IBD Shorts July 2018

DJ Gracie et al. Gastroenterol 2018; 154: 1635-46. This study of 405 adults indicated that IBD triggers anxiety and that anxiety triggers IBD. Specifically: “Baseline CD or UC disease activity were associated with an almost 6-fold increase in risk for a later abnormal anxiety score (hazard ratio [HR], 5.77; 95% CI, 1.89-17.7).  In patients with quiescent IBD at baseline, baseline abnormal anxiety scores were associated with later need for glucocorticosteroid prescription or flare of IBD activity (HR 2.08; 95% CI, 1.31-3.30).”

RL Dalal, B Shen, DA Schwartz. Inflamm Bowel Dis 2018; 24: 989-96.  This review provides updated information on epidemiology, diagnosis, and treatment recommendations for pouchitis.

A Alper et al. JPGN 2018; 66: 934-6. Key finding: Celiac disease is “not increased in children with IBD compared with non-IBD children with gastrointestinal symptoms.”  False-positive tTG serology can occur.

AK Shaikhkhalil et al. JPGN 2018; 66: 909-14. The authors showed that using a quality-improvement effort, there was increase utilization of enteral exclusive therapy (EEN).  Baseline 5.was <5% and by completion of intervention, utilization increased to approximately 50%. The interventions to achieve this are specified in this article, including talking points.  EEN is described as “nutrition therapy.” Patients are offered oral EEN and if not adequate by 3-4 days, nasogastric feedings are initiated (~15%).  Interestingly, of those to complete EEN therapy, 97% did not need NG placement.

Pictures from Ameilia Island:

Amelia Island


Position Paper: Nutrition in Pediatric Inflammatory Bowel Disease

E Miele et al. JPGN 2018; 66: 687-708.

Full text linkNutrition in Pediatric Inflammatory Bowel Disease: A Position Paper on Behalf of the Porto Inflammatory Bowel Disease Group of the European Society of Pediatric Gastroenterology, Hepatology and Nutrition

This position paper from ESPGHAN makes a total of 53  recommendations and 47 practice points.  There are too many to summarize in this blog post, but I will highlight a few.


  • Due to insufficient data, we do not recommend routine measurement or supplementation of zinc and selenium in children with IBD (EL 2).
  • We recommend monitoring vitamin D levels in all children with IBD (EL 2).
  • We recommend monitoring folic acid annually (EL 2).
  • We do not recommend routine measurement or supplementation of vitamin B1, B2, B3, B6, B7 and vitamin C in children with IBD (EL 2).
  • We recommend folic acid supplementation (either 1 mg daily or 5 mg weekly) in children with IBD receiving MTX therapy (EL 2).
  • We recommend that either serum cobalamin levels or methylmalonic acid level in blood or urine should be measured in children with active ileal CD, children with ileal resection of >20 cm and UC children ileal pouch surgery at least annually (EL 4)

Enteral Nutrition:

  • EEN has the same efficacy as oral steroids in the induction of remission of children with active luminal CD (EL 1). EEN is recommended for a period of at least 8 weeks (EL 1).
  • The use of standard polymeric formula, with a moderate fat content, is recommended unless other conditions are present (eg, cow’s milk protein allergy) (EL 1).
  • Due to the highly demanding adherence, EEN should not be considered as an option for long-term maintenance therapy.
  • EEN is not efficacious in the induction and maintenance of remission of pediatric UC (EL 4).
  • PEN is a treatment option to maintain remission in selected patients with mild disease and low risk of relapse (EL 4).
  • A specific carbohydrate diet (SCD) for induction or maintenance of remission in pediatric IBD patients should not be recommended (EL 4). More evidence on the benefit of SCD from RCTs is needed before such a dietary restriction can be recommended to pediatric IBD patients

My take: This position paper provides a lot of useful information and makes some recommendations that are practical.  The use of diets for maintenance therapy does not receive a favorable view.

Related blog posts:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

“Eternal Nutrition” Therapy

NASPGHAN twitter feed (with links to enteral therapy podcasts) was probably a typo &/or autocorrect issue:

“Podcast series must! Eternal Nutrition as Primary Therapy for Crohn’s disease.

