Category Archives: Gastroenterology

Low Risk of Solid Organ Transplantation with Celiac Disease

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JB Doyle et al. Clin Gastroenterol Hepatol 2026; Risk of solid organ transplantation in individuals with celiac disease: a nationwide cohort study

Background: “Celiac Disease (CeD) is associated with immune-mediated diseases of the liver, including autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis. Individuals with CeD are also at increased risk for non-autoimmune diseases of the liver, including metabolic dysfunction-associated fatty liver disease…CeD has also been associated with chronic kidney disease and cardiovascular disease. Multiple studies have demonstrated that individuals with CeD have increased rates of end-stage renal disease than the general population, with particularly strong associations between CeD and
autoimmune nephropathy, diabetic nephropathy, and systemic lupus erythematosus (19-22).
Population-level data also suggests that individuals with CeD have an increased risk of
cardiovascular disease and ischemic heart disease>”

Methods: Population-based matched cohort study in Sweden. We identified individuals with biopsy-proven CeD diagnosed between 2000-2023 using the nationwide histopathology cohort ESPRESSO. We calculated the incidence of solid organ transplantation (liver, heart, kidney, and lung) in CeD patients and estimated the risk relative to the general population. There were  41,277 individuals with CeD and 196,863 age- and sex-matched comparators with a mean follow-up of 12.1 years.

Key findings:

  • There were 85 solid organ transplantations in patients with CeD (17.0 per 100,000 person-years) and 111 in matched comparators (4.6 per 100,000 person-years). This corresponded to an adjusted hazard ratio (HR) of 2.76 
  • The highest relative risk was for liver transplantation: HR 7.26; for kidney HR 1.85. For heart, HR was 2.35 did not reach statistical significance (CI: CI 0.84-6.61)

Discussion:

“Shared genetic susceptibility may explain physiological links between CeD and autoimmune liver disease, especially since we also detected an increase in liver transplantation prior to CeD diagnosis…owever, CeD patients in our analysis had an increased risk of liver transplantation relative to their nonaffected siblings, suggesting that CeD itself may be a risk factor beyond genetic predisposition”

My take: While nearly triple the incidence compared to the general population, the absolute increased risk of needing a solid organ transplant was about 1 in 10,000. For comparison, the risk of dying in a bicycle accident in one’s lifetime is about 1 in 5,000. Nevertheless, it may be worthwhile to screen for CeD in those with end-organ disease. Additionally, checking liver tests periodically in patients with CeD would be reasonable.

Related blog posts:

Vonoprazan-Tetracycline: Effective Dual Rescue Regimen for H Pylori

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W Gao et al. Gastroenterol 2026; 170: 1473-1483. Open Access! Vonoprazan-Tetracycline Dual Regimen as Rescue Therapy for Helicobacter pylori Infection: Randomized Controlled Trial

Methods: In this prospective, open-label, randomized controlled trial(n=350), H pylori–positive adults with at least 1 prior eradication failure were allocated 1:1 to VT dual therapy (vonoprazan [20 mg, twice a day] and tetracycline [500 mg, 3 times a day]), or bismuth quadruple therapy (BQT; lansoprazole [30 mg, twice a day], colloidal bismuth [150 mg, 3 times a day], tetracycline [500 mg, 3 times a day], and metronidazole [400 mg, 3 times a day]) for 14 days.

Key findings:

Discussion:

  • “Potent acid suppression broadens the applicability of dual therapy, allowing a single sensitive antibiotic to achieve reliable eradication when gastric pH is maintained at ≥6 with potassium-competitive acid blockers.13–15“
  • “Antibiotic resistance is a major obstacle to the successful eradication of H pylori, particularly in rescue treatment. Surveillance data from the Asia-Pacific region (1990–2022) have shown persistently high resistance rates to metronidazole (52%), levofloxacin (26%), and clarithromycin (22%), whereas resistance to tetracycline and amoxicillin has remained low, both at ∼4%.17“
  • “Although high-dose amoxicillin dual therapy has been well studied and incorporated into guidelines for first-line treatment, the clinical potential of tetracycline-based regimens deserves similar attention.19,20“

Limitations: This was an open-label trial from a single center and did not include antibiotic resistance testing, which may limit generalizability to other regions or clinical settings.

My take (borrowed from authors): Vonoprazan combined with tetracycline is a simplified, penicillin-free rescue regimen, and may offer a practical option for the rescue treatment of H pylori infection. Its eradication rate was comparable to that of traditional tetracycline-metronidazole–based bismuth quadruple therapy, and was associated with fewer adverse events and better adherence. 

