International scientists and clinicians gathered in Warsaw for the 243rd International Symposium of the Falk Foundation e.V., "Gastrointestinal Inflammation and Neoplasia". Over two days of presentations and discussion, expert clinicians and scientists explored the epidemiology, pathophysiology, diagnostics, and treatment of a broad range of immune-mediated gastrointestinal (GI) disorders. A major theme across the program was that patient-reported symptoms correlate only moderately with what is actually happening in the gut, and that good long-term care depends on combining clinical, endoscopic, histologic, and patient-centered endpoints, along with tailoring disease management to each individual.

Eosinophilic esophagitis: Why symptoms alone are not enough

PD Dr. Ulrike von Arnim (Magdeburg, Germany) explored the current diagnostic and monitoring strategies for eosinophilic esophagitis (EoE), a chronic, immune-mediated disease of the esophagus, characterized by symptoms of esophageal dysfunction and, histologically, by eosinophilic inflammation. Diagnosis of EoE requires both clinical and pathological confirmation. The diagnostic work-up combines esophagogastroduodenoscopy (EGD) with biopsies showing at least 15 eosinophils per high-power field, structured assessment of endoscopic features using the Eosinophilic Esophagitis Endoscopic Reference Score (EREFS) score, and exclusion of other causes of esophageal eosinophilia [1]. Patient symptoms change with age. While infants present with food intolerance and failure to thrive, adults experience dysphagia and food impaction. Patients often develop compensatory eating behaviors without realizing it, masking the actual disease severity. As allergic comorbidities are present in 60–80% of patients [2], Dr. von Arnim urged clinicians to ask their patients about both eating behavior and allergic background.

Standardized scoring matters. The EREFS runs 0 to 9, with values above 2 indicating active disease. It discriminates EoE from controls with high sensitivity and specificity, has been validated in children and adults, and correlates with treatment response across multiple clinical trials [3,4]. Since EREFS has come into use, reports of normal-appearing esophagus have fallen from 21% to 7%. Even so, about 11% of active EoE still looks endoscopically normal, usually in younger patients with atypical symptoms, so biopsies should be taken regardless of how the mucosa appears. For histology, the expert recommended that pathologists adopt the EoE Histology Scoring System, which captures eosinophil-independent features that contribute substantially to symptoms, such as basal zone hyperplasia and lamina propria fibrosis [5].

Symptoms alone are an unreliable guide and monitoring of EoE patients is essential as more than one-third of patients in apparent clinical remission on conventional therapy still have endoscopic or histologic activity [6,7]. A retrospective Swiss cohort of around 160 adults on topical corticosteroid maintenance therapy found significantly more stricture formation among those not followed up within 18 months [8]. Exclusive symptom-based follow-up is not recommended because symptoms only moderately correlate with endoscopic and histologic disease. Dr. von Arnim recommended both endoscopic and histologic reassessment 8–12 weeks after induction or any major treatment change. Stable patients should be reviewed every 12–24 months, with shorter intervals for those with strictures or other complications. As no blood, breath, stool, urine, or minimally invasive biomarker is currently recommended for routine monitoring, EGD with biopsy remains the gold standard.

IBD: Treatment goals in 2026

Inflammatory bowel disease (IBD) is a complex and heterogeneous condition with substantial symptom burden and impaired quality of life, said Prof. Alessandro Armuzzi (Milan, Italy). 
Around 40% of patients with IBD still experience active intestinal disease along with high hospitalization and surgery rates, and an approximately 1.8 times higher risk of colorectal cancer than the general population. Multiple advanced therapies with similar efficacy and safety profiles are available for ulcerative colitis (UC) and Crohn's disease (CD), targeting different drivers of inflammation. The absence of reliable biomarkers of disease progression and treatment response remains a major gap.

The STRIDE-II (Selecting Therapeutic Targets in Inflammatory Bowel Disease) update (2021) fundamentally shifted IBD management from managing symptoms to a "treat-to-target" approach [9]. While symptoms matter most to patients, they do not always closely correlate with objective disease measures. The CALM trial in patients with CD showed that normalizing standard biomarkers (i.e., fecal calprotectin and C-reactive protein) delivers superior mucosal healing at one year compared with a symptom-based approach [10].

