Crohn’s disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract that often leads to intestinal fibrosis, an irreversible complication associated with strictures and the need for surgical intervention. Fibrosis occurs due to prolonged inflammation and abnormal wound healing, involving complex interactions between immune cells, mesenchymal cells, cytokines, and the gut microbiota. Key fibrogenic mechanisms include the activation of fibroblasts and myofibroblasts, cytokine signaling, and disrupted turnover of the extracellular matrix. Advancements in imaging techniques, such as MRI and CT enterography, have improved the detection and monitoring of fibrosis. Additionally, molecular techniques targeting fibroblast activation proteins show promise as a new imaging method. However, there are currently no approved anti-fibrotic therapies for CD. Emerging strategies focus on key pathways and novel therapeutic targets, including growth factor modulators, intracellular enzyme and kinases modulators, and interventions targeting the modulation of inflammation and extracellular matrix, which are being evaluated in preclinical and clinical settings. This review discusses the pathophysiology, diagnostic advancements, and therapeutic perspectives related to intestinal fibrosis in CD, emphasizing the urgent need for targeted anti-fibrotic therapies to prevent long-term complications and improve the life quality of patients.

Background: Pyoderma gangrenosum (PG) is a rare inflammatory cutaneous disorder that frequently occurs in association with systemic diseases such as inflammatory bowel disease (IBD). This case report describes a 23-year-old female with Crohn’s disease (CD) who developed PG and was successfully treated with adalimumab. The objective of this study is to present the clinical course, treatment approach, and outcomes while reviewing the existing literature on the efficacy of adalimumab in PG management. Methods: A case report is presented, detailing clinical presentation, diagnostic evaluation, and treatment strategy. Additionally, a systematic review was conducted using PubMed to assess studies on adalimumab in PG, focusing on treatment response, remission rates, and adverse effects. Results: The patient presented with ulcerative lesions on her lower extremities and sacroiliitis. After corticosteroid therapy, adalimumab was initiated, leading to significant ulcer healing, reduced back pain, and CD remission. The systematic review identified seven studies on adalimumab in PG. Findings suggest that adalimumab is effective in steroid-refractory cases, with remission achieved in a significant proportion of patients. The most common adverse effects were infections, but overall, adalimumab showed a favorable safety profile. Conclusions: This case highlights the importance of early diagnosis and multidisciplinary management of PG in CD patients. Adalimumab appears to be a promising therapeutic option, particularly for steroid-resistant PG, though further research is needed to establish standardized treatment protocols.

Inflammatory bowel diseases (IBDs) and metabolic disorders are increasingly recognized as interconnected conditions that frequently coexist and influence each other’s clinical course. Accumulating evidence indicates that patients with IBD face a substantial burden of obesity, metabolic syndrome, metabolic dysfunction-associated steatotic liver disease, osteoporosis, and type 2 diabetes. These associations appear to be driven by shared and interacting mechanisms, including intestinal barrier disruption, gut microbiota dysbiosis, chronic systemic inflammation, and adipose tissue-mediated immunometabolic pathways. Metabolic comorbidities may worsen IBD activity, reduce response to therapy, increase complications, and contribute to higher health care utilization. Conversely, intestinal inflammation and commonly used treatments, particularly corticosteroids, can adversely affect glucose metabolism, lipid metabolism, body composition and bone homeostasis. Advanced therapies have demonstrated variable metabolic effects, some of which may be beneficial through suppression of systemic inflammation. Recognition of these bidirectional interactions highlights the importance of routine metabolic screening and integrated, multidisciplinary management. Lifestyle interventions, nutritional optimization and individualized therapeutic strategies represent central parts of comprehensive management.

Background: Short bowel syndrome (SBS) is the leading cause of chronic intestinal failure and is frequently associated with long-term dependence on parenteral nutrition (PN) and intravenous fluids. Teduglutide, a glucagon-like peptide-2 (GLP-2) analogue, promotes intestinal adaptation and has been demonstrated to reduce parenteral support requirements. However, real-world data from the Greek population are scarce. Methods: We conducted a non-interventional, multicenter, retrospective cohort study across 5 centers in Greece, including adult patients with SBS receiving teduglutide therapy. Demographic and clinical characteristics, parenteral nutrition and intravenous fluid requirements, body mass index (BMI), laboratory parameters, and adverse events were recorded at baseline and during follow-up at weeks 4, 12, 26, and 52. Results: Eight adult patients with SBS were included (75% female), with a median age of 53 years (range 19–71). Over 52 weeks of treatment, mean parenteral nutrition requirements decreased by approximately 45% compared with baseline (from 1430 to 788 kcal/day), while mean intravenous hydration requirements decreased by approximately 80% (from 5170 to 1000 mL/week). Complete independence from parenteral nutrition was achieved in 2 of 8 patients (25%). Nutritional status improved, with a 10.6% increase in mean BMI at Week 52. Teduglutide was generally well tolerated; mild adverse events occurred in 3 of 8 patients, were predominantly gastrointestinal, and did not lead to treatment discontinuation. Conclusions: This study provides data from the Greek population and supports the effectiveness and favorable safety profile of teduglutide in adult patients with SBS and chronic intestinal failure. Further prospective studies are warranted to better define predictors of response and optimize long-term management strategies.

Introduction: Despite proven efficacy of anti-TNF agents in inflammatory bowel disease, primary non-response affects up to one-third of patients, while secondary loss of response occurs at 13–21% per patient-year, often requiring dose optimization or switching to alternative advanced therapies. Methods: The present single-center cohort study at the University Hospital of Ioannina included biologic-naïve patients receiving anti-TNF therapy as their first biologic treatment. First anti-TNF treatment failure was defined as discontinuation due to persistent IBD activity despite maximal dose optimization (infliximab 10 mg/kg every 4 weeks, adalimumab 40 mg weekly). Patients with measurable anti-drug antibodies prior to anti-TNF dose intensification or discontinuation were excluded. Of 528 anti-TNF-treated patients, 286 (173 with CD, 113 with UC) met the inclusion criteria and were included in the final statistical analysis. Results: Anti-TNF failure occurred in 32.7% of Crohn’s (CD) and 32.9% of ulcerative colitis (UC) patients. Multivariable Cox regression identified complicated phenotype (stricturing or/and penetrating CD; HR = 1.9, p = 0.032) and concomitant corticosteroid use at anti-TNF initiation (HR = 2.03, p = 0.012) as independent predictors of anti-TNF failure in CD. Age at CD diagnosis showed a trend for statistical significance (HR = 1.02, p = 0.061), and after stratification, age at diagnosis ≥ 40 years conferred higher risk (HR = 1.93, p = 0.016), alongside persistent effects of complicated phenotype (HR = 1.83, p = 0.027) and corticosteroid use (HR = 2.01, p = 0.013). In UC patients, female sex predicted anti-TNF failure (HR = 2.13, p = 0.025). IBD-related bowel resection occurred in 26.6% of patients with CD and in 5.3% of patients with UC. Conclusions: Anti-TNF failure remains common despite optimization. Identifying immunogenicity-independent predictors may enable personalized treatment strategies and improve outcomes.

Introduction: Clostridioides difficile (C. difficile) is a major cause of antibiotic-associated diarrhea and healthcare-associated infections, with rising global incidence and severity due to the emergence of hypervirulent strains. Methods: This review synthesizes recent literature on the epidemiology, pathogenesis, diagnostic approaches, and therapeutic strategies related to C. difficile infection (CDI). Sources were selected from peer-reviewed journals, clinical guidelines, and emerging research between 2020 and 2025. Results: Advances in molecular diagnostics have improved the accuracy and speed of CDI detection. New therapeutic options such as fidaxomicin offer narrower-spectrum antibiotic activity with reduced recurrence rates. Fecal microbiota transplantation (FMT) has emerged as a highly effective option for recurrent CDI. Preventive efforts, including antibiotic stewardship programs and early-phase vaccine trials, show potential in reducing