Related blog posts:

Comparative Safety of Advanced Therapies for Ulcerative Colitis

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D Ahuja et al. Am J Gastroenterol 2026;121:1192–1201. Comparative Safety of Advanced Therapies in Patients With Ulcerative Colitis: An Administrative Claims-Based Study

Methods: Using an administrative claims database (OptumLabs Data Warehouse) with a ‘real-world’ cohort, the authors identified 9,430 patients with UC treated with TNF antagonists (n = 4,111), anti-integrins (n = 3,165), anti-ILs (n = 1,342), JAK inhibitors (n = 701), or sphingosine-1 phosphate receptor modulators (n = 111), followed over median 27 months.

Key findings:

Overall, the risk of serious infections was higher with infliximab than with the other therapies. The incidence of VTE in patients with UC was very low and comparable across all advanced therapies, including JAK inhibitors. Also, the incidence of MACE in patients with UC was
very low and comparable across all advanced therapies, including anti-ILs and JAK inhibitors.

From the discussion: “In a recent network meta-analysis and corresponding clinical guidelines on the management of moderate-to-severe UC, upadacitinib was ranked as having the highest efficacy for induction ofremission compared with all other agents (2,14). However, safety concerns with JAK inhibitors were raised in the pivotal ORAL Surveillance trial (15). In this noninferiority trial, tofacitinib, particularly at higher doses, was associated with a higher risk of serious and opportunistic infections, VTE, and MACE, compared with TNF antagonistsi n patients with rheumatoid arthritis. Following this, the US Food and Drug Administration changed JAK inhibitors’ labeling across all indications, restricting its use in patients with previous failure or intolerance to TNF antagonists…the ORAL Surveillance trial focused on older patients aged 50 years or older with rheumatoid arthritis and at least one cardiovascular risk factor…

[In this study, the] lack of an apparent increase in the risk of JAK inhibitors compared with other medications may be related to superior disease control achieved with JAK inhibitors or reverse causality where patients at high risk of MACE and/or VTE events are not prescribed JAK inhibitors.”

My take: This study provides additional reassurance that newer advanced therapies have similar or better safety than infliximab.

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Don’t Rush to Judge Risankizumab Effectiveness for Ulcerative Colitis

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R Panaccione et al. Clin Gastroenterol Hepatol 2026; 24: 1424-1433. Open Access! Impact of Extended Risankizumab Treatment in Patients With Ulcerative Colitis Who Did Not Respond to Induction Treatment

Methods:

  1. In the AbbVie-funded phase 3 INSPIRE induction study, 209 initial nonresponders to 12 weeks of 1200 mg intravenous (IV) risankizumab induction were rerandomized to receive 12 weeks of additional 1200 mg risankizumab (weeks 12, 16, and 20) or 180 mg or 360 mg subcutaneous [SC] risankizumab (weeks 12 and 20) in a double-blind fashion
  2. Then, the delayed responders continued to receive blinded risankizumab at their assigned dose in the phase 3 COMMAND maintenance study
  • Clinical response per adapted Mayo Score (AMS): decrease from baseline ≥2 points and ≥30% from baseline, plus a decrease in RBS ≥1 or an absolute RBS ≤1
  • Clinical remission per AMS: SFS ≤1 and not greater than baseline, RBS = 0, and endoscopic subscore ≤1 without the evidence of friability

Key findings:

  • Initial nonresponders (1200 mg IV [n = 68], 180 mg SC [n = 71], or 360 mg SC [n = 70]) had week 24 clinical response rates of 50%, 56.3%, and 57.1%, respectively
  • Patients also achieved clinical remission, histologic endoscopic mucosal improvement (8.8%, 12.7%, and 15.7% for both endpoints), endoscopic improvement (17.6%, 18.3%, and 24.3%), and endoscopic remission (1.5%, 8.5%, and 5.7%)

My take: A longer trial of risankizumab is often needed to know with certainty if it will work for ulcerative colitis. More than half of initial nonresponders acquire a clinical response with extended therapy. A similar pattern was noted for risankizumab with Crohn’s disease.

Related blog post: Over 60% of Initial Nonresponders Improve with Extended Risankizumab Therapy for Crohn’s Disease

This Day in Gastroenterology History

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From a previous blog post (538: Gut Science Week):

One of the major leaps forward in gut science began with an accidental shooting at a trading post on June 6, 1822. A fur trader named Alexis St. Martin took a bullet in the abdomen, leaving him with a hole ripped through his muscle, bone and internal organs…

His doctor, William Beaumont, could literally tie a bit of food on a string, shove it into St. Martin’s stomach through the hole, and pull it back out again. Using this one weird trick, Beaumont extracted samples of the man’s gastric juices. Over eight years and more than 200 awkwardly invasive experiments, St. Martin and Beaumont gave humanity its first real understanding of how digestion works.

Earlier today

Appendectomy for Refractory Ulcerative Colitis: 2026 COSTA Study

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Visser E, Reijntjes M, Heuthorst L et al.The Lancet Gastroenterology & Hepatology, 2026; 11, 190-203. Appendicectomy versus switching to a JAK inhibitor in inducing remission in patients with active ulcerative colitis after biologic therapy failure (COSTA): 1-year results of a multicentre, prospective, cohort study

Last year, the ACCURE Trial (see blog post link below), showed that laparoscopic appendicectomy, in addition to standard medical therapy, significantly reduced the relapse rates for ulcerative colitis (UC) within 1 year. Most patients were treated with mesalamine.

The COSTA study examined adult patients (n=125) who were not responding to advanced therapy. Patients were offered one of three treatments: laparoscopic appendicectomy while continuing their existing advanced therapy at a stable dose; switching their advanced therapy to a JAK inhibitor; or colectomy. 116 patients were included in the modified intention-to-treat-analysis (67 received appendicectomy and 49 received JAK inhibitor (primarily tofacitinib).

Key findings:

  • 22 (32.8%) of 67 patients in the appendicectomy group were in clinical remission without therapy failure at 12 months compared with six (12.2%) of 49 patients in the JAK inhibitor group (p=0.016)
  • At 12 months, corticosteroid-free clinical remission without therapy failure was attained in 22 (32.8%) of 67 patients in the appendicectomy group compared with six (12.2%) of 49 patients in the JAK inhibitor group  (p=0.010). Clinical response in 49 (73.1%) of 67 patients compared with 26 (53.1%) of 49 patients (p=0·025), and endoscopic response in 31 (48.4%) of 64 patients compared with 11 (25.6%) of 43 patients (p=0·018)

My take (borrowed in part from the authors): “Appendicectomy as an adjunct to advanced therapy in biologic-exposed patients with active ulcerative colitis was associated with higher clinical remission rates at 12 months compared with switching to a JAK inhibitor.” We don’t know how appendectomy would influence disease course in pediatric patients. We also don’t know how this information will be incorporated into adult guidelines.

Interestingly, there have been studies (two cited below) indicating that appendectomy lowers the risk of developing inflammatory bowel disease:

Related blog post: ACCURE Trial: Appendectomy As an Adjunct Ulcerative Colitis Treatment Plus One

Kiawah Island at Sunrise

    “Evidence-Practice Gap” and How It Applies to H pylori Treatment

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    There is a well-described “evidence-practice gap” which has been cited to describe the lag between initial discovery and widespread, evidence-based clinical implementation (M Beauchemin et al. ANS Adv Nurs Sci. 2019 Oct-Dec;42(4):307–324); it has been suggested that this gap is typically about 17 years.

    I was looking this up after reading a “practice tips” article on H pylori and was surprised at how infrequentlly practitioners follow guidelines for optimal treatment.

    M Ventoso, SF Moss. Gastroenterology & Hepatology 2026; 22: 80-86. Open Access! Practice Tips From the Updated Helicobacter pylori Treatment Guidelines 

    Background: “The American College of Gastroenterology (ACG) recently published H pylori management guidelines6 with significant updates to the prior recommendations published in 2017.7 Importantly, the 2017 management guidelines relied heavily upon extrapolation from studies performed outside of North America. Since then, new data from US patients have become available that highlights the rising rates of resistance of commonly used antibiotics for treatment of H pylori.”

    Key points:

    • “Bismuth Quadruple Therapy Is First Line and Should Be Optimized” (see below). A 14-day course is recommended (except when using Pylera which is a 10 day treatment).
    • “3 new regimens have received US Food and Drug Administration (FDA) approval for H pylori therapy, each based on high levels of gastric acid inhibition. “
    • “The first is a combination tablet of rifabutin with amoxicillin and omeprazole (Talicia, RedHill Biopharma), given in daily doses of 150 mg, 3 g, and 120 mg, respectively. If the combination tablet is not available, generic equivalents can be substituted at similar doses (omeprazole 40 mg and amoxicillin 1 g each 3 times daily). Because the lowest available dose of generic rifabutin is only 150 mg, the best option is likely 150 mg twice daily”
    • “The second regimen is based on vonoprazan (Voquezna, Phathom Pharmaceuticals), the first potassium-competitive acid blocker (P-CAB) approved in the United States. substituting the P-CAB vonoprazan for lansoprazole in clarithromycin triple therapy produced higher eradication rates (81% compared with 69%). Similar statistically high rates (77%) were achieved with a dual vonoprazan-amoxicillin combination in the same trial, leading to FDA approval of both the triple and dual regimens14“
    • For “both rifabutin- and vonoprazan-containing regimens use amoxicillin and cannot be used in the confirmed penicillin-allergic patient. For patients with unproven penicillin allergy (approximately 10% of the US population), allergy testing is recommended”
    • “Use Clarithromycin or Levofloxacin Only If Antimicrobial Susceptibility Is Confirmed“
    • “The majority of practitioners continue to use clarithromycin-based triple therapy and have not followed the 2017 ACG H pylori guidelines …It is striking that clarithromycin-PPI triple therapy still dominates the US market, comprising greater than 80% of all treatments in 2016 to 2019.11 Notably, in approximately half of the cases where clarithromycin-PPI triple therapy failed, exactly the same prescription was given a second time.11 Thus, a massive implementation gap exists.”

    My take:

    1. While this article focuses on adult guidelines, there are similar issues in pediatrics. There is an even greater need for research involving children with H pylori. As vonoprazan appears to improve eradication rates, more guidance is needed regarding drug regimens with vonoprazan in kids.
    2. I frequently see patients who have received empiric clarithromycin-based therapy. Based on this article, I should be less surprised that this is so commonplace.

    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.

    Rising Rates of Extensively Drug-Resistant Shigellosis

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     Logan N, Birhane MG, McDonald SL, et al. MMWR Morb Mortal Wkly Rep 2026;75:173–178. Open Access! Emergence of Extensively Drug-Resistant Shigellosis — United States, 2011–2023. DOI: http://dx.doi.org/10.15585/mmwr.mm7513a1

    Background: “Shigellosis is a nationally notifiable diarrheal illness caused by gram-negative bacteria. Shigella infection is spread through fecal-oral transmission (infection can occur with as few as 10 organisms) and sexual contact. Although most infections are self-limited, antibiotics are indicated for severe illness or to reduce transmission in settings with high risk for spread. Since 2015, a growing proportion of cases has been caused by extensively drug-resistant (XDR) Shigella species, defined as being resistant to ampicillin, azithromycin, ceftriaxone, ciprofloxacin, and trimethoprim-sulfamethoxazole. No Food and Drug Administration–approved oral antimicrobial agents are available to treat these XDR infections.”

    Key finding:

    • The percentage of Shigella isolates with resistance data that were XDR increased from 0% during 2011–2015 to 8.5% in 2023

    Limitations included the following:

    • “Surveillance likely underestimated XDR Shigella isolate incidence: not all isolates were sequenced or had AST, many specimens that were positive by culture-independent diagnostic tests were not cultured, underdiagnosis and incomplete reporting occurred>”

    My take (borrowed from authors): “It is concerning that resistance is increasing.”XDR Shigella infection is an emerging concern in the United States. Because no oral antimicrobial agents are FDA approved, prevention, early detection, AST-guided therapy, and timely reporting are important to protect populations at higher risk for XDR Shigella infection”

    Related blog posts:

    Achalasia: Immune-Mediated Disease

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    S Grover et al. Gut 2026;75:476–485. doi:10.1136/gutjnl-2024-334498. Open Access! First genome-wide association study reveals immune mediated aetiopathology in idiopathic achalasia

    Key findings:

    • This genome-wide association study (GWAS) confirms the idiopathic achalasia (IA) “association of variants in HLA-DQB1 and HLA-DQA1, but also points to a more complex genetic risk architecture at this locus that involves an IA risk variant in HLA-DRB1. Moreover, the GWAS resulted in the identification of three novel disease variants outside HLA. One leads to an amino acid substitution with functional effect in PTPN22. One further novel IA risk variant leads to a downregulated expression of TNFSF8, TNFSF15 and TNC in immune-relevant cells. The remaining disease variant is located near ZNF365, but the cellular pathogenic mechanism remains unknown.”
    • “On the polygenic level, this study provides the first IA heritability estimate and shows that immune-mediated mechanisms that are shared with Crohn’s disease (CD) contribute to IA aetiopathology.”

    My take: This study “highlights that immune-mediated mechanisms influenced by genetic risk are of major relevance for disease development.”

    Related blog posts:

    “Corkscrew Method;” A Quick Trick For Esophageal Food Impactions

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    C Thellin, Y Urrutia. Gastroenterology and Endoscopy News, March 17, 2026. Open Acess! ‘Uncorking’ the Esophageal Food Impaction: Why Twisting Works Better Than Pulling

    An excerpt from this recent article:

    Yet, just as one wouldn’t simply yank a cork from a bottle, it may be time to rethink how we approach food bolus removal. Torsional stress—twisting rather than pulling—may provide a more efficient and atraumatic method for managing these impactions, a technique we refer to as the “corkscrew method.”

    Less force is required because rotation gradually disengages the bolus, decreasing the need for strong pulling or pushing. This method also poses a lower risk for mucosal injury. Shear forces are distributed rather than focused, reducing trauma.

    My take: This is probably worth a try for the next food impaction requiring endoscopic removal.

    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.