Related blog posts:

Why Does Enteral Nutrition Work for Crohn’s Disease? Is it due to the Microbiome?

A recent study (K Gerasimidis et al. Am J Gastroenterol advance online publication 3 November 2015; doi: 10.1038/ajg.2015.357. Full Text: Extensive Modulation of the Fecal Metagenome in Children With Crohn’s Disease During Exclusive Enteral Nutrition) finds that treatment with Exclusive Enteral Nutrition further reduces microbiome diversity compared to healthy controls. This was an unexpected finding as the authors state: “we would expect EEN treatment to normalize the perceived ‘dysbiotic’ microbiota toward a healthier state.”

Reference from KT Park’s twitter feed. Here’s the abstract:


Exploring associations between the gut microbiota and colonic inflammation and assessing sequential changes during exclusive enteral nutrition (EEN) may offer clues into the microbial origins of Crohn’s disease (CD).


Fecal samples (n=117) were collected from 23 CD and 21 healthy children. From CD children fecal samples were collected before, during EEN, and when patients returned to their habitual diets. Microbiota composition and functional capacity were characterized using sequencing of the 16S rRNA gene and shotgun metagenomics.


Microbial diversity was lower in CD than controls before EEN (P=0.006); differences were observed in 36 genera, 141 operational taxonomic units (OTUs), and 44 oligotypes. During EEN, the microbial diversity of CD children further decreased, and the community structure became even more dissimilar than that of controls. Every 10 days on EEN, 0.6 genus diversity equivalents were lost; 34 genera decreased and one increased during EEN. Fecal calprotectin correlated with 35 OTUs, 14 of which accounted for 78% of its variation. OTUs that correlated positively or negatively with calprotectin decreased during EEN. The microbiota of CD patients had a broader functional capacity than healthy controls, but diversity decreased with EEN. Genes involved in membrane transport, sulfur reduction, and nutrient biosynthesis differed between patients and controls. The abundance of genes involved in biotin (P=0.005) and thiamine biosynthesis decreased (P=0.017), whereas those involved in spermidine/putrescine biosynthesis (P=0.031), or the shikimate pathway (P=0.058), increased during EEN.


Disease improvement following treatment with EEN is associated with extensive modulation of the gut microbiome.

My take: We really don’t know why EEN works and we have a lot to learn about a ‘healthy’ microbiome.

Related blog posts:

Nutrition Symposium Georgia AAP (Part 1)

At this year’s nutrition symposium, Dr. Stan Cohen presented the latest information on nutrition and inflammatory bowel disease.  His entire presentation will be on the Nutrition4Kids website.  While I took a few pictures, my notes from his presentation were minimal, mainly because I had to give a talk afterwards.  He reviewed how the microbiome can be influenced by diet and that this in turn can result in phenotypic changes.  Specific complications from poor diet/nutrient deficiencies were discussed.  In addition, data from exclusive enteral nutrition and the specific carbohydrate diet were presented. Here are some slides from his lecture (also available at Georgia AAP Symposium Website):

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Related blog posts:


Head-to-Head: Nutritional Therapy versus Biological Therapy in Pediatric Crohn’s Disease

The best data to date: D Lee et al. Inflamm Bowel Dis 2015; 21: 1786-93. In this prospective study, the authors studied treatment initiation in children (N=90), comparing partial enteral nutrition (PEN, n=16), exclusive enteral nutrition (EEN, n=22), and anti-TNF therapy (n=52).


  • Clinical response, defined by PCDAI reduction ≤15 or final PCDAI ≤10, was achieved by 64% PEN, 88% EEN, and 84% anti-TNF.
  • Fecal calprotectin ≤250 noted in 14% PEN, 45% EEN, and 62% anti-TNF

Because of the discrepancy between EEN and PEN, the authors speculate that the “efficacy of EEN may be a consequence of elimination of table food rather than providing a uniquely therapeutic method of delivering nutrients.”  They note that “choice of formula has not impacted the efficacy of enteral nutrition.”

More extensive information on this subject: D Lee et al. Gastroenterol 2015; 148: 1087-1106.

Bottomline: Anti-TNF therapy was as effective or more effective than EEN. And, “for patients who prefer treatment with a nutrition-based therapy, EEN seems superior to PEN.”

Related blog posts:

Street Art, NYC

Street Art, NYC

N2U -Part 3: EoE, IBD, and Cystic Fibrosis

2015 N2U Syllabus & Presentations

EoE Dietary Pointers (Syllabus pg 83-94): Sally Schwartz, Valeria Cohran

  • Even with SFED, elemental supplements helpful
  • Drink elemental beverages from covered glass with straw (improves palatability)
  • Cross-contamination –big issue
  • Label reading critical

Related posts:

IBD EEN Pointers (Syllabus pg 95-102): Rebecca Pipkorn, Justine Turner

  • Polymeric formulas –most palatable and least expensive. Oral EEN is used costly/not covered
  • EEN particularly helpful with microperforation/flare-up presentation and with infections (eg. TB)
  • EEN induces mucosal healing and improved symptoms


  • Levin et al. Inflamm Bowel Dis. 2014;20:278-285.
  • Johnson et al. Gut 2006;55:356-361.
  • Sigall-Boneh et al. Inflamm Bowel Dis. 2014;20:1353-1360.
  • Wilschanski et al. Gut 1996;38543–548.
  • Critich et al. J Pediatr Gastroenterol Nutr. 2012;54: 298–305. NASPGHAN Guidelines


  • Enteral therapy offers an alternative to steroids in patients with CD
  • Has potential to improve growth and IBD symptoms
  • Avoids the side effects of steroids
  • Need further research:
  1. – Unclear of the mechanism
  2. – Unclear of the best protocol
  3. – No standard protocol for reintroduction of food

Related posts:

Cystic Fibrosis (Syllabus pg 34-50) Justine Turner

Case in point: 10 yo with CF and poor growth, hx/o DIOS, poor intake, and distention.  Family had refused tube feedings previously.

Key point: Long-term survival is linked to nutritional status

  • Zemel et al. J Pediatr. 2000; 137(3):374-380.
  • Stallings et al. J Am Diet Assoc. 2008; 108(5):832-839.
  • McPhail et al. J Pediatr. 2008; 153(6):752-757.
  • Sharma et al. Thorax 2001; 56:746-750.

Other Caveats:

  • Intervene early
  • Breast milk (often with supplements) is optimal for infants
  • Poor oral intake àcould need periactin and/or supplemental feeds
  • Discussion re: pros/cons of Gtubes (pg 47 in syllabus)
  • Psychology support

Nutrition Goals

  • – Normal growth and optimal nutritional status
  • – Ages 0-2 year: Weight for length >50th percentile
  • – Ages 2-20 year: BMI percentile at or above 50th percentile
  • – BMI for males:23
  • – BMI for females: 22

Nutritional assessment at every visit & review:

  • – Weight, length/height, weight for length, BMI, head circumference in infants
  • – Nutritional education & dietary counseling
  • – Review PERT
  • – Review need for micronutrient supplementation: fat soluble vitamins (A, D, E, K), Ca, Fe, Zn, Na (salt), essential fatty acids

PERT (Pancreatic enzyme replacement therapy):

  • Infants 2000-4000 U lipase with 120 mL breast milk or formula– Mouth care for infants (and breast feeding mother)
  • Children 500-2500 U lipase/kg per meal (≤10000 U/kg/day or ≤ 4000 U/g fat/day); half meal dose with snacks
  • Ideally taken with meals and orally
  • Microspheres preferred formulation
  • Acid blockade (used to optimize enzyme activity)
  • Gold standard to assess adequacy is 72h fecal fat collection

Cystic Fibrosis Related Diabetes

  • Rare before 10 years of age
  • Increases mortality risk 6-fold
  • Weight loss and pulmonary decline begin 2-4 years prior to
  • diagnosis of CFRD

Related posts:


Robie House (at Univ Chicago)

Robie House (at Univ Chicago)