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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.

Inability to Burp: How Effective is Botox?

Briefly noted: S Sanagapalli et al. The American Journal of Gastroenterology 120(9):p 2051-2058, September 2025. Prospective Controlled Study of Endoscopic Botulinum Toxin Injection for Retrograde Cricopharyngeus Dysfunction: The Inability to Belch Syndrome

This study explored a treatment with botulinum toxin (aka. Botox) for people who can’t belch due to a condition called retrograde cricopharyngeus dysfunction (R-CPD), which causes gas-related discomfort. Researchers used high-resolution manometry (HRM) with carbonated drink provocation to diagnose R-CPD. Then, they tested a treatment involving botulinum toxin injections into the cricopharyngeal muscle.

Out of 65 participants, 52 received the treatment, and 92% of those who received the treatment were able to belch after three months, significantly improving their symptoms and quality of life. In contrast, the control group, which included participants who deferred or declined treatment, saw no improvement. After 3 months, 43/51 (84%) of the treatment group reported being satisfied or very satisfied with therapeutic outcome.

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In the News: Fewer Peanut Allergies, Possibly Improving Obesity Rates in U.S., Best Fruit for Constipation

10/20/25 NY Times: Peanut Allergies Have Plummeted in Children, Study Shows “The new study, published Monday in the journal Pediatrics, found that food allergy rates in children under 3 fell after those guidelines were put into place — dropping to 0.93 percent between 2017 and 2020, from 1.46 percent between 2012 and 2015. That’s a 36 percent reduction in all food allergies, driven largely by a 43 percent drop in peanut allergies.”

Referenced article (Open Access!): S Gabryszeweki et al. Pediatrics e2024070516. Guidelines for Early Food Introduction and Patterns of Food Allergy

Related blog posts:

10/16/25 ABC News: Obesity remains high in the US., but more states showing progress, a new report finds “For the first time in more than a decade, the number of states with rates of obesity of 35% or more dropped, an encouraging sign that America’s epidemic of excess weight might be improving.  But cuts to federal staff and programs that address chronic disease could endanger that progress, according to a new report released Thursday. Nineteen states had obesity rates of 35% or higher in 2024, down from 23 states the year before, according to an analysis of the latest data collected by the U.S. Centers for Disease Control and Prevention”

M Warren et al. Trust for America’s Health. Open Access! The State of Obesity 2025 Report (140 pages)

Related blog post: Worldwide Trends in Underweight and Obesity (2024)

10/13/25 NBC News: What to eat to ease chronic constipation, according to new guidelines This article revies the new dietary guidelines from the British Dietetic Association.

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Why Pediatric Patients Need Higher Dosing of Infliximab

E Stenke et al. Inflamm Bowel Dis 2025; 31: 2331-2337. Higher-Dose Infliximab Induction Achieves Better Maintenance Trough Levels in a National Pediatric IBD Cohort—A Retrospective Study

In this single center retrospective study from Ireland, the authors examined 122 patients (93 with Crohn’s disease [CD], 18 with ulcerative colitis [UC], 1 with IBDU) who received infliximab and had prospectively-collected data. The earlier cohort 2018-2019 received 5 mg/kg/dose and the later group 10 mg/kg/dose. Both groups had proactive therapeutic drug monitoring (pTDM).

Key findings:

  • The 5 mg/kg group, compared to the 10 mg/kg group, was less likely to have target pre-third TLs (6% vs 80%, P < .001) with the stated goal of >/= 15 microgm/mL
  • Fewer patients in the 5 mg/kg than 10 mg/kg group had pre-fourth TLs ≥5 µg/mL (6/48 [12.5%] vs 28/50 [56%], P < .001; mean [SD] TL 3.5 [6.3] vs 10.0 [9.9], P < .001)
  • Concurrent immunomodulator therapy was more common in the 5 mg/kg group (43% compared to 24%)
  • 80% of patients were still receiving infliximab at 1 year including 87% of patients with CD and 54% with UC
  • The higher dose group had a lower CRP at 1 year followup. 26% of patients receiving the lower dose had a CRP > 5 mg/L compared with 9% in the higher dose group.
  • Some other measures of long term outcome (eg. IFX durability, clinical remission) were slightly better but did not reach statistical significance (see below)

