions –this is something the government can be quite good at.

Here’s the link: How to Handle Vaccine Skeptics -NY Times

Here’s an excerpt:

They [States} can require parents to write a letter elaborating on the reason their child should be exempt. They can require that the letter be notarized. They can insist that parents read and sign a form that discusses the risks of nonvaccination. Better yet, they should mandate in-person counseling so that the decision not to vaccinate is truly informed.

States can also require that parents obtain an exemption form by specifically requesting one from the state or local health department, rather than downloading it online. They can insist that these parents acknowledge that they will be responsible for keeping the children away from school during outbreaks. Moreover, they should have procedures to review each request for exemption rather than automatically approving them, as many states do now. And they should require parents with exemptions to apply annually for renewal…

 In a 2012 study, which my colleagues and I [Saad Omer] published in The New England Journal of Medicine, nonmedical exemption rates were 2.3 times higher in states with easy administrative policies for granting exemptions (like Connecticut, Missouri and Wisconsin) than in states with difficult policies (like Florida, Minnesota and Texas). Moreover, the annual rate of increase in nonmedical exemptions was about 60 percent higher in states with easy exemption policies compared with states with difficult policies.

“Origins of Cystic Fibrosis Lung Disease”

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Origins of Cystic Fibrosis Lung Disease — NEJM (NEJM 2015; 372: 351-62) is a good read.  The authors note that the basic defect in Cystic Fibrosis (CF), the loss of the cystic fibrosis transmembrane conductance regulator (CFTR), has been recognized for a long time.  However, the connection between this defect and the progressive lung disease/inflammation has remained uncertain.

Now, new animal models have provided a wealth of information that closes the knowledge gap.

Here are the key points:

  • CF affects the lungs very early: Bronchiectasis is present in nearly one in three children with CF by 3 years of age and CT scans are abnormal in most babies with CF as early as 3 months of age.
  • Infection precedes inflammation: “During the first hours after birth, piglets with CF show no evidence of inflammation in their airways…yet,…they fail to eradicate bacteria as well…[which] can initiate a cascade of airway inflammation and airway remodeling.”
  • There are multiple “hits” on the airways.  While many have suggested that increased sodium leads to a ‘dehydrated’ state, this does not seem to be correct.
  • More recent studies point to loss of bicarbonate secretion as a crucial factor.  This results in a reduced pH which in turn leaves the lungs more vulnerable to infection.  Lower acidity reduces the effectiveness of a “complex soup of antimicrobial peptides, proteins, and lipids in airway-surface liquid.”
  • Poor mucociliary transport, “which guards the lungs by trapping invading pathogens and particulates in mucus,” is another important “hit” on the lungs.

Implications:

  • CF needs to be diagnosed early and treated early
  • Improving even one of these defects in host defenses is likely to be beneficial.
  • Animal models remain important in understanding pathophysiology.  They allow “investigating the disease at its genesis and before the onset of secondary manifestations.”

Related blog posts:

Progress in Cystic Fibrosis over 18 Years

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A recent study (J Pediatr 2014; 165: 1091-7) showed significant improvement in lung function among 6-year-olds with Cystic Fibrosis (CF) between 1994-2012.

Using the Cystic Fibrosis Foundation Patient Registry with a total of 11,670 children, the authors found that the mean FEV1 and FVC z-scores increased significantly over the period in the entire cohort.  In addition, the height-for-age (HFA) also improved.  These results are easy to see graphically in Figures 1 & Figure 2.  The authors note that in 2012, children who were identified by screening had improved HFA, FEV1, and FVC compared to children who were not identified by screening.

Take-home points:

  • These data show impressive improvement in lung function and growth over the past two decades
  • These values are going to improve further now that all 50 states mandate newborn screening for CF
  • While there is improvement, 6-year-olds with CF still have measurable pulmonary dysfunction; thus, more work is needed, perhaps with novel therapies.

Related blog posts:

What We Know Now: Therapeutic Drug Monitoring for Inflammatory Bowel Disease

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This blog has discussed the utility of obtaining drug levels for both biologic agents and thiopurines.  A recent article (Inflamm Bowel Dis 2015; 21: 182-97) provides a concise up-to-date review.

