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.

Breastfeeding: protection from asthma

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Good news for breastfed babies –breastfeeding may reduce risk of wheezing and asthma for several years (J Pediatr 2012; 160: 991-6).

In this prospective birth cohort study of 1105 infants from New Zealand, detailed feeding information was obtained at 3, 6, and 15 months which allowed calculation of breastfeeding duration. This information was correlated with information about wheezing and asthma collected at 2, 3, 4, 5, and 6 years.

Findings (after controlling for confounding variables):

  • Each month of exclusive breastfeeding was associated with significant reductions in asthma at all timepoints.  The effect was most prominent at younger ages.
  • The authors estimate that if every infant in the cohort had been exclusively breastfed for 6 months, that asthma would have been reduced by 50% at 2 years, 42% at 3 years, 30% at 4 years, 42% at 5 years, and 32% at 6 years.
  • In atopic children, the effects of exclusive breastfeeding are more pronounced.  In this study, exclusive breastfeeding for ≥3 months reduced asthma at ages 4, 5, and 6 by 62%, 55%, and 59% respectively.

The authors note that not all studies have found that breastfeeding improves asthma.  However, most of these studies reported outcomes in older children.

Related Posts:

Breastfed babies less likely to develop fatty liver

More evidence that breastfeeding improves cognitive development

Additional references:

  • -NEJM 2011; 364: 701, 769.  Living on a farm decreases risk of childhood asthma.
  • -Thorax 2009; 64: 604-9. Breastfeeding and asthma in children followed for 8 years.
  • -Br Med J 2007; 335: 815-20.  Longer time of breastfeeding does not reduce allergy/asthma. n=17,046 pairs of mother-infant (13,889 followed up at age 6.5yrs)

NAFLD Guidelines 2012

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Given the pervasiveness of Non-alcoholic Fatty Liver Disease (NAFLD), updated practice guidelines are worth a look (Hepatology 2012; 55: 2005-23, also in Gastroenterology 2012; 142: 1592-1609)).  While the review includes updated information on incidence, prevalence, risk groups, natural history, the focus remains on specific graded recommendations.

These AGA/AASLD/ACG guidelines do not recommend screening adults due to uncertainties surrounding diagnostic tests and treatment.  This includes high risk populations such as diabetics and bariatric patients.  In addition, unlike recent obesity guidelines from the AAP (Pediatrics 2007; 120: S164-192), these guidelines do not recommend screening children for NAFLD.

Specific management recommendations:

  • Exclude competing etiologies in patients with suspected NAFLD: iron studies, autoantibodies, Wilson’s, viral hepatitis, celiac serology, muscle disease
  • Consider liver biopsy in higher risk patients: metabolic syndrome patients, patients with higher NAFLD Fibrosis score, or before treatment
  • Serum/plasma CK18 is promising biomarker.  Not recommended for routine practice at this time.

Treatment Recommendations:

  • Weight loss (3-5%) helps steatosis and greater losses (up to 10%) may be needed to improve necroinflammation.
  • Metformin –not recommended for liver disease in NASH/NAFLD.
  • Pioglitazone can be used to treat steatohepatitis; however, “long-term safety and efficacy of pioglitazone in patients with NASH is not established.”
  • Vitamin E at 800 units/day improves liver histology in biopsy-proven NASH.  Not recommended without biopsy-confirmed NASH, in diabetic patients, or patients with cirrhosis.  Concern with Vitamin E in adults has been an association with increased all-cause mortality in some studies (but not in others).
  • Avoid alcohol in patients with NAFLD

Website to download PDF version:

http://www.gastro.org/journals-publications/news/societies-develop-new-nafld-clinical-practice-guideline

Another opinion on which patients to biopsy:

http://www.gastro.org/journals-publications/aga-perspectives/june-july-2012/should-we-routinely-do-liver-biopsy-in-nafld-patients

Related posts:

A liver disease tsunami

What do you know about the “exposome”?

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I had not heard of the term “exposome” until last week (Gastroenterology 2012; 142: 1403-4).  However, this term was coined in 2005 (Cancer Epidemiol Biomarkers Prev 2005; 14: 1847-50).    This term is meant to describe the environmental analog of the genome.

