gutsandgrowth

Pediatric Gastroenterology

gutsandgrowth

Does It Matter How Hard Your Poop Is?

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A recent study (MH Vriesman et al. J Pediatr 2017; 190: 69-73) with 1835 children examined the issue of stool consistency, comparing the Bristol Stool Scale (BSS) and the Questionnaire on Pediatric Gastrontestinal Symptoms-Rome III (QPGS-RIII). Most of the patients in this study were older children, with 803 (43.7%) age 8-12 years and 1032 (56.3%) ≥13 years.

Key findings:

  • Surprisingly (to me) there only slight agreement between BSS and QPGS-RIII for assessing stool consistency (κ = .046; P=.022).
  • With the BSS, hard stools (types 1 & 2) were reported more frequently than QPGS-RIII: 18.0% vs. 7.1%.
  • Both scales reported similar levels of functional constipation, 9.3% for BSS and 8.6% for QPGS-RIII. The presence of hard stools or painful defecation is only 1 of 6 Rome criteria for the diagnosis of functional constipation.

These results indicate significant variability in how often pediatric patients considered their stools hard based on the instrument (BSS vs QPGS-RIII).  The reason why there is fairly close agreement on functional constipation is due to the fact that Rome III criteria combine the presence of hard stools and painful defecation into a single criteria and the fact that there are multiple criteria needed.  “Not all children with hard stools have painful defecation and vice versa, with only 21% of children with painful defecation reporting hard stools.”

My take: This study suggests that painful defecation is more important to ascertain than if the stools are hard. In addition, this may explain why softening the stools as a stand alone strategy is not effective in many children.

Related study: S Muddasani et al. J Pediatr 2017; 190: 74-8.  This retrospective study showed that pelvic floor physical therapy was effective in the majority of children (n=64,mean age 8.7 yrs) with fecal incontinence due to pelvic floor dyssynergia. It is notable that there were only two physical therapists involved; thus, in order to replicate these results, one would need quite capable PTs.

Related blog posts:

Does Celiac Disease Increase the Likelihood of Clostridium difficile infections?

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Thanks to Mike Hart for the following reference:  Risk of Clostridium difficile in patients with Celiac Disease: A Population-Based Study B Lebwohl et al. AJG 2017; doi:10.1038/ajg.2017.400

Abstract

Objectives:

Patients with celiac disease are at increased risk for infections such as tuberculosis, influenza, and pneumococcal pneumonia. However, little is known about the incidence of Clostridium difficile infection (CDI) in patients with celiac disease.

Methods:

We identified patients with celiac disease based on intestinal biopsies submitted to all pathology departments in Sweden over a 39-year period (from July 1969 through February 2008). We compared risk of CDI (based on stratified Cox proportional hazards models) among patients with celiac disease vs. without celiac disease (controls) matched by age, sex, and calendar period.

Results:

We identified 28,339 patients with celiac disease and 141,588 controls; neither group had a history of CDI. The incidence of CDI was 56/100,000 person-years among patients with celiac disease and 26/100,000 person-years among controls, yielding an overall hazard ratio (HR) of 2.01 (95% confidence interval (CI), 1.64–2.47; P<0.0001). The risk of CDI was highest in the first 12 months after diagnosis of celiac disease (HR, 5.20; 95% CI, 2.81–9.62; P<0.0001), but remained high, compared to that of controls, 1–5 years after diagnosis (HR, 1.85; 95% CI, 1.22–2.81; P=0.004). Among 493 patients with CDI, antibiotic data were available for 251; there were no significant differences in prior exposures to antibiotics between patients with celiac disease and controls.

Conclusions:

In a large population-based cohort study, patients with celiac disease had significantly higher incidence of CDI than controls. This finding is consistent with prior findings of higher rates of other infections in patients with celiac disease, and suggests the possibility of altered gut immunity and/or microbial composition in patients with celiac disease.

Silver Bridge crossing Colorado River. Part of Grand Canyon’s Bright Angel Trail.

Therapeutic Drug Monitoring for Vedolizumab

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A recent observational study (N Williet et al. Clin Gastroenterol Hepatol 2017; 15: 1750-7) provides some important information about where we are heading with regard to therapeutic drug monitoring (TDM) with vedolizumab (VDZ).

This study enrolled 47 consecutive patients with either Crohn’s disease (CD, n=31) or ulcerative colitis (UC, n=16). In those without a clinical response at week 6, an additional dose of 300 mg of VDZ was administered at week 10.

Key findings:

  • VDZ levels were higher in responders than in nonresponders, which is in agreement with previous studies ( (NEJM 2013; 369: 711-21, NEJM 2013; 369: 699-710)
  • A low therapeutic drug level as early as week 2 (<24.5 mcg/mL) and at the end of induction (week 6) (<18.5 mcg/mL) was associated with the need for drug optimization within 6 months in all patients
  • All patients with a level <19.0 mcg/mL at week 6, regained a secondary response after optimization at week 10.
  • The authors note that in the GEMINI trial, anti-VDZ antibodies were detected in 56 of 1434 patients (3.7%).  In this cohort, no anti-VDZ were detected using the same methods.

My take: Low trough levels of VDZ at week 6 are associated with the need for drug optimization/increased dosing.

How to Talk About Childhood Obesity

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Pont SJ, et al. Pediatrics. 2017. doi: 10.1542/peds.2017-3034. A policy statement from the American Academy of Pediatrics addresses the issue of stigma associated wtih pediatric obesity.  This is summarized in the following links:

An excerpt form NY Times piece:

Dr. Pont is one of the lead authors of a new policy statement from the American Academy of Pediatrics titled “Stigma Experienced by Children and Adolescents With Obesity.” The statement, published online Monday in the journal Pediatrics, advises pediatricians to use neutral words like “weight” and “body mass index” rather than terms like “obese” and “fat.” …

In a study published earlier this year in the journal Preventive Medicine, Dr. Puhl and her colleagues looked at the longitudinal effects of teenagers being teased about their weight. The study involved over 1,800 people who had been followed for 15 years and are now in their mid 30s…

“These teasing experiences have long-lasting implications for health and for health behavior.” For women especially, these adolescent experiences of teasing by peers or family members were associated with binge eating, poor body image, obesity, and a higher B.M.I. 15 years later, she said; for men there were some of the same associations, including obesity as adults, if they had been teased by their peers as adolescents…

Weight stigma does exactly the opposite; criticizing and inducing shame only make people feel terrible about themselves, not motivated or capable of making changes…

“Recognize that a child is far more than what their weight is, praise them for all the positives, so when we get to some of the more challenging topics, they can still maintain their self-esteem,”…

The most effective way for parents to help a child is to make healthy changes for the whole family, regardless of shape or size, Dr. Pont said. Try making small changes slowly, like adding one new green vegetable into the family diet, not keeping sugary drinks in the home or walking to school instead of driving.

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Smoke in Grand Canyon after recent brush fires

Fatty Liver Disease with Craniopharyngioma and with Down Syndrome

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A recent retrospective study (SY Yung et al. Ann Pediatr Endocrinol Met 2017; 22 https://doi.org/10.6065/apem.2017.22.3.189 –thanks to Jeff Schwimmer for this reference) describes the problem of nonalcoholic fatty liver disease (NAFLD) in long-term survivors of childhood-onset (CO) craniopharyngioma.

This study reviewed 75 children with CO-craniopharyngioma who had surgery prior to 15 years of age. The mean followup was 4.3 years.

Key findings:

  • 51 had either elevated AST or ALT above 40 IU/L. ALT ≥60 IU/mL was observed in 15 patients.
  • Estimated prevalence of NAFLD based on mainly imaging was 47%. 27 underwent ultrasonography and 5 underwent CT scan.
  • Among those with available growth data, 41% were obese and 18% were overweight.
  • NAFLD developed within a year after surgery in many patients.

This study had many limitations, including reliance of ultrasonography for diagnosis and incomplete evaluations.  Despite this, it is clear that hypothalamic obesity places patients at a high risk for developing NAFLD.  In addition, NAFLD in this population may be more aggressive.

My take: This study documents the well-recognized phenomenon of NAFLD in CO-craniopharyngioma with obesity.  Current treatment relies on trying to preserve hypothalamic function and optimizing lifestyle/nutrition.

Briefly noted: D Valentini et al. J Pediatr 2017; 189: 92-7.  Using ultrasound in 280 Italian children with Down syndrome, the authors identified NAFLD in 45% of those considered nonobese and 82% of those overweight/obese. In a related commentary (pg 11-13 Full text: Down syndrome and Pediatric NAFLD …), the authors (AD Matteo, P Vajro) note that Down syndrome patients may have increased NAFLD due to less activity, more obesity including possible excess adiposity in those with normal BMI, obstructive sleep apnea, or perhaps other mechanisms.

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Autoimmune Liver Disease in Children with Sickle Cell Disease

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A recent retrospective study (S Jitaruch et al. J Pediatr 2017; 189: 79-85) documents the important association of autoimmune liver disease in children with sickle cell disease (SCD).  I have seen  children with hemoglobinopathy and autoimmune hepatitis.

Key findings:

  • 13 of 77 patients with SCD were diagnosed with autoimmune liver disease
  • 2 patients presented with acute liver failure
  • 6 patients had cholangiopathy on cholangiogram “suggesting autoimmune sclerosing cholangitis”
  • At median follow-up of 3.8 years, 5 achieved full remission, 4 partial remission, 1 had liver transplant, 1 died of subdural hemorrhage (prior to liver disease treatment), and 2 were lost to followup

My take: this report is a good reminder that though there are a good number of reasons for abnormal liver blood tests in children with SCD, it is important to follow these children closely and to obtain serology (including ANCA) in those with persistent elevations.

Related blog post: Blood is not enough

South Kaibab Trail at the basin of the Grand Canyon (Colorado River)

 

Cytosponge for Eosinophilic Esophagitis

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A recent prospective study (DA Katzka et al. Am J Gastroenterol 2017; 112: 1538-44 -thanks to Ben Gold for this reference) provided more information regarding the potential utility of the cytosponge for eosinophilic esophagitis (EoE); the cytosponge has been studied for Barrett’s esophagus.

Background: 86 adult patients were recruited; 6 could not swallow sponge.  In the remainder, 105 procedures were performed comparing the cytosponge to standard endoscopic biopsies. The cytosponge technique can be completed in ~5 minutes without sedation. “All that is required is centrifuging the cytosponge specimen in its preservative to create a pellet followed by routine paraffin embedding and processing.”

Key findings:

  • Cytosponge was considered to have adequate specimen in 102 of 105 cases, compared with 104 of 105 with endoscopic sampling
  • Using a cutoff of <15 eos/hpf for inactive disease, the authors found that the cytosponge had a sensitivity of 75% and a specificity of 86%.
  • Six patients had active EoE on cytosponge with negative endoscopic biopsies.
  • 14 patients with active EoE with endoscopic biopsies had <15 eos/hpf with cytosponge
  • No complications were noted with cytosponge.

The sensitivity of 75% is likely due to inadequate contact between cytosponge and esophageal wall which could be related to technique, especially in those with a normal caliber esophagus.

My take: The cytosponge appears to identify active EoE in the majority of adult patients.  In those with abnormal cytosponge, the likelihood of active EoE would be very high; as such, it could be a useful biomarker.  It is still probable that many with normal cytosponge result would need endoscopy due to suboptimal sensitivity.

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NEJM 2017; 377: e22. In this patient with lingual papillomas, hx/o melenoma, and both hyperplastic and adenomatous polyps, a genetic mutation identifying Cowden syndrome was identified.

Fatty Acid Intake and Risk of Ulcerative Colitis Flare

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A recent study (Barnes EL et al. Clin Gastroenterol Hepatol 2017; 15: 1390-6) found an association between the intake of certain fatty acids and the risk of an ulcerative colitis flare.  This is nicely summarized in the AGA Journals Blog.

Here’s the link: Does Consumption of Certain Fatty Acids Increase Risk of Ulcerative Colitis Flares?

Here’s an excerpt:

Diets with high levels of fatty acids such as myristic acid (found in palm oil, coconut oil, and dairy fats) increased risk of flare in patients with ulcerative colitis (UC), researchers report in the September issue of Clinical Gastroenterology and Hepatology. Their findings, from a prospective study of more than 400 patients in remission during treatment with aminosalicylates, could guide future studies of supplements or compounds that reduce risk of flares in patients with UC in remission…

Edward L. Barnes et al performed a prospective study of dietary patterns among 412 patients, from 25 sites, with UC in remission during monotherapy with an aminosalicylate (mesalamine, sulfasalazine, or balsalazide for at least 3 months before enrollment). Patients completed a validated food frequency questionnaire (on consumption of dairy, fruits, vegetables, eggs, meat, fish, cereals, breads, and starches, beverages, sweets, and baked goods) at enrollment and were followed for 12 months…

Forty-five patients (11%) had a relapse of UC within 1 year of study enrollment… In multivariable analysis, higher intake of myristic acid (odds ratio, 3.01) and alpha linolenic acid (odds ratio, 5.50) were associated with increased risk of relapse, although a dose–response relationship was retained only for myristic acid intake.

Other foods previously implicated in flares of UC, such as processed meat, alcohol, and foods high in sulfur, were not associated with an increased risk of flare.

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From Andy Warhol Exhibit at the High Museum