Here are the key points:

  • Primary nonresponse to anti-TNF therapy (PNR) “is most commonly defined as lack of improvement of clinical signs and symptoms after the induction phase leading to discontinuation of the drug.”
  • “We think that patients who respond but fail to achieve remission…are likely almost all due to insufficient drug.”
  • Table 2 provides a list of predicting factors, both negative and positive, for PNR.  This list includes genetic mutations (e.g.. IL23R, NOD2/CARD15 variant), mucosal gene expression, clinical factors (e.g. young age, isolated colitis, smoking, nonstricturing disease, concomitant immunomodulators) and serologic (eg. CRP, hemoglobin, and presence of pANCA).
  • Patients with PNR to a TNF antagonist, “despite therapeutic concentrations of drug and no anti-drug antibodies (ADA), would likely benefit from a switch to an alternative drug with a different mechanism of action.”
  • “Patients with a high baseline inflammatory load…and increased clearance of drug because of a high turnover would likely benefit from higher induction doses.”  This hypothesis has been proven in rheumatoid arthritis patients in which patients with high TNF concentrations had a clinical response to 10 mg/kg that was “significantly better than the response to 3 and 6 mg/kg of infliximab.”
  • Patients (with ADA) with an “early immunogenic response against the TNF antagonist are unlikely to respond to dose escalation and thus should be switched to another TNF antagonist, and it should be considered to give higher induction doses in combination with an IMM [immunomodulator] to reduce the risk of immunogenicity.”

Take-home message: New definition of primary nonresponse to anti-TNF agent: “a lack of improvement of objectively assessed signs of active inflammation at baseline, after the induction phase despite the presence of adequate concentrations of drug and the absence of anti drug antibodies.”

Also noted: “Surgical management of ulcerative colitis in the era of biologicals” Inflamm Bowel Dis 2015; 21: 208-10. Key point: “Sacrificing the non responsive diseased colon is an underused or unnecessarily delayed chance to normalize ..health and life.”  “Deconditioning of patient with unreasonably long escalations of ineffective medications adds to the morbidity of surgical intervention.”

“Automimmune Features are Associated with Chronic Antibiotic-refractory Pouchitis”Inflamm Bowel Dis 2015; 21: 110-20. Key point: “Microsomal antibody expression and elevated IgG4-positive plasma cell infiltration were independent risk factors” for chronic antibiotic-refractory pouchitis.”

Update on MOC (recent blog:Resistance to Maintenance of Certification | gutsandgrowth) American Board of Internal Medicine “We Got It Wrong” “We launched programs that weren’t ready and we didn’t deliver an MOC program that physicians found meaningful. We want to change that.”

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“Using Drugs to Discriminate”

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A recent commentary (Jacobs DB, Sommers BD, NEJM 2015; 372; 399-402) highlighted a growing problem.  Many insurers are using drug benefit plans to dissuade sicker people from enrolling in their plans.

Prior to the Affordable Care Act (ACA), insurers charged high premiums to people with chronic conditions.  The ACA attempted to address this problem; in fact, the “individual mandate” was necessary to make sure that insurance companies had enough healthy people in their insurance pool to make it financially feasible.

Yet, insurance companies make more money if they can limit insuring sicker, chronically-ill people.  One way this is happening is through “Adverse Tiering” which substantially increases out-of-pocket expenses for individuals with HIV, cancer, diabetes, mental illness, and arthritis. The difference in out-of-pocket costs, for example, with for each HIV drug was more than $3000 (on average) between adverse-tiered plans and those that were not adverse-tiered.  Even for generic drugs, the cost was nearly a $2000 difference.

A few problems with this approach:

  • Insurer’s drug prices are not usually available to public when choosing a plan; thus, these higher out-of-pocket costs are often unanticipated. (*Price transparency could accelerate rather than hinder this process.)
  • If sicker patients flock to plans without “adverse tiering,” this could make these non-adverse-tiered plans lose money and result in similar design to avoid “adverse selection.”

Conclusion: “Preventing [this adverse tiering and] other forms of financial discrimination on the basis of health status — with the attendant risks of adverse selection in the marketplace –will require ongoing oversight.”

Here’s the NY Times Report on this study: Study Finds HIV Drugs Priced Out of Reach

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