Particularly with the gastrointestinal tract, environmental exposures are often considered a cofactor in disease development.  While there has been an increased understanding of the role of genes in the development of disease, it is abundantly clear that environment exposures can independently cause disease or act as a ‘second hit.’  The gastrointestinal tract is exposed to fluids which contain a multitude of elements and microorganisms, and to foods with their variability in nutrients, microbes and pollutants.  Other environmental factors include smoking, ionizing radiation, noise, breastfeeding, medications, and antimicrobials.

This cited commentary explains how environmental scientists are trying to unravel the ‘exposome.’

  • Bottom-up strategy:  measure external sources of the individual exposome at multiple time points.  This strategy may benefit from improvement in informatics, remote & personal sensing devices.
  • Top-down strategy: examines internal milieu including blood, biologic specimens, and transcriptomics/proteonomics.  Early examples include distinct signatures associated with specific environmental exposures.

Both strategies require validation to understand how external exposures trigger internal changes and disease expression.  Promising fields in gastroenterology for the study of the exposome include IBD, gastrointestinal cancers, functional disorders, and even obesity.  It is likely that studies of the exposome will answer questions about why the frequency of so many diseases are changing much more readily than studies of the genome.

Related blog posts:

Eat your veggies…if you don’t want to get sick

Why are we seeing so many more cases

Additional references:

  • -PLoS One 2010; 5 e10746.  Novel associations between type 2 diabetes and specific chemical exposures.
  • -Nature 2006; 444: 1027-31.  Obesity-associated gut microbiome.
  • -BMC Med Genomics 2010; 3: 17.  Chemical factors associated with disease-related gene expression data.

Unknown unknowns for Hepatitis C

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“ [T]here are known knowns; there are things we know that we know.
There are known unknowns; that is to say there are things that, we now know we don’t know.
But there are also unknown unknowns – there are things we do not know, we don’t know.		 ”
—United States Secretary of Defense, Donald Rumsfeld February 2002

Reading a recent epidemiology article reminded me of the preceding referenced quote  (Hepatology 2012; 55: 1652-61).  This study took a close look at knowledge of being infected with hepatitis C virus (HCV) and what HCV infection may indicate.

The study identified 30,140 participants through the National Health and Nutrition Examination Survey (NHANES) conducted from 2001-2008.  The Centers for Disease Control (CDC) obtains nationally representative data on the health and nutritional status of noninstitutionalized civilians across the U.S.  NHANES uses a ‘complex, stratified, and mulitstage probability sampling design and collects information from approximately 5,000 persons per year using standardized household interviews, physical examinations, and testing of biologic samples.’

Participants 6 years of age or older who tested positive for anti-HCV antibodies were sent a report.  Out of the 30,140 participants, 393 (1.4%) had evidence of past or current HCV infection; 170 were available for the study investigators.  Only 49.7% were aware of HCV status prior to receiving NHANES letter.  Furthermore, only 3.7% were first tested for HCV because they or their doctor thought they were at risk for infection; most were tested as part of a routine exam (perhaps detected after elevated ALT values) (46.7%), due to symptoms (15.9%), or blood donation (9.7%).

Another aspect of the study was determining the participants’ understanding of HCV infection.  Correct responses to the HCV survey were more likely in individuals between 40-59 years of age, white non-Hispanics, and patients who had seen a doctor about their HCV infection.  Specific questions often answered incorrectly included the following:

  • whether HCV could be contacted by kissing –only 68% knew this was false
  • whether HCV could be transmitted sexually –only 64% knew this was true
  • whether HCV could be acquired during birth if mother had HCV –only 57% knew this was true

Take home points:

  • Risk-based screening for HCV will continue to fail.  Physicians may not elicit adequate information and patients may deny risky behaviors even if asked.
  • Approximately half of patients in this cohort were unaware of HCV infection.
  • Many misconceptions about HCV persist even among those who had received counseling.

Related blog posts:

Pediatric HCV Guidelines

HCV now more deadly than HIV

The cost of progress in treating Hepatitis C

Additional resource:

http://www.cdc.gov/hepatitis/RiskAssessment/  This website allows individuals to assess their risk for hepatitis.

TODAY is worrisome for a lot of tomorrows

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The TODAY study (NEJM 2012; 366: 2247-56 and editorial 2315-16) =Treatment Options for Type 2 Diabetes in Adolescents and Youth.

While the study has a catchy acronym, the findings are disturbing.  Eligible patients (n=699) were 10 to 17 years old were followed on average over 3.86 years; they were divided into three groups:

  • Metformin 1000mg BID –48% achieved primary outcome (glycated hemoglobin <8% for at least 6 months).
  • Metformin with lifestyle changes –53% achieved primary outcome.  The lifestyle counseling that patients received in the study likely exceeded the typical counseling that most patients receive in clinical practice.
  • Metformin with rosiglitazone (4mg BID) –61% achieved primary outcome.  While this group had the best glycemic response, this group also had the greatest increase in BMI.

Other findings:

Comorbid conditions were common:

  • Hypertension: at baseline in 81 (11.6%) and new cases during study 155 (22.2%)
  • Dyslipidemia (LDL): at baseline in 23 (3.3%) and new cases during study 49 (7%)
  • Triglyceridemia: at baseline in 127 (18.2%) and new cases during study 70 (10%)
  • Microalbuminurina: at baseline in 44 (6.3%) and new cases during study 72 (10.3%)

Frequent adverse events noted with medications (Table 2 in study): gastrointestinal symptoms noted in about half of all study participants in each group, rash noted in about 40%, and elevated LFTs in about 40%.

Take home messages (borrowed from editorial):

“Most youth with type 2 diabetes will require multiple oral agents or insulin therapy within a few years after diagnosis”

“Fifty years ago, children did not avoid obesity by making healthy choices; they simply lived in an environment that provided fewer calories and included more physical activity.”

“Public-policy approaches–sufficient economic incentives to produce and purchase healthy foods and to build safe environments that require physical movement…will be necessary to stem the epidemic of type 2 diabetes and its associated morbidity.”

Related posts:

Treating diabetes with surgery

Cardiovascular disease for the entire family

Staggering cost of obesity

Lower leptin with physical activity

Reasons for refeeding syndrome

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Refeeding syndrome (RFS) is defined as the potentially fatal shifts in fluid and electrolytes that may occur in malnourished patients who are abruptly refed either enterally or parenterally.  The biochemical hallmark is hypophosphatemia.  Other changes can include hypokalemia, hypomagnesemia, and thiamin deficiency.  RFS can worsen the prognosis of children with celiac crisis as well (JPGN 2012; 54: 522-5).

A chart review from Lucknow, India from Jan-Dec 2010, identified 5 cases of RFS among 35 celiac patients.  All were severely malnourished.  All had anemia, hypoalbuminemia, hypophosphatemia, hypokalemia, and hypomagnesemia.  All improved with initial caloric restriction followed by gradual escalation of caloric intake along with electrolyte supplementation.

This article shows that a variety of causes of malnutrition can lead to refeeding syndrome. Considering refeeding syndrome in any severely malnourished child may help improve the prognosis by altering the nutritional management.

Additional references:

  • Nutr Clin Pract 2012; 27: 34-40. Reviewed refeeding syndrome publications since 2000.  Hypophosphatemia occurred in 96% of cases (26 of 27).
  • Crit Care Med 2010; 14: R172-R178.  Refeeding syndrome with anorexia.
  • Nutrition 2010; 26: 156-67. Review of refeeding syndrome treatment.
  • Nutr Clin Pract 2008; 23: 166-71.  Death due to refeeding syndrome.
  • JPEN 1990: 14.1; 90-97. Refeeding syndrome review.
  • Crit Care Med 1990; 18: 1030-1033. Review.

Pediatric HCV Guidelines

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A useful recent article, ‘NASPGHAN Practice Guidelines for pediatric HCV’ (JPGN 2012; 54: 838-55) needs to be a handy reference.  However, given the rapid changes in the HCV field, it is likely that this reference will need to be updated soon to incorporate new information (eg. IL28b) as well as emerging therapies.

Highlights:

Epidemiology: 0.2% of children & 0.4% of adolescents are HCV-infected; primary mode is mother to child (vertical) transmission which occurs in 5-7% if mother not coinfected with HIV

Testing: For infants of HCV-infected mothers, check HCV antibody after 18 months or HCV RNA at younger ages.  Need two negative HCV RNAs to exclude infection (guidelines suggest checking 6 months apart).  Most individuals should be screened with antibody testing and confirmed with RNA test.

Screening for HCC (U/S, AFP): suggested only “for those with significant liver disease (ie. cirrhosis)” due to rarity of HCC in pediatric HCC.

Treatment:

  • Not if patient younger than 3 years
  • Probably Pegylated-interferon with ribavirin –references for pediatric studies indicate response rates of about 50% for genotype 1 and about 80% for types 2 & 3.
  • Who should be treated? Not always clear.  Probably those with elevated aminotransferases or progressive disease based on liver biopsy.  Possibly those with mild disease to eradicate virus.
  • Dosing: ribavirin  15/kg/day divided twice daily; weekly PEG-IFN-α-2a 180 microgram/1.73 m2 or weekly PEG-IFN-α-2b 60 microgram*m2

Treatment monitoring (Table 8):

  • CBC/diff, Hepatic panel, glucose 0, 1, 2, 4, 8, 12 weeks, then every  4-8 weeks
  • T4/TSH 0, 12, 24, 36, 48 weeks
  • Urine HCG 0, 24 weeks (if female >12 years)
  • Prothrombin, Urinalysis at week 0
  • HCV RNA 0, 24, 48, 72 weeks

Anticipatory Guidance: “no legal requirement” to disclose HCV infection in U.S.; however, CDC suggests revealing this information to sexual partners (http://www.cdc.gov/hepatitis/hcv/)

  • Avoid sharing toothbrush, shaving equipment with household contacts, unprotected sexual activity with multiple partners, tattooing/piercing
  • Do not need to screen household or casual contacts

Special issues:

  • Vaccines: HCV patients should receive all standard vaccines
  • Obesity and alcohol both can worsen the outcome
  • Fetal scalp probes and prolonged rupture of membranes but not route of delivery may increase risk of HCV transmission
  • Breastfeeding is not contraindicated but should be avoided during mastitis/bleeding

Additional related blog links:

HCV now more deadly than HIV

The cost of progress in treating Hepatitis C

Increased ferritin predicts poor response in Hepatitis C

Curing Hepatitis C without interferon

Looking for trouble

Additional references:

  • –Hepatology 2011; 54: 1433. AASLD guidelines.  See teleprevir & boceprevir as well.-http://www.aasld.org/eweb/docs/hepatitisc
  • -Hepatology 2011; 53: 1468. PEG/RBV have minimal effect on QOL/cognitive/emotional outcomes, n=114.
  • -Gastroenterology 2011; 140: 389, 450-58. HEP-C STUDY. Comb RBV (15mg/kg div BID) & PEG-2a (180mcg/1.73m2 body surface q week) is better than PEG monotherapy. 53% SVR in combo group. Neutropenia in 40% –needed to reduce dose see below). “The Combination of Ribavirin and Peginterferon Is Superior to Peginterferon and Placebo for Children and Adolescents With Chronic Hepatitis C.”
  • -Hepatology 2009; 49: 1335. Comprehensive review and guidelines
  • -J Hepatology 2010; 52: 501-07. n=107. Pediatric study. Wirth et al. Efficacy of PEG alfa-2b (1.5/g/d) & RBV (15/kg/day): Genotypes 2/3 96% SVR, genotype 1 55%.
  • -JPGN 2006; 43: 499.  Study of PEG-IFN-α-2a in children.  dose BSA m2/1.73 x 180microgm weekly x 48 weeks.  6/14 (43%) had sustained response.  all genotype 1.  Article states that IFN (3/week) + RBV has now been approved by FDA for those over 3 years

PEG-Interferon Dosing:

Dosing adjustment from hep C study in children –needed in ~40%

PEG -2a
original: 180mcg/1.73m2
1. level 1: 135 mcg, level 2: 90mcg, level 3: 45 mcg

If ANC 750-999 week 1-2: level 1 adjustment, weeks >3: no adjustment
If ANC 500-749: week 1-2: hold dose ’til >750, then level 1; weeks >3, level 1 adjustment
If ANC 250-499: week 1-2, hold until >750, then level 2 adjustment, weeks >3, then hold ’til 750, then level 1 adjustment
If ANC <250, stop drug

If PLTs 35-49K, hold til >50, then level 1
If PLTs 25-34, hold til >50, then level 2
If PLTs <25, stop drug

If Hgb <10, reduce RIBA dose by 1/2 & increase dose when hgb>10
If hgb <8.5, stop RIBA

If indirect bili >5, stop drug.  If <2.5, restart dose at one-half and if remains less than 2.5, can resume full dose after 4 weeks.

IF ALT 5-10 ULN, recheck in 1 week.  If stays high, level 1 adjustment.
IF ALT10 ULN for more than 1 week, then if drops to 5-10, level 1 but if remains >10 ULN, then stop drug.

Side effect frequency:
flu symptoms: 91%, h/a, 62%, GI symptoms 56%, injection pain 45%, muscle aches 36%, irritable 31%, fatigue 27%, rash 20%, itching 15%, anorexia 13%, trouble sleeping 11%, depression 4-12%

TNF-α antagonists and infections

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In our pediatric patients who receive tumor necrosis factor-α (TNF-α) antagonists, fortunately we see few infectious complications.  In older patients, infections are much more important source of morbidity.  The main TNF-α inhibitors in clinical use include infliximab, etanercept, adalimumab, and certolizumab. Two large studies help quantify this risk:

  • Grijalva CG et al. JAMA 2011; 306: 2331-39.
  • Strangeld A et al. Ann Rheum Dis 2011; 70: 1914-20.

The first study assembled retrospective cohorts between 1998-2007 with rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and psoriasis/psoriatic arthritis or ankylosing spondylitis (group 3).  This study’s acronym is SABER: Safety Assessment of Biologic Therapy. This data was compiled from 4 large US automated databases.  In total, there were 10,484 RA, 2323 IBD, and 3215 group 3 patients.  1172 serious infections were identified, mostly (53%) pneumonia or skin/soft tissue infections.  Among IBD patients, hospitalization rates were 10.91 (per 100 person-years) for TNF-α antagonists and 9.6 for comparison group.  The rates of hospitalization were similar in RA (8.16 with TNF-α antagonists) and lower in the group 3 patients (5.41 with TNF-α antagonists).   In all groups, baseline glucocorticoid use was associated with a dose-dependent increase in infections.  Overall, there was not an increase risk of hospitalizations with TNF-α antagonists compared with nonbiologic treatments.

The second cited reference examined patients from Germany with RA, enrolled in the RABBIT registry.  Data was available for 5044 patients.  There were 392 serious infections in this cohort with fewer infections noted after 3 years.  Risks for infection included age (>60), chronic lung or renal disease, history of serious infections, and treatment with glucocorticoids.  Treatment with 7.5-14mg conferred at relative risk (RR) of 2.1; treatment with ≥15mg conferred a RR of 4.7.  The rates of serious infections has an exponential change when risk factors are added together.  In Figure 3, estimated risk of serious infections for patients receiving ≥15mg  glucocorticoids along with three additional risk factors was 45% per year; with two risk factors the risk was approximately 20% and with one additional risk factor approximately 10%.

While these studies confirm significant risks of infections with biologic agents, the absolute risk is low particularly when other risk factors are not present.  In pediatric populations, glucocorticoids are the most prominent risk factor.  In addition, the risk of serious infections may be reduced by effective therapy.  In the SONIC study, serious infectious complications were less frequent in patients on combination therapy (infliximab and azathioprine) than with either monotherapy.  This result was likely due to the decreased need for glucocorticoids.

Additional references/relevant previous blogs:

  • NEJM 2010; 362: 1383. Sonic study. Combination AZA/IFX with greater efficacy. 56.8% remission in combo Rx.
  • -IBD 2008; 14: 721.  Pneumocystis jiroveci (carinii) w infliximab -review of 84 cases.  Dig Dis Sci 2007; 52: 1481-84.  PCP most likely to occur on average 3 weeks after 2nd infusion (possibly due to concommitant drug use)
  • -Gastroenterology 2008; 134: 929.  n=100 consecutive IBD patients with opportunistic infections.  Any of drugs associated w ~2.9 OR in adutls (greatest in >50yrs).  OR 14.5 when multiple immune drugs. Steroids more associated with Candida. AZA/6MP more with viral: HSV, VZV (shingles), CMV.  IFX less commonly with infections -though increased histoplasma and atypical mycobacterium
  • -Gastroenterology 2009; 136: 1182.  Review of biologics.
  • -IBD 2007; 13: 769.  Review of safety of wide range of biologics
  • –Clin Gastroenterol Hepatol. 2006; 5:621-30.  TREAT registry.  Steroids but not biologics associated with increased mortality risk.
  • Only one chance to make first impression

Look of improvement on an EoE diet

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In this month’s Gastroenterology, 50 adults with Eosinophilic esophagitis (EoE) were treated with a 6-food elimination diet (SFED) (Gastroenterology 2012; 142: 1451-1459).  Repeat endoscopy after 6 weeks determined responsiveness.  Histologic response was defined by having <5 eosinophils/high power fields (eos/hpf).  In 20 patients, reintroduction of foods followed by repeat endoscopy was undertaken.

After SFED, 32 (64%) had peak eosinophil counts <5 eos/hpf.  Symptom scores decreased in 94%.  After trigger food reintroduction, eosinophil counts returned to pretreatment values.  The changes are clearly visible in Figure 5.  The pictures are almost like the weight loss commercials on TV –striking improvement.  I contemplated putting in a scan of the Gastroenterology cover, but have not received permission from the publisher.  Check out this link to view it yourself:

http://download.journals.elsevierhealth.com/pdfs/journals/0016-5085/PIIS0016508512006257.pdf

Based on reintroduction, the foods most commonly associated with EoE were wheat (60%), and milk (50%).  Skin-prick testing predicted only 13% of foods associated with EoE.  In general, these study results mirror results from pediatric studies, with the exception that milk allergy has been found to be more common in some pediatric studies.

Only 20 patients completed the reintroduction process.  This process involved adding 1 food group every 2 weeks.  If the patient had symptoms during reintroduction or remained on regimen for 4 weeks, then  endoscopy with biopsies was performed.  If recurrence noted based on symptoms or histology, this required a 6 week washout before additional food reintroduction.  Of note, median time for recurrence of symptoms was 3 days after reintroduction.

Six foods: milk, wheat, eggs, soy, shellfish/fish, nuts.

This study shows that, as in children, adult EoE is predominantly a food-allergy disease

Related blog entries:

Eosinophilic Esophagitis -Six Food Group Diet

Guidelines for Eosinophilic Esophagitis

MicroRNA signature for eosinophilic esophagitis

The undiscovered country

Upper endoscopy useful for identifying Crohn’s disease

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In a large pediatric study, the value of upper endoscopy in detecting Crohn’s disease (CD) is evident (JPGN 2012: 54: 753-57).

While the majority of pediatric patients with suspected inflammatory bowel disease probably undergo both upper endoscopy and colonoscopy, the added value of upper endoscopy remains unclear.  In this retrospective study with 171 pediatric patients (70 with CD, 33 with UC, 68 Non-IBD), 11% of children with CD had the diagnosis established based “solely” on the finding of granulomatous inflammation in upper intestinal tract (along with clinical symptoms).

Other key findings:

  • Presence of histologic gastric inflammation in CD patients compared to control patients was significantly higher (p<0.0001) but not significantly higher compared to UC patients (p=0.19).
  • Duodenal inflammation was highly suggestive of CD compared with both UC and non-IBD patients.  This occurred in 19% of CD patients compared with 0% and 1% in the other groups respectively.
  • 21 children (30%) had granulomas identified in upper GI tract (19 in stomach).  In 8 (11%), the diagnosis was changed based on this finding.  Prior to histology, the tenative diagnosis: 2 UC, 4 IC, 2 non-IBD.
One curious finding was a the presence of “perianal abscess/fistula” with similar frequency in CD patients and UC patients based on their Table 2 Patient Characteristics.
Additional references:
  • -IBD 2009; 15: 1101-4.  Presence of UGI disease in IBD.
  • -JPGN 2007; 44: 653.  NASPGHAN report on discriminating/labelling UC vs. Crohn’s.
  • -JPGN 2002; 35: 636-40. Advocates panendoscopy for all new IBD.  Granulomas in 28% of EGDs & 71% of UC pts c some abnl on EGD; 82% Crohn’s c abnl EGD.
  • -JPGN 2005; 41: abstract 181 (page 549).  UGI identified granulomas in 15% that were not identified elsewhere.
  • -JPGN 2004; 39: 257-61. Diagnostic role of EGD for pediatric IBD.
  • Magnetic resonance enterography for Crohn’s disease