Mucosal healing is consistently associated with improved long-term outcomes in both UC and CD, while stricter endoscopic targets are considered optimal [11,12]. Despite this, Prof. Armuzzi cautioned that one in three patients who achieve complete mucosal healing still reports moderate disability. Pursuing healing is generally worthwhile, but it may not be justified to persist at any cost if it cannot be achieved despite optimized therapy and treatment switching. Only around 30% of patients with 8 to 10 years of disease duration achieve full mucosal healing on treat-to-target strategies. Prof. Armuzzi proposed that the field should consider defining a "minimal disease activity" state for advanced CD, analogous to the concept long established in rheumatology.

Histologic healing in UC and transmural healing in CD are emerging as the next key targets. For example, the ongoing VERDICT trial compares treat-to-symptoms, treat-to-endoscopy and treat-to-histology strategies in UC [13]. The ongoing VECTORS study is evaluating intestinal-ultrasound-guided transmural healing as a basis for therapy adjustment in CD [14]. Prof. Armuzzi expects both endpoints to be incorporated as adjunctive targets in the next STRIDE update. He argued for a patient-centered composite remission score that combines clinical, endoscopic, 
histologic and biomarker remission with quality-of-life measures, which he summed up as feel well, heal well, avoid damage. Prof. Armuzzi regards surgery as a legitimate therapeutic option rather than a last resort. In selected patients with limited ileocecal CD who have failed conventional therapy, a minimal ileocecal resection can deliver 5 to 10 years of wellness before biologics are needed [15,16].

Immune-mediated gastrointestinal disorders during pregnancy and lactation

Prof. Uma Mahadevan (San Francisco, USA) addressed what “high-risk pregnancy” means in different healthcare environments. Given that immune-mediated GI diseases are often diagnosed during a woman's reproductive years, it is essential to consider evidence-based management of fertility, pregnancy and lactation. IBD management decisions in pregnancy often result in treatment withdrawal, putting the pregnancy at greatest risk. Evolving guidelines emphasize controlling disease activity for both maternal and fetal health.

The human placenta is uniquely vulnerable to immune dysfunction. Abnormal placentation (i.e., issues with placental position, attachment, or invasion) can result in severe, life-threatening maternal hemorrhage and adverse fetal outcomes, as well as a higher risk of preterm preeclampsia and intrauterine growth restriction. Monoclonal antibodies cross the placenta by active transport via the Fc receptor, which develops at around weeks 12–14 of gestation. As this is after the bulk of organogenesis, biologics have not been associated with increased congenital anomalies. Small molecules are different, however, as they cross the placenta during organogenesis, and therefore warrant greater caution.

Prof. Mahadevan presented the 2025 Global Consensus Consortium recommendations for the management of pregnancy in IBD [17]. According to these recommendations, aminosalicylates, thiopurines, anti-TNF agents, anti-integrins, and selected IL-12/23 and IL-23 inhibitors may be continued during pregnancy and lactation. Methotrexate is teratogenic and should be discontinued at least one month prior to conception. Steroids may be used when needed, but switching to steroids from an effective biologic is not safer. JAK inhibitors and S1P modulators should be avoided unless no alternative exists for maternal health. Early data on 55 women exposed to a JAK inhibitor during pregnancy showed no birth defects, although definitive safety conclusions cannot yet be made [18,19].

Based on findings from the ASPRE trial, low-dose acetylsalicylic acid initiated between weeks 12–16 of gestation has been shown to reduce the risk of preterm preeclampsia in women at high risk [20].

Regarding treatment while breastfeeding, monoclonal antibodies transfer minimally into breast milk and are largely digested in the infant gut, leaving negligible levels in serum. Multiple agents are considered to be safe during lactation, including 5-aminosalicylic acid (5-ASA, mesalamine), sulfasalazine, thiopurines, steroids, anti-TNFs, anti-integrins, and anti-IL-23s (and respective biosimilars). Small molecules, however, should be avoided, including JAK inhibitors, S1P modulators, and methotrexate. For infants exposed to biologics in utero, inactivated vaccines should be given per national schedule. Live vaccines can also be given on schedule, with one exception: Bacillus Calmette-Guérin (BCG) vaccination should be delayed until at least six months of age or until drug levels are undetectable, owing to documented cases of fatal disseminated BCG. Live attenuated rotavirus vaccine is now considered safe regardless of biologic exposure. No serious adverse reactions were identified in retrospective data from over 300 biologic-exposed infants after live rotavirus vaccination, or in a prospective Canadian Immunization Research Network study of 191 infants exposed to immunomodulatory biologic agents [22]. The take-home message is that all pregnancies in IBD should be followed as high-risk, with monitoring tailored to disease severity.

Source

243^rd Symposium "Gastrointestinal Inflammation and Neoplasia", April 24 and 25, 2026, Warsaw (Poland)

References:

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