Discussion Points:

  • “Our data show higher rates of below-target infliximab levels during and after induction in the 5 mg/kg group. Higher rates of dose escalation in this group during the first year resulted
    in similar dosing regimens…Thus, the similar infliximab durability and clinical outcomes
    at 1-year follow-up reflect early-dose optimization leading to dose equalization between the 2 groups, rather than a lack of benefit to higher dosing regimens”
  • “Our data affirm that proactive TDM with pre-emptive dose escalation restores
    below-target infliximab TLs and sustains clinical response…Indeed, in our cohort, some patients with low IFX levels pre-third dose were given their fourth dose 6 weeks later, rather
    than the standard 8 weeks. Without proactive TDM results, our rate of suboptimal TLs pre-fourth and during maintenance therapy would have been higher in both groups”
  • “Rates of immunomodulator use in the 10 mg/kg group were lower than in the earlier cohort of 5 mg/kg, reflecting changes in clinical practice over time”

My take:

  1. This study shows that 94% of pediatric patients did NOT achieve adequate levels of infliximab at the pre-third dose with “standard” therapy. This was true even with 43% of the lower dose cohort receiving combination therapy (which often helps improve pharmacokinetics)
  2. Proactive therapeutic drug monitoring helped mitigate the clinical outcomes, especially in the lower dosed cohort
  3. “Children with IBD treated with the historic standard dose of 5 mg/kg induction are at increased risk of pharmacokinetic treatment failure related to high rates of suboptimal TLs”

Related blog posts:

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.

Consensus Recommendations on Functional Bloating and Distention

C Melchior et al. United European Gastroenterology Journal, 2025; 00:1–39. Open Access! European Consensus on Functional Bloating and Abdominal Distension—An ESNM/UEG Recommendations for Clinical Management

A total of 21 experts (authors of article), recommended by ESNM, The European Association for Gastroenterology, Endoscopy and Nutrition (EAGEN) and The European Society for Primary Care Gastroenterology (ESPCG), from different countries agreed to participate as the International Working Group for the European Consensus on Bloating to vote on the Delphi statements.

This article regarding bloating/distension in adults is summarized in two tables. Table 1 has 75 statements. Table 2 is a summary –here are many of its recommendations:

Patients with functional bloating and abdominal distention should receive a lactose‐limiting diet trial based on their self‐reported symptoms or the presence of intolerance during a breath test after ingestion of a defined lactose load

  • A low FODMAP diet is effective in reducing functional bloating and abdominal distention
  • Rifaximin may be useful for the treatment of functional bloating and abdominal distention with efficacy
  • Among antispasmodic agents, pinaverium and otilonium bromide have been shown to be the most effective drugs for the treatment of functional bloating and abdominal distension
  • Lubiprostone, plecanatide and linaclotide are effective in improving constipation associated with functional bloating and abdominal distension
  • Linaclotide is the most effective secretagogue for functional bloating, although limited data is available for lubiprostone and plecanatide as well
  • Selective serotonin reuptake inhibitors (SSRI’s) are effective in reducing symptoms of functional bloating
  • Tricyclic antidepressants (TCA) such as amitriptyline are effective in reducing symptoms of functional bloating
  • In patients with discrete episodes of visible abdominal distension, biofeedback‐guided techniques to re‐educate abdominothoracic muscular activity are safe and effective for correction of abdominal distention and are associated with improvement in the subjective sensation of abdominal bloating
  • “Hypnotherapy improves symptoms of bloating in patients with IBS. However, its effect on functional bloating and abdominal distension was not explored and cannot be recommended”
  • Figure 1 provides an algorithm. For workup, it suggests checking the following in all patients: TSH, HgbA1c, CBC, CRP, TTG IgA, IgA, Glucose
  • In those with alarm features (eg. anemia, wt loss, suspicion of organic disease), more extensive evaluation is recommended

My take: One of my colleagues would often say that if there are a lot of treatments for a disease it usually indicates that none of them are very good.

