Tag Archives: eosinophilic esophatitis

NASPGHAN Postgraduate Course 2014 -3rd Module

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This blog entry has abbreviated/summarized the presentations. Though not intentional, some important material is likely to have been omitted; in addition, transcription errors are possible as well.  All of the speakers had terrific presentations.  The course syllabus is attached:

PG Course Syllabus 2014

The 3rd Module had a “potpourri” of GI problems.

Extraesophageal Manifestations of Gastroesophageal Reflux –Ben Gold, MD (GI Care For Kids, Atlanta) (pg 86)

“Is reflux really the scurge of the earth and the cause of every malady known to human-kind in the head, neck, and lungs…?“

Key points:

Airway protection: “Aerodigestive disease reflexes are intact by 38 weeks gestation.”

Central deglutition apnea: a normal protective mechanism to prevent aspiration during swallowing. (Hasenstab KA, Jadcherla, S. J Pediatr 2014; 165:250-255).  No proof at present that central apnea is caused by reflux though there is a biologic plausibility.

“Although reflux causes physiologic apnea, it causes pathologic apneic episodes in only a very small number of newborns and infants.”  “When reflux causes pathological apnea, the infant is more likely to be awake and the apnea is more likely to be obstructive in nature.”

Laryngeal Reflux:

  • Chronic cough, chronic laryngitis, hoarseness, and asthma may be associated with GERD BUT the data showing a relation between reflux and upper airway disease are weak
  • Airway symptoms attributed to reflux in adults include hoarseness, chronic cough, and globus sensation
  • Affected adults rarely have typical reflux symptoms
  • The sensitivity of laryngoscopic findings to identify reflux disease are poor. Sherman et al. Am J Gastroenterol. 2009;104:1278-95. Vandenplas et al. J Pediatr Gastroenter Nutr. 2009;49:498-547.

Asthma:

“Chronic cough, chronic laryngitis, hoarseness and asthma are multifactorial disease processes and acid reflux can be an aggravating cofactor.” GER is an unlikely contributor to asthma if reflux testing is negative.

“Two NIH-funded blinded, randomized placebo-controlled trials (RCT), one in adults (using esomeprazole), one in children (using lansoprazole) showed NO difference in asthma outcomes comparing placebo and acid suppression therapy”

Multi-Channel Intraluminal Impedance/pH probe studies: Pediatric studies are critically needed to determine if knowing the amount of nonacid reflux changes treatment or outcome

Proton Pump Inhibitors can cause gastric bacterial overgrowth (Rosen R et al JAMA Pediatr 2014; JAMA Pediatr. doi:10.1001/jamapediatrics.2014.696)

Ben Gold (speaker) and Jay Hochman prior to 5K Run

Ben Gold (speaker) and Jay Hochman prior to 5K Run

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EoE: PPI, PPI-REE, TCS, OVB, SFED, 4FED….…Alphabet Distress — Sandeep K Gupta, MD (Indiana University) pg 105 in Syllabus

Treatment endpoints discussed -histologic, symptomatic, fibrosis, etc.

  • Proton pump inhibitor responsive eosinophilic esophagitis (PPI-REE) may work by blocking STAT6 binding to Eotaxin-3 promoter rather than by acid suppression (PLos ONE 2012;7:e50037).  PPIs work (eos <6/hpf) in in 30-40%.  May need high dose to work long-term (Dr Molina-Infante – DDW 2014)
  • Topical corticosteroids (TCS) -higher dose = better response.  (Budesonide. Gupta SK, Vitanza J, Collins, MH Clin Gastro Hepatol 2014 [ePub], Fluticasone. Butz BK. Gastroenterology 2014). Clinical symptoms do not correlate with histologic response. Discussed long term safety concerns.
  • Reviewed diets -elemental, targeted, 4-food elimination and 6-food elimination.

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“Gotta keep on movin”: New tricks and treatments for motility disorders –Carlo DiLorenzo (Nationwide Children’s Hospital) pg 116 in Syllabus

Key points:

  1. Most important motility study is a normal study.  If normal study, then there is more concern for sensory dysfunction.   Look for significant findings on motility studies not minor changes.
  2. Key to confirm if motility disorder is present. Hx/o small intestinal transplant in medical child abuse/Munchausen syndrome by proxy (Trans Proc 1996; 28: 2790)
  3. New tool: wireless motility capsule (J Pediatr. 2013;162:1181-7)
  4. Easier to obtain full thickness biopsies (Gastrointest Endosc 2011;73:949-54)

Treatments reviewed -“try everything”

  • prucalopride (JPGN 2014; 57: 197-203
  • cisapride -still available
  • lubiprostone (JPGN 2014;58:283–291)
  • linaclotide boxed warning not for <17 years of age –though has been used by motility specialists
  • cyproheptadine (J Pediatr 2013; 163: 261-7) –use in dyspepsia
  • fludrocortisone -used in orthostatic intolerance
  • augmentin -for small bowel motility (JPGN 2012;54: 780–784)
  • octreotide -for bowel motility
  • pyridostigmine (Colorectal Disease 2010 12, 540–548)
  • iberogast
  • botulinum toxin (Gastrointest Endosc. 2012 ;75:302-9)
  • treat bacterial overgrowth
  • surgery: Jube, GJ tube, ileostomy. “Every child with pseudoobstruction on TPN needs a gastrostomy and an ileostomy –(me, now)”
  • gastric electrical stimulation
  • emerging treatment: Elobixibat (for constipation) Expert Opin. Investig. Drugs

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What’s New in the Diagnosis and Management of Constipation –Manu Sood (Children’s Hospital of Wisconsin) -page 130 in Syllabus

Reviewed recent guidelines from NASPGHAN

“Miralax is considered a 1st line agent”

Outcomes in children with constipation:

  • Almost 50% of patients experienced at least one relapse in first 5 yrs.
  • Almost 20% of children were symptomatic at 10 yrs. follow up (Bongers ME, et al. Pediatrics. 2010)

Pointers:

  • Slow transit is common
  • Rectal compliance does not predict success with treatment. Van den Berg MM, et al. Gastroenterology 2009.  Patients with mega-rectum may have motility disturbance as well.
  • Success rates for antegrade continence enemas (ACE) 65% to 89%. Colon manometry can help predict ACE success.  Up to 40% may be able to stop ACE w/in 2 years

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Systemic Review of Dietary Treatments for Eosinophilic Esophagitis

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A recent analysis of the literature for dietary treatment of eosinophilic esophagitis (EoE) has been published (Gastroenterology 2014; 146: 1639-48). Only 33 references out of 581 screened were included, yielding 1317 patients (1128 children and 189 adults).

Key findings:

  • Elemental diets were effective in 90.8%
  • Six-food elimination diets were effective in 72.1%
  • Allergy test-directed diets were effective in 45.5%
  • Adults responded similarly to children to dietary interventions with remission in 67.2% compared to 63.3%.

Bottomline: This study reiterates the dietary response rates from multiple previous studies. The finding that adults respond similar to children is less well-recognized, perhaps because dietary treatments are used less often in adults with EoE.

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Looking behind and looking forward in EoE (part 1)

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Two important articles are provide additional insight into eosinophilic esophagitis (EoE).

In the first (Gastroenterol 2013; 145: 1230-36), the authors performed a retrospective review of the Swiss EoE Database (SEED). This SEED should not be confused with our SEED center (Home- The SEED Center of Atlanta– SouthEast Eosinophilic …).  While the database contains 783 EoE patients, only 200 who were followed by the senior author and had complete data were included.  The enrollment period dates back to 1989.

Demographics: 153 men, mean age 39 years old, 94.5% had dysphagia at time of diagnosis and 35.5% had chest pain.  66% had concomitant allergies.

Terminology: The authors defined strictures as low-grade if a standard 9 mm endoscope could pass but met resistance, intermediate if a 6 mm endoscope could pass, and high-grade if it could not be passed with a 6 mm endoscope.

Results:

  • 37.5% (n=75) had strictures (other endoscopic findings noted in Table 2)
  • Peak eosinophil count (median): 35 proximally and 28 distally
  • Figure 2 showed the evolution of endoscopic features based on diagnostic delay.  With increasing diagnostic delay, there developed a preponderance of a mixed fibrotic/inflammatory picture whereas in those whose symptoms were of much shorter duration, the endoscopic features were often inflammatory without fibrosis.
  • For example, if diagnostic delay was between 0-2 years, then fibrotic findings were noted in 46.5%; in contrast, 87.5% had fibrotic features if symptoms had been present for > 20 years.
  • Strictures increased from 17.2% in those without significant diagnostic delay to 70.8% in those with symptoms present for > 20 years.
  • The authors note that diagnostic delay was greatest in those who developed symptoms in the first decade of life.

Study limitations: The categorization of strictures is straightforward; however, newer tools like the EndoFlip can detect esophageal narrowing more accurately.  Other limitations are related to retrospective nature of study and its reliance on patient’s reported outcomes (subject to recall bias).  Thus, the estimation of diagnostic delay may be inaccurate.

Take home message:

This article reinforces the concept that the presentation of EoE changes with time and that the long-term consequence of untreated EoE is increasing fibrosis and stricturing of the esophagus.

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