Collagenous gastritis (CoG) is a rare disorder characterized by subepithelial collagen band deposition in the gastric mucosa. In this report, we describe a case of a 33-year-old woman presenting with chronic, episodic, postprandial nausea and vomiting later found to have biopsy proven CoG. She symptomatically improved following proton pump inhibitor and budesonide initiation and cessation of nonsteroidal anti-inflammatory drugs. This case underscores the insidious nature of CoG; it should be considered in functional or undifferentiated nausea and vomiting. Moreover, it demonstrates associations between CoG, nonsteroidal anti-inflammatory drug use, and isolated immunoglobulin A deficiency.

We report a patient with Hoyeraal-Hreidarsson syndrome (HHS), a telomere biology disorder, who developed severe chronic enterocolitis with inflammatory bowel disease-like features. Vedolizumab led to improvement in stool frequency, reduced fecal calprotectin, and clinical remission without infectious complications. Remission was maintained with vedolizumab monotherapy for 2 years after discontinuation of budesonide and parenteral nutrition. This report highlights vedolizumab as a potentially safe therapeutic option for enterocolitis in HHS, emphasizing the value of gut-selective therapy when systemic immunosuppression is risky. Further studies are needed to establish the long-term efficacy and safety of vedolizumab in patients with telomere biology disorders.

Collagenous gastritis is a rare disorder characterized by subepithelial collagen deposition in the gastric mucosa and is frequently associated with iron deficiency anemia. We report two girls aged 8 and 16 years with persistent iron deficiency anemia, abdominal pain, bloating, and constipation. Upper endoscopy revealed severe follicular pangastritis in both patients. Histopathology demonstrated collagenous gastritis, with subepithelial collagen bands measuring 23 and 18 μm, respectively, accompanied by eosinophilic infiltration and absence of Helicobacter pylori infection. One patient had a history of cow's milk allergy and autoimmune family history, whereas the second had positive celiac serology with negative HLA-DQ2/DQ8. Individualized management included dietary modification, iron replacement, proton pump inhibitor therapy, systemic corticosteroids in one patient, and oral budesonide in the other. Both patients showed clinical improvement and recovery from iron deficiency anemia. These cases highlight collagenous gastritis as an important diagnostic consideration in children and adolescents with refractory iron deficiency anemia and follicular pangastritis.

Airway remodeling is a pathological hallmark of asthma that is difficult to reverse and effective therapeutic interventions remain limited. The present study investigated whether fucoidan, a natural sulfated polysaccharide derived from seaweed, attenuates airway remodeling in ovalbumin (OVA)-induced asthmatic mice. In total, 40 female Kunming mice were randomly assigned to four groups (n=10/group): Asthma, budesonide, fucoidan and control. Asthma was induced by OVA sensitization and challenge. Budesonide was administered via nebulization, while fucoidan was given by oral gavage prior to OVA challenge. Bronchoalveolar lavage fluid was collected for total and differential cell count and levels of interleukin-21, thymic stromal lymphopoietin, α-smooth muscle actin and collagen I in the lavage fluid were measured by ELISA. Lung sections were evaluated by hematoxylin and eosin staining for histopathological changes and immunohistochemistry for protein expression. Fucoidan significantly alleviated asthma-like behavior, including scratching, shortness of breath and restlessness, and reduced total cells, neutrophils, lymphocytes and eosinophils in bronchoalveolar lavage fluid compared with the OVA group (P<0.05). Fucoidan decreased the elevated levels of interleukin-21, thymic stromal lymphopoietin, α-smooth muscle actin and collagen I (P<0.05), with effects comparable with those of budesonide (P>0.05). Histological examination revealed that fucoidan attenuated peribronchial inflammatory infiltration, bronchial wall thickening and luminal narrowing. Immunohistochemical analysis confirmed that fucoidan suppressed the expression of IL-21, thymic stromal lymphopoietin, α-smooth muscle actin and collagen I in lung tissue, as reflected by significantly decreased integrated optical density values relative to the model group (P<0.05). Collectively, these findings indicated that fucoidan attenuates airway remodeling in asthmatic mice, which may be associated with downregulation of interleukin-21 and thymic stromal lymphopoietin. Although the underlying mechanisms and clinical applicability require validation, the present results suggest that fucoidan merits investigation as a potential candidate for asthma therapy.

Fidanacogene elaparvovec is an adeno-associated virus (AAV)-based gene therapy that enables endogenous factor IX (FIX) expression in hemophilia B, potentially eliminating the need for prophylactic FIX replacement. Post-treatment monitoring focuses on FIX durability, hepatic safety, and immune-mediated loss of expression. A 40-year-old man with severe hemophilia B received a single intravenous dose of fidanacogene elaparvovec in the phase 3 BENEGENE-2 trial (NCT03861273). FIX activity was assessed by one-stage and chromogenic assays. Liver enzymes, clinical parameters, and adverse events were monitored. Prednisolone was initiated for liver enzyme elevation and later switched to budesonide in response to declining FIX levels. Follow-up continued for 4 years. FIX activity peaked at week 6 (~30 IU/dL) and remained stable until week 16. Moderate ALT elevation (peak ~70 U/L) responded to prednisolone. Between weeks 22-28, FIX levels declined without ALT elevation. Budesonide (9 mg/day) was started at week 25 for 3 months and gradually tapered, stabilizing FIX activity at 10-20 IU/dL. This level has been maintained for 4 years without bleeding episodes or FIX replacement. Fidanacogene elaparvovec provided sustained, clinically meaningful FIX expression. Budesonide may offer an effective hepatocyte-targeted alternative to systemic corticosteroids while supporting long-term transgene expression.

Canine chronic inflammatory enteropathy (CIE) frequently requires a sequential therapeutic approach in which treatment is escalated according to clinical response. This prospective, open-label clinical study evaluates selected dietary, antimicrobial, microbiome-directed, and corticosteroid interventions used within a step-up treatment strategy in dogs with CIE under routine clinical conditions. Fifty-six dogs were enrolled. Clinical response was assessed using the Canine Chronic Enteropathy Clinical Activity Index (CCECAI), together with faecal calprotectin, serum folate, and serum cobalamin concentrations. In the dietary stage, both novel-protein and hydrolysed diets significantly reduced CCECAI and faecal calprotectin. Clinical remission, defined as a final CCECAI score ≤ 3, was achieved in 64% and 60% of dogs, respectively. Baseline-adjusted analyses likewise showed no significant between-group differences in CCECAI, faecal calprotectin, or cobalamin. In dogs receiving second-line treatment, both metronidazole and probiotics combined with fibre significantly reduced CCECAI and faecal calprotectin, while baseline-adjusted comparisons demonstrated no significant differences between treatments for the evaluated outcome. In dogs receiving corticosteroid-containing treatment, substantial numerical reductions in CCECAI and faecal calprotectin were observed in both the prednisone-containing and budesonide-containing regimens; however, the very small subgroup sizes and concomitant dietary, probiotic, and fibre interventions precluded definitive conclusions regarding the specific effects or comparative efficacy of the individual corticosteroids. These findings provide real-world clinical evidence supporting a structured step-up approach to canine CIE and provide a rationale for larger, adequately powered controlled studies to determine whether non-antibiotic microbiome-directed strategies and locally acting corticosteroid-containing therapy can reduce reliance on empirical antimicrobial treatment and systemic corticosteroids, thereby minimising the potential adverse consequences associated with these therapies.

Nefecon is a targeted-release formulation of the corticosteroid budesonide. It is specifically engineered to selectively target the ileal gut-associated lymphoid tissue to reduce galactose-deficient IgA1 (Gd-IgA1) production and IgA immune complex formation. Irbesartan is an angiotensin II receptor blocker that is widely used to reduce proteinuria in chronic kidney disease. The study aimed to investigate the effects of the concomitant administration of both drugs in treatment-naïve patients with primary IgA nephropathy (IgAN). We conducted a retrospective study of 12 patients with primary IgAN at a single institution who received a 6-month combination therapy with Nefecon and irbesartan. Irbesartan was administered at a fixed dose of 150 mg/day, and Nefecon was given at a dosage of 16 mg/day. Treatment effectiveness was assessed by evaluating the alterations in 24-hour urinary protein and estimated glomerular filtration rate (eGFR). We measured the levels of Gd-IgA1 and analyzed the correlations between Gd-IgA1 and clinical outcomes. Linear mixed models assessed urinary protein, albumin, creatinine, and eGFR over time. Estimated mean urinary protein reductions from baseline were -28.28% (1 month), -32.78% (3 months), and -51.46% (6 months) (P < .001). eGFR was stable at 1 month (+4.08 mL/min/1.73 m2) but rose significantly at 3 months (+10.40) and 6 months (+8.80) (P = .009). Gd-IgA1 levels before and 1 month after treatment were 15.81 ± 1.43 and 15.16 ± 1.71 U/mL. Changes in Gd-IgA1 at 1 month correlated with changes in urinary protein (r = 0.664, P = .018). Urinary dysmorphic red blood cells decreased from 108.5 (37.5, 308.8) to 14 (6, 74.2) cells/μL at 6 months (P = .012). In treatment-naïve patients with primary IgAN, combined use of Nefecon and irbesartan was associated with reduced proteinuria and stable kidney function. However, given the single-arm design, these changes cannot be attributed to the combination itself and may reflect the effects of either agent alone, natural fluctuation of proteinuria, or regression to the mean. Although early changes in Gd-IgA1 correlated with reduced proteinuria, this exploratory finding requires confirmation. In addition, subgroup findings - such as the sex-based difference in proteinuria reduction - are exploratory and hypothesis-generating. These retrospective observational findings require confirmation in adequately powered controlled studies.