Related blog posts:

Bouquet of Flowers, Claude Monet

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.

New Era in Cholestatic Liver Diseases

H Sutton, RJ Sokol, BM Kamath. Hepatology 2025; 82: 985-995. Open Access! IBAT inhibitors in pediatric cholestatic liver diseases: Transformation on the horizon?

This review article is one of many in the same issue (#4) of Hepatology.

Key points:

  • “In the last few years, a novel class of agents, intestinal bile acid transporter (Ileal bile acid transporter (IBAT); also known as apical sodium-dependent bile acid transporter [ASBT]) inhibitors, has emerged and gained approval from the FDA… the pivotal studies on which these approvals were granted were all performed in rare pediatric cholestatic diseases, namely Alagille syndrome (ALGS) and progressive familial intrahepatic cholestasis (PFIC).3 Additional expansion of these approvals will possibly follow as there are ongoing trials of IBAT inhibitors in primary biliary cirrhosis, primary sclerosing cholangitis, and biliary atresia.”
  • “The role of bile acids in promoting hepatic injury in cholestasis is perhaps best illustrated in human infants with ABCB11 (bile salt export pump; BSEP) disease or PFIC type 2…The response to IBAT inhibition in this disease further supports the notion that retained bile acids are a key factor leading to progressive liver injury and cholestatic symptoms including pruritus, fat-soluble vitamin deficiencies, and growth failure.4
  • These medications may improve liver histology and not just reduce pruritic symptoms: “Using the MDR2−/− mouse cholangiopathy model, Miethke et al22 demonstrated that ASBT inhibition led to a reduction in both serum and intrahepatic bile acid concentrations by 98% and 65%, respectively. These reductions in bile acid concentrations were associated with improved liver biochemistry and a reduction in peri-portal inflammation and fibrosis on histology. The histopathologic improvements seen in these treated MDR2−/− are important to highlight, as they support the rationale of this therapeutic approach: that lowering serum bile acid (sBA) with IBAT inhibition leads to a reduction in intrahepatic bile acid accumulation and toxicity, improvements in liver inflammation and fibrosis, and ultimately improved liver disease biology.”
  • Numerous clinical trials are listed in Table 1 (completed trials) and Table 2 (ongoing).
  • Physiology: “Bile acids are key regulators of their own enterohepatic circulation, predominately through activation of the farnesoid X receptor (FXR)…the fecal elimination of bile acids in IBAT inhibitor–treated patients appears to far exceed the rate of synthesis of new bile acids in the liver; thus, IBAT inhibitors reduce the total bile acid pool size and the bile acid load presented to the liver.22,34,39
  • Alagille syndrome (ALGS): Key trials are summarized including the ICONIC trial with maralixibat and the ASSERT trial with odevixibat.
  • PFIC (Type 1 and 2) Trials: Key trials are summarized including the MARCH-PFIC trial with maralixibat and the PEDFIC1 & PEDFIC 2 trialswith odevixibat.
  • Safety: These medications are well-tolerated with self-limiting diarrhea and abdominal pain especially at the initiation of these medications. Liver blood test abnormalities have been noted in up to 20%. “This is an interesting finding, and the underlying etiology is unknown. Maralixibat is largely luminally restricted and so, without systemic absorption, a direct hepatotoxic effect is unlikely. It may reflect an alteration in the speciation of the bile acid pool with increasing bile acid synthesis or alterations in the gut-liver axis signaling. More importantly, it is not known if there are any clinical consequences to the increase in ALT.”
  • Cost: The authors note that ursodeoxycholic acid and antihistamines are frequently used for management of pruritus. They also not that “from a cost standpoint, it seems appropriate to offer rifampin before IBAT inhibitors in the treatment of cholestatic pruritus.”
  • Conclusions: “The clinical trial data are encouraging. As more physicians gain experience prescribing IBAT inhibitors, we will continue to learn how to best apply them to our patient populations. Like any new drug, there are still several unknowns. One of these unknowns is the potential for loss of efficacy…The short-term to medium-term clinical effects of IBAT inhibitors are clear, but we have not yet begun to see the long-term benefits. Whether durable reductions in oncogenic and fibrogenic bile acids reduce rates of HCC or slow the progression of (or reverse) portal hypertension remains to be seen.”

