Category Archives: Pediatric Gastroenterology Intestinal Disorder

Extent of Eosinophilic Esophagitis and Response to PPI Therapy

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DA Hartnett et al. Clin Gastroenterol Hepatol 2026; 24: 375-384. Open Access! Distribution of Esophageal Eosinophilia as a Predictor of Proton Pump Inhibitor Response in Eosinophilic Esophagitis

Methods: This was a retrospective cohort study of newly diagnosed adult patients with EoE — All patients received ≥8-week PPI trial and underwent repeat biopsies to assess response. There were including 66 with isolated distal and 200 with proximal/diffuse disease. 86% of patients received twice daily PPI therapy (73% in those with isolated distal disease and 87% in the diffuse/isolated proximal disease.

Key findings:

PPI response was higher among patients with isolated distal disease:

  • histologic remission [<15 eosinophils/hpf post-PPI]: 63.6% vs 44.5%; P = .01
  • deep remission [<6 eosinophils/hpf]: 54.5% vs 31.0%; P = .001
  • symptom improvement: 92.4% vs 81.0%; P = .03).

The discussion noted that there has been limited studies of EoE distribution and response to treatment. “Godat et al observed that the distribution of esophageal eosinophilia had no impact on clinicohistologic remission rates (defined as ≤2 on a scale of 0–10 for dysphagia/odynophagia in the last 7 days and a peak eosinophil count <5 eos/hpf) in patients treated with budesonide orodispersible tablets.19“

“The generally higher PPI response with isolated/predominant distal disease suggests that acid suppression and improved mucosal barrier function likely play a key role in how PPI may lead to EoE remission…prior studies have demonstrated no correlation between findings on ambulatory pH monitoring and PPI response in EoE.25 Therefore, the differential response to PPI based on eosinophil distribution phenotypes may be due to more than comorbid GERD alone.”

My take: While the pathophysiology of how PPIs work for EoE is unclear, it appears that the response to PPIs is better with in those with isolated distal EoE. The difference in response may have been even more pronounced if both groups had a similar percentage of receiving twice daily PPI treatment.

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Prospective Study: Acute Gastroenteritis Increases Risk of Disorders of Gut-Brain Interaction

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A Palorath et al. Am J Gastroenterol 2026; 121: 242-247. Acute Gastroenteritis Is a Risk Factor for the Development of Disorders of Gut-Brain Interaction in Children

Methods:  A prospective, controlled, cohort study. Children (1-15 years) with recent AGE (cases) and siblings (controls) were followed for 6 months. We assessed DGBIs using a validated questionnaire (QPGS IV) per Rome criteria. Patients with underlying GI disorders (eg. Celiac, IBD, recent abdominal surgery) were excluded.

Key findings:

  • Among children without a history of DGBI before the AGE, 6 (12.2%) cases vs 0 control were diagnosed with DGBI (P = 0.01) at follow-up at 3 months
  • At 6 months, 5 cases (1 lost to follow-up) vs 0 control had persistent DGBI (P = 0.03)
  • Severity of AGE was correlated with PI-DGBI. Severe AGE included abdominal pain, ED consullt, and need for IV fluids

My take: It is well-known that previous AGE increases the risk of PI-DGBIs, especially irritable bowel syndrome. However, this is the first prospective cohort study showing this association between AGE and DGBIs in a nonoutbreak setting. In addition, it correlates the risk of DGBI with the severity of AGE.

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Chronic Nonbacterial Osteomyelitis Associated with Pediatric Inflammatory Bowel Disease

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M Matar et al. J Pediatr Gastroenterol Nutr. 2026;82:487–494. Chronic nonbacterial osteomyelitis associated with pediatric inflammatory bowel disease: : A multicenter retrospective study from the Paediatric inflammatory bowel disease Porto Group of ESPGHAN

Methods: Retrospective study with 45 pediatric patients with inflammatory bowel disease (n=32 with Crohn’s disease, n=8 with ulcerative colitis, n=5 with IBD-U)

Key findings:

  • CNO presented in 15 patients (33%) within 3 months of IBD diagnosis, and in additional 20 (44%) patients after IBD diagnosis; in 10 (22%) patients CNO preceded the diagnosis of IBD with a median time 46 (25–248) weeks
  • 11 (24%) subjects displayed at least one additional extra-intestinal manifestations, including arthritis (6, 13%), erythema nodosum (4, 9%), sacro-ileitis (2, 4%), psoriasis (1, 2%), and pyoderma gangrenosum (1, 2%).
  • Complications occurred in six patients and included vertebral collapse, bone fracture, and bone deformity. In eight (18%) subjects vertebral collapse was present already at the time of diagnosis.
  • “While in most patients, diagnosis of CNO was associated with either clinical or laboratory indices of active IBD, especially CD, in some cases, the intestinal disease was quiescent.”
  • “All patients achieved remission of CNO at some point during follow-up, which may support the hypothesis that anti-TNF treatment is unlikely to promote CNO development and does not reinforce the theory of a paradoxical effect that has been suggested by Cordesse et al.22“

My take: This is a useful review highlighting the association of CNO with both active disease and quiescent IBD. The authors argue that their data does not support the development of CNO as a paradoxical effect. I disagree with this premise. Many of the extraintestinal manifestations, that anti-TNF agents can treat, rarely can be caused by them. Besides CNO, paradoxical reactions to anti-TNF agents have included the development of rheumatoid arthritis, psoriasis, hidradenitis suppurativa and autoimmune liver disease.

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QI Project: Increasing H Pylori Eradication

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KR Arellanos et al (Senior Author S Bonilla). JPGN Reports. 2026;7:19–27. Standardizing a protocol for Helicobacter pylori gastric biopsy culture: From implementation to sustained practice

Background: “The availability of antibiotic susceptibility data is essential for understanding local and regional resistance patterns and for informing future guidelines on optimal treatment regimens for children.” This quality improvement project report documents how “using a standardized checklist, in combination with educational initiatives for staff physicians and collaborative efforts with endoscopy and laboratory teams, were effective strategies to increase the use of gastric biopsy culture as a diagnostic tool for H. pylori infection and, to a lesser extent, to improve culture yield in patients with positive histology.”

Key steps:

  1. Standardized checklist for biopsy collection used by nurses
  2. Standardized transport protocol
  3. Prompt refridgeration/transportation
  4. Using a single lab for testing (Mayo clinic)

Key findings:

  • There was a consistent increase in culture positivity for H pylori and this was associated with improved eradication rates
  • Overall, antimicrobial resistance was highest for metronidazole (27.5%) and clarithromycin (18.7%), and lower for rifampin (12.2%), levofloxacin (10.1%), and amoxicillin (4.3%). Only one isolate showed resistance to tetracycline

Discussion: “Among the various interventions implemented during the QI project, the one that appears to have contributed most significantly to the dramatic improvement in culture yield among patients with H. pylori-positive histology was the consolidation of specimen processing to a single specialty laboratory [Mayo clinic].” Specific logistics included using a simple sterile container with saline-moistened tissue for collection and sending samples to specialty lab on the same day as collection.

My take: During this project, there was improved use of gastric culture and in culture yield. This resulted in meaningful improvement for patients. However, without clinical leadership to implement these changes, there will continue to be suboptimal eradication rates at other centers.

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How to Improve the Value of Biologic Infusions: Reduce Lab Testing and Frequency

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T Shah et al. JPGN Reports 2026;1–5. Responsible laboratory surveillance of pediatric patients with inflammatory bowel disease on biologic infusion therapy

This retrospective single-center study with 34 pediatric patients with inflammatory bowel disease examined the laboratory costs (2020-2021) associated with monitoring biologic therapy.

Methods: “Routine laboratory studies were defined as those part of the standardized infusion protocol at SBCH and were obtained with each scheduled infusion. The following laboratory studies were considered routine/standard: complete blood count with differential, basic metabolic panel, liver function tests, amylase, lipase, erythrocyte sedimentation rate, C-reactive protein, vitamin D, iron, ferritin, vitamin B12, folate, urine hCG (if a subject was female). Other laboratory studies that were collected, but not considered routine studies included QuantiFERON-TB, and biologic drug and antibody level.”

Key findings:

  • The average hospital charge for studies obtained per infusion was $1308.36 with an average annual cost of $9543.44 per patient
  • Fifteen (6%) instances of change in clinical management were found. “Only a limited subset of the 15 laboratory studies included were utilized in making changes: biologic drug, Vitamin D, and iron level”
  • During the study, 248 infusions were administered with a “total annual charge amongst all patients in the study was $324,447”

Discussion:

  • “Our study population had well controlled disease as evident by low PCDAI and PUCAI scores…Our observations suggest the utility of routine laboratory surveillance at each biologic infusion is minimal, favoring decreased testing for IBD patients, especially those in clinical remission.”
  • “We propose obtaining laboratory tests twice a year, or with every third infusion, for patients with mild disease or in remission based on their disease activity index scores. In our small cohort of patients, this change in practice would reduce the total annual costs by 66% ($214,154.82)”

My take: It has been my practice, for most patients with IBD, to obtain labs with every other infusion (~3 times per year). Typically, I will obtain a CBC/d, CMP and CRP and obtain other labs like Vit D, GGT, Quantiferon Gold and drug level monitoring less frequently. I rarely check Vit B12, ESR, Folate, Amylase, and Lipase.

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician. Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure. 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.

VedoKids Study: Vedolizumab for Extraintestinal Manifestations of Inflammatory Bowel Disease

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G D’Arcangelo et al. J Pediatr Gastroenterol Nutr. 2026;82:495–502. Open Access! Vedolizumab for extraintestinal manifestations in pediatric inflammatory bowel disease: Results from the VedoKids study

Background: “Since vedolizumab is a gut-selective anti-α4β7 integrin, its effect on EIMs has been a matter of debate, with relevant data lacking in pediatric IBD. A systematic review, which included three interventional studies, five non-interventional studies, and three case series, concluded that there is insufficient evidence supporting the efficacy of vedolizumab for treating pre-existing EIMs in adults.3“

Methods: This was a subgroup analysis of the pediatric VedoKids cohort, a multicenter, prospective “real-life” study of children (aged 0–18 years) with IBD treated with vedolizumab and followed through 54 weeks.

Key findings:

  • EIMs were identified in 18/142 (12.6%) children at baseline
  • Children with EIMs had an average age of diagnosis of 9 yrs compared to 12 yrs in those without EIMs
  • Children with EIMs had higher rate of pancolitis in UC and ileocolonic distribution in CD
  • Prior anti-TNF medication was noted in 16 (89%) of EIM cohort compared to 74 (60%) of non-EIM cohort
  • Concomitant medications were administered in 72% of EIM cases and to a similar number of non-EIM patients. For EIM patients, ASA were given in 7, steroids in 10, thiopurines in 4 and methotrexate in 2
  • Children with EIMs had more active disease (see below)
  • EIM resolution rate of 89%, mainly occurring within the early weeks of vedolizumab treatment

My take: While this study has several limitations, including the high rate of concomitant medications, it shows that most patients receiving vedolizumab had resolution of their EIMs. In addition, it shows that patients with EIMs had a more severe IBD phenotype.

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Pediatric Data for Mirkizumab –SHINE-1 Trial

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Briefly noted:

Jess L et al. The Lancet Gastroenterology & Hepatology 2025; 11: 100 – 109. Efficacy and safety of mirikizumab in paediatric participants with moderately-to-severely active ulcerative colitis (SHINE-1): a multicentre, open-label, non-randomised phase 2 trial

Background: Mirikizumab, a immunoglobulin G4 monoclonal antibody, targets the p19 subunit of IL-23, with demonstrated efficacy and safety in adults with ulcerative colitis and Crohn’s disease.

Methods: This 52-week, multicenter, open-label, non-randomized, phase 2 study enrolled pediatric participants (n=26, 2 to <18 years) with moderately-to-severely active ulcerative colitis with inadequate or loss of response or intolerance to corticosteroids, immunomodulators, biologics, or JAK inhibitors.

Key findings:

  •  At week 12: 18 (69·2%) participants had a clinical response by modified Mayo score (mMS), ten (38·5%) achieved clinical remission by mMS, 14 (53·8%) achieved endoscopic remission
  • At week 12: 20 (76·9%) of the 26 participants had a clinical response based on Pediatric Ulcerative Colitis Activity Index (PUCAI), and ten (38·5%) achieved clinical remission at week 12
  • At week 52: 14 (53·8%) of 26 participants achieved mMS-based clinical response, ten (38·5%) were in mMS-based clinical remission, ten (38·5%, 95% CI 22·4–57·5) of 26 patients were in endoscopic remission
  • At week 52:  14 (53·8%) had a PUCAI-based clinical response and 13 (50·0%) were in PUCAI-based clinical remission
  • Three (12%) participants experienced serious adverse events across induction and maintenance periods (non-infective appendicitis, worsening of ulcerative colitis, and pseudarthrosis), of which one (worsening of ulcerative colitis) led to study discontinuation

My take: In this pediatric population with high prior advanced therapy exposure, there was a good response to mirikizumab. This trial which was limited by a lack of an active comparator group was started prior to the medication approval in adults. Overall, the IL-23 class of medications has emerged as an effective drug class for inflammatory bowel disease.

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    Use of Neostigmine as Adjunct for Manual Disimpaction

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    M Mostavi, S Lee, V Martin. JPGN Reports. 2026;7:55–58. When manual disimpaction isn’t enough: Case report and review of neostigmine’s role in refractory constipation management

    This was a case report of a 21 yo with  chronic constipation and likely undiagnosed autism spectrum disorder hospitalized for severe fecal retention, unresponsive to nasogastric polyethylene glycol. He underwent a manual disimpaction but due to residual stool in more proximal colon, Neostigmine was administered with good results.

    Methods: “The patient underwent manual disimpaction under general anesthesia with a large amount of hard stool removed from the rectum. He was noted to have ongoing abdominal distension with significant palpable stool more proximally. A trial of 1 mg intravenous (IV) neostigmine was given. This was done without anticholinergic co-administration due to his persistent tachycardia (HR ~ 120 s) and with close heart rate monitoring. Passive passage of stool occurred within 5 min of drug administration. Subsequently, neostigmine was titrated in additional 1 mg IV doses every 3–5 min. His heart rate remained above 90bpm. He received a total of four doses of neostigmine over 20 min. Each administration, combined with abdominal massage, produced large amounts of soft stool along with marked reduction in distension and palpable stool burden. 

    Before NG cleanout and disimpaction:

    After NG cleanout and disimpaction/Neostigmine:

    Pharmacokinetics:

    ” Neostigmine has been clinically utilized by anesthesiologists to reverse the effects of non-depolarizing neuromuscular blocking agents…In the gastrointestinal (GI) tract, the accumulation of acetylcholine in the neuromuscular junction of the small intestine and colon results in increased contractility and peristalsis, thus promoting defecation. Neostigmine is predominately administered intravenously with typical dose ranges from 0.03 to 0.07 mg/kg, up to maximum 5 mg. The peak effect typically occurs between 7 and 10 min, while the duration of action lasts approximately 55–75 min in adult patients…

    Because of its cholinergic effects on the muscarinic receptors of the cardiac parasympathetic nervous system, neostigmine results in a significant decrease in heart rate. Therefore, when neostigmine is bolused to reverse non-depolarizing paralytics at the clinically appropriate dose (~3–5 mg IV), it is always co-administered with glycopyrrolate or atropine to prevent bradycardia at a 1:1 volume ratio.”

    My take (borrowed from authors): “This case demonstrates that intravenous neostigmine can be a safe and effective adjunct to manual disimpaction in severe refractory constipation when administered in a monitored setting.”

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    Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician. Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure. 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.

    Why Are Kids in U.S. Picky Eaters?

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    Helen Zoe Veit, NY Times 2/15/26: There’s a Reason American Kids Are Such Picky Eaters:

    An excerpt:

    In historical documents of all kinds, from medical treatises to diaries to school records, Americans described children as curious omnivores who appreciated bold flavors and interesting textures…

    This was unrelated to socioeconomic status — children at every income level happily ate a diversity of foods. But today, appreciation of sharp and varied flavors can be hard to find among American kids. Parenting message boards are filled with questions about getting reluctant children to eat vegetables, and kids’ menus across the country offer dishes aimed at narrow palates.

    Many adults assume that prolonged pickiness is a hard-wired stage and that kids naturally dislike many foods. But mass childhood pickiness is a modern phenomenon created largely by junk food companies that marketed products like sugary cereals as food specifically for children, convincing Americans that kids need different, easily likable foods...widespread pickiness didn’t exist until the 20th century. Before then, kids sometimes disliked individual foods, just as some adults did. But people in earlier eras didn’t think that pickiness was related to age.

    All this changed as food companies like General Foods and Nestlé poured money into designing products in laboratories to target humans’ biological instincts and make their foods very hard to refuse. By the mid-20th century, thousands of seductively sweet, salty and crunchy factory foods crowded grocery shelves, and many of them were marketed aggressively to children — from Goldfish crackers to SpaghettiOs…

    Junk food companies also started pushing portable, calorie-dense snacks…

    As marketers glorified personalized eating, family eating habits fractured. Before the mid-20th century, most family meals centered on communal food. But as kitchens filled with shelf-stable products, many Americans stopped sharing food in the same way. One 1950s mother noted that she ate whole-wheat bread, her husband ate rye bread, and her children ate white bread…Cooking had also transformed. As more food was processed in factories, meal preparation could mean warming up or even just assembling. It suddenly became feasible to “cook” separate meals for different family members...

    We’ve been told that urging kids to eat any particular dish can cause lasting aversions and dysfunctional relationships with food...

    Parents can warmly encourage children to eat family foods and avoid offering alternatives. They can also counter corporate marketing with their own enthusiastic messages about the foods they love to eat, whether it’s a crunchy salad or slippery green olives.

    My take: The advice in this article is not for everyone – especially for patients with ARFID, sensory processing disorders, and autism. Also, this problem is not solely related to ‘big food’ marketing. There are other factors shaping our eating habits. For example, one factor for many households, especially if both parents are working, is less time for meal preparation.

    Some books that may be helpful for families working through these issues:

    • Laura Jana and Jennifer Shu: Food Fights: Winning the Nutritional Challenges of Parenthood
    • Ellyn Satter: Child of Mine and Secrets of Feeding a Healthy Family
    • Keith E. Williams and Laura J. Seiverling: Broccoli Boot Camp: Basic Training for Parents of Selective Eaters

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    The Lancet Cover: Robert F Kennedy Jr: 1 year of failure

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    Here’s link to editorial: Open Access! Robert F Kennedy Jr: 1 year of failure

    A lengthy excerpt:

    “Kennedy promised a receptive and collaborative relationship, and to the public from whom he claims his mandate, he promised a new era of unbiased science without hidden conflicts of interest, secrecy, or profiteering. Radical transparency, gold-standard science, ethics, compassion, competency, and pride would restore to HHS the unimpeachable authority that the USA needs and deserves. Politicians are known to break promises, but Kennedy’s record, 1 year in, has been a failure by most measures, especially his own.

    10 days after his speech about trust and openness, HHS rescinded a 54-year-old policy of soliciting public comments for new rules and regulations, silencing the voices of many of the stakeholders he pledged to serve. Kennedy has summarily dismissed advisers and experts, communicated policy changes on pay-walled media, fired a whistleblower, and overseen the revisions of guidelines and recommendations, contradicting decades of established science, often to the benefit of industries he formerly condemned. Under Kennedy’s leadership, the National Institutes of Health (NIH) shuttered programmes studying the health effects of air pollution, HHS withheld a report linking alcohol consumption to cancer, and the Food and Drug Administration (FDA) withdrew warnings of potential harm from consuming products (such as raw milk and chlorine dioxide) falsely marketed as treatments for autism. His changes at CDC have driven 26 states to reject official guidance on vaccine policy, and in December the CDC awarded an unsolicited $1·6 million grant to conduct a vaccine study in Guinea-Bissau that raised so many ethical concerns—the design would have risked exposing thousands of unvaccinated children to hepatitis B—that it has been compared to the infamous Untreated Syphilis Study at Tuskegee.

    HHS under Kennedy has made a habit of throwing good money after bad science. Amid the Trump administration’s cuts to research funding and personnel there has been a harmful shift in priorities. Cutting-edge discoveries and clinical investigations—on subjects ranging from mRNA vaccines to diabetes and dementia—are denied crucial resources while junk science and fringe beliefs are elevated without justifiable explanation. Under Kennedy’s leadership, politicisation at the NIH, FDA, and CDC is imperilling the future of US science and innovation and throttling the public health enterprise that keeps the country safe today.

    The mechanisms maintained by the Federal Government to monitor and report health concerns such as drug overdoses, maternal mortality, and food security have been as beleaguered as the doctors and scientists who rely on them; thousands of datasets are no longer publicly available, leaving Americans—and the world—unprepared to respond to future crises. And crises are looming: in November, 2025, the first human infection (and death) from the H5N5 strain of avian flu was recorded in Washington state; pertussis, which killed 13 people in the USA in 2025, continues to spread across the country; and the measles outbreak that began in January of last year now threatens the elimination status of the USA and Mexico.”

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