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. I have authored numerous publications/presentations including original research, case reports, review articles, and textbook chapters on various pediatric gastrointestinal problems.
Currently, I am the 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 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, 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 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. For many families, more practical matters 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
– 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. I like to read, walk/hike, exercise, swim, and play tennis with my free time as well as go to baseball games.
I do not have any financial relationships with pharmaceutical companies or other financial relationships to disclose. I have participated in industry-sponsored research studies.
A prospective pediatric eosinophilic esophagitis (EoE) study (C Gutierrez-Junquera et al. JPGN 2018; 67: 210-6) examines the use of proton pump inhibitors (PPIs) for long-term management for this disorder.
After diagnosis of EoE, children received esomeproazole (1 mg/kg/dose BID). For those with a response (<15 eos/hpf), they were maintained on 1 mg/kg/day for one year.
Of the initial cohort of 109, 72 (66%) had response to esomeprazole.
57 of these responders were subsequently followed in this study. At the lower daily esomeprazole dose, 70.1% (n=40) continued with <15 eos/hpf and 29.9% (n=17) had relapse.
Maintaining response was more common among those who achieved an initial response (with BID esomeprazole) of <5 eos/hpf compared to those who had achieved an initial response of 6-14 eos/hpf. At 1 year, in those with who had a more complete response, 81% maintained eosinophil count <15/hpf compared with only 50% in those with a lesser initial response.
Adverse events with prolonged treatment were uncommon and included self-resolving diarrhea in three, headache in one and urticaria in one; the latter two adverse effects responded to change to lansoprazole
PPI treatment is effective in probably 40-50% of individuals with EoE (though higher response in this study)
Some individuals need higher doses of PPIs
Due to the high response rate, this underscores the need to diagnose EoE prior to using PPIs or after they have been discontinued.
What this latest study suggests, in the context of other studies, is that if people can’t shop for elective M.R.I.s, there’s hardly a chance they are going to do so with other health care procedures that are more complicated and variable.
Even if 40 percent of health care is shoppable, people are not shopping. What seems likelier to work is doing more to influence what doctors advise.
For example, we could provide physicians with price, quality and distance information for the services they recommend. Further, with financial bonuses, we could give physicians (instead of, or in addition to, patients) some incentive to identify and suggest lower-cost care.
Leaving decisions to patients, and making them spend more of their own money, doesn’t work.
Briefly noted: A Muntaner-Mas et al. J Pediatr 2018; 198: 90-7. This cross-sectional study with 250 Spanish children (10-12 year olds) examined obesity measures, physical fitness measures and academic performance. Key finding: “Children considered fit had better academic performance than their unfit peers…the association between body mass index and GPA was mediated by cardiorespiratory fitness and speed-agility.” The design of this study precludes establishing this association as a causal relationship.
I remember back to college chemistry when one of my professors pondered what type of person would purposely delve into sulfur-related research. Similarly, I have wondered how some of my colleagues can put their nose right in the middle of a heavy-soiled diaper and use their olfactory sense to narrow the differential diagnosis.
Now, more research involving the olfactory sense has been published: “The development of an international odor identification test for children: the Universal Sniff Test” also called the U-Sniff test (VA Schriever et al. J Pediatr 2018; 198: 265-72) and fortunately it does not involve any offensive odors.
This multicenter (19 countries) with 1760 children age 5-7 years, validated the U-sniff with twelve odors. Key finding: The U-Sniff “enabled discrimination between normoosmia and children with congenital anosmia with a sensitivity of 100% and specificity of 86%.”
Specific odors that are part of U-Sniff: lemon, banana, coffee, flower, strawberry, fish, cut grass, orange, onion, butter, apple, peach, chocolate, tomato, cheese, biscuit, and honey.
My view is that Clostridium difficile infection (CDI) in children with inflammatory bowel disease is often overdiagnosed due to detection of a carrier state in many when tested by PCR assays and the overlapping clinical features. This is particularly important when considering fecal microbiota transplantation (FMT) due to the potential risks of this treatment.
Recently, I had a letter to the editor (J Pediatr 2018; 199: 283) on this topic that was accepted:
The author’s reply suggested that their approach followed IDSA guidelines by checking CDI with PCR in those who were clinically-symptomatic. Yet, the IDSA guidelines (link here: IDSA C diff guidelines) do not focus on the issue of IBD flare-ups which cause identical symptoms. Expert IBD specialists have recommended the following for identifying CDI in patients with IBD:
“Start with enzyme immunoassay-based tests with a reflex to PCR test for discordant enzyme immunoassay results.” Rationale: “PCR is quite sensitive for the presence of toxigenic C difficile, it may increase the detection of asymptomatic colonization and shedding.” (K Rao, PDR Higgins. Inflamm Bowel Dis 2016; 22: 1744-54.)
In a recent study (C Canova et al. J Pediatr 2018; 198: 117-20) from Padua, Italy compared 1233 individuals with celiac disease to a comparison group of 6167 (from a population-based cohort of >200,000 individuals). In this longitudinal study with a maximum followup, the authors found no increase risk of fractures in youths diagnosed with celiac disease (HR of 0.87).
22 individuals had fractures compared to 128 in the reference population
Median age of celiac diagnosis was 6 years
While celiac disease is linked to osteoporosis, “the vast majority of individuals with childhood celiac disease are likely to heal shortly after the introduction of a gluten-free diet.”
My take: Institution of a gluten-free diet for children with celiac disease likely removes the risk of osteoporosis.
Related blog posts:
Good News for Celiac Disease –Gastroenterology 2010; 139: 763. Mortality NOT worsened in undiagnosed celiac disease (identified by review of serology) in Olmstead County, though bone density decreased. n=129 of 16,847. (?milder cases undiagnosed)
A clinical review, “Antibiotics in IBD: Still a Role in the Biological Era?” (O Ledder, D Turner, Inflamm Bowel Dis 2018; 24: 1676-88). While this article provides a detailed review of the use of antibiotics for Crohn’s (including perianal disease), Ulcerative colitis and the effects on the microbiome, the potential use for very early onset (VEO) IBD caught my attention:
“We have recently begun considering oral vancomycin and gentamicin as sole firstline therapy in the rare form of infantile (ie <2 years of age) mild to moderate IBD, with promising success…this is merely investigational” at this time. (Ref: Lev-Tzion R et al. Digestion 2017; 95: 310-13).
My take: Antibiotics can be a helpful adjunct therapy in both Crohn’s disease and Ulcerative colitis. It is unclear what role antibiotics will have for VEO-IBD.
A recent commentary (R Khanna et al, Inflamm Bowel Dis 2018; 24: 1619-23) examines the role of biomarkers. While much of this topic has been reviewed extensively, I found the part about calprotectin helpful. One of the topics with discrepant data has been the negative predictive value of calprotectin for detecting inflammatory bowel disease. The data in this review:
From a meta-analysis in patients with symptomatic ulcerative colitis, calprotectin had a sensitivity of 0.88 and specificity of 0.79 compared to endoscopic inflammation. For Crohn’s disease, the respective values were 0.87 and 0.67.
For histologic remission in ulcerative colitis, a study found that with a threshold of 155 mcg/g, calprotectin had a sensitivity of 78% and specificity of 71%.
Another study suggested that values <100 mcg/g indicate quiescent disease, values 100-250 suggest possible active inflammation, and values >250 mcg/g suggest active inflammation.
A cross-sectional study indicated that calprotectin ≥57 mcg/g had a sensitivity of 91% and specificity of 90% to identify endoscopically-active disease (Gastroenterol 2016; 150: 96-102)
My take: Sensitivity/specificity vary greatly based on the likelihood of disease; in populations at lower risk for IBD, a calprotectin has a high level of excluding active inflammation/IBD. In populations with IBD, levels more than 250 mcg/g indicate a high likelihood of active inflammation whereas levels between 100-250 are indeterminate.