Related article: M Trauner, SJ Karpen, PA Dawson. Hepatology 2025; 82: 855-876. Open Access! Benefits and challenges to therapeutic targeting of bile acid circulation in cholestatic liver disease

“Recent advances in understanding bile acid (BA) transport in the liver… This has led to new treatments targeting BA transport and signaling. These include inhibitors of BA transport systems in the intestine and kidney (IBAT/ASBT inhibitors) and liver (NTCP inhibitors), as well as receptor agonists that modify BA synthesis and transport genes. BA analogs like norucholic acid also show promise. This review discusses the molecular and clinical basis for these therapies, particularly for cholestatic liver disorders.

Principal therapeutic targets within the entero-nephro-hepatic circulation of BAs in cholestasis.

My take (borrowed from Trauner et al): “We have arrived at a new era in the treatment of cholestatic disorders. This has been made possible by incorporating findings from discoveries into the molecular pathogenesis of cholestasis and adaptive processes that direct rational therapeutics to improve patients’ lives.”

Related blog posts:

NSAIDs for Severe Acute Pancreatitis

L Huang, et al. Gut 2025;74:1467–1475. doi:10.1136/gutjnl-2024-334038. Open Access! Parecoxib sequential with imrecoxib for occurrence and remission of severe acute pancreatitis: a multicentre, double-blind, randomised, placebo-controlled trial

Background: “COX-2 inhibitors (COX-2-Is) have shown potential in reducing pancreatitis severity and improving renal and respiratory function in animal models.” However, at this time, “there is no effective drug treatment for organ failure (OF) caused by severe acute pancreatitis (SAP)” in humans.

Methods: “In this multicentre, double-blind, randomised, placebo-controlled, investigator-initiated trial, 348 patients with acute pancreatitis aged 18–75 years, <1 week from onset of illness to admission, and Acute Physiology and Chronic Health Evaluation II Score ≥7 or modified Marshall Score ≥2, were randomly assigned (1:1) to the COX-2-Is group (parecoxib sequential with imrecoxib) or the placebo group.”

The authors chose to adopt a sequential regimen of intravenous (3 days) to oral COX-2-Is. “Parecoxib labelling recommends intravenous administration for no more than 3 days due to limited clinical experience beyond this period.”

Key findings:

  • “Compared with the placebo group, SAP occurrence was reduced by 20.7% (77.6% vs 61.5%, p=0.001) and the persistent OF duration in SAP was shortened by 2 days (p<0.001) after COX-2-Is treatment.” 
  • “For patients enrolled within or after 48 hours from symptom onset, SAP occurrence was reduced by 23.8% (p=0.001) and 8.5% (p=0.202), and the persistent OF [organ failure] duration in SAP was shortened by 3 days (p=0.001) and 2 days (p=0.010) after COX-2-Is treatment, respectively.” 
  • “The serum levels of inflammatory mediators and 30-day mortality (from 8.6% to 3.4%) were significantly reduced after COX-2-Is treatment, p<0.05.”
  • “The incidence of adverse events was similar between the two treatment groups.”

My take: This study showed that NSAIDs (starting with IV x 3 days) improved outcomes with severe acute pancreatitis (in adults). Prior studies have also showed reduced pancreatitis with NSAIDs following ERCP.

Related blog posts:

Diets for Obesity and Steatotic Liver Disease Plus Patient Information from FISPGHAN

S Karjoo et al. JPGN 2025;81:485–496. Evidence-based review of the nutritional treatment of obesity and metabolic dysfunction-associated steatotic liver disease in children and adolescents

This invited commentary reviews the data for several diets that may improve weight loss and metabolic dysfunction-associated steatotic liver disease (MSALD).

Several points:

  • “Extremely restricted plant‐based diets may have deficiencies of vitamin D, calcium, and vitamin B12 which are nutrients found in animal products, and can be minimized by vitamin supplementation or increasing consumption of fish, mushrooms, egg yolk, cod liver oil, salmon, herring, and sole fish. VitaminB12 supplementation is recommended in plant‐based diets because this vitamin is primarily found in animal products”
  • Table 1 compares the structure of these diets and their advantages/drawbacks
  • “Low to moderate weight loss can be seen in the anti-inflammatory diet, plant-based diets, or Mediterranean diet. These diets are nutritionally complete. However, restrictive plant-based diet carries a risk of micronutrient deficiencies, which can be corrected with appropriate supplementation. These diets are effective in treating MASLD independent of weight loss due to their anti-inflammatory profile.”
  • “The ketogenic diet, certain carbohydrate-restricted diets, and intermittent fasting can lead to more weight loss but carry a higher risk of malnutrition. Children on these diets must be followed by nutritionists.”

My take: Each of the diets reviewed can help MASLD and obesity. Most patients pursuing dietary therapy would benefit from working with a nutritionist.

Related news: TEVA Press release, August 28, 2025: Generic liraglutide (need for daily injections) is now available.

Related blog posts:

Also, related patient advice from Federation of International Societies for Pediatric Gastroenterology, Hepatology, and Nutrition (FISPGAN) –outlines risk factors and prevention tips for metabolic dysfunction-associated steatotic liver disease (MASLD):

The Rise of Oral Obesity Therapies: Semaglutide and Orforglipron

SWharton et al. N Engl J Med 2025;393:1077-1087. Oral Semaglutide at a Dose of 25 mg in Adults with Overweight or Obesity

Methods: The participants were randomly assigned in a 2:1 ratio to receive oral semaglutide (25 mg) or placebo once daily, plus lifestyle interventions.

Key Findings:

In their discussion, the authors note that the reasons why “patients may prefer oral administration over the subcutaneous route are most often needle aversion and local skin reactions.7,8 In addition, unlike injectable agents, oral agents may not require a refrigerated chain of delivery and could widen the reach of obesity care in many regions of the world where a lack of refrigeration represents a barrier to access.”

In addition, the results were similar to the “STEP 1 (Semaglutide Treatment Effect in People with Obesity) trial of weekly subcutaneous semaglutide at a dose of 2.4 mg (12.4 percentage points more than that with placebo),16

As with prior trials of semaglutide, “treatment was also associated with substantial reductions in cardiometabolic risk factors including BMI, waist circumference, and levels of glycated hemoglobin, fasting plasma glucose, fasting serum insulin, lipids (very-low-density lipoprotein and triglycerides), and C-reactive protein.”

My take: Effective oral therapy is a big advance for management of obesity. The entire field of pharmacology for obesity has seen remarkable advances in the past few years. For me, it is reminiscent of the proliferation of published studies for hepatitis C around 10 years ago.

Related article in same NEJM issue: J Rosenstock et al. N Engl J Med 2025;393:1065-1076. Orforglipron, an Oral Small-Molecule GLP-1 Receptor Agonist, in Early Type 2 Diabetes

In the ACHIEVE-1 Trial: Key Findings (n=559 adults):

The associated editorial by DB Lowe (N Engl J Med 2025;393:1133-1134) notes that Orforglipron is a small molecule that manages to mimic the effects of glucagon-like peptide-1 (GLP-1) at the GLP-1 receptor. “The incretins, like many peptide hormones, are fairly small as proteins go — a few dozen amino acids long. But that makes them gigantic as compared with small-molecule drugs. Their molecular weights are at least 10 times as high as the 300 to 500 mass units that medicinal chemists have traditionally aimed for, and being peptides, they have generally undesirable properties as well. Many have short half-lives in the circulation, which can be a desirable feature for endogenous peptides but is nowhere near what is needed for the administration of a once-daily dose.”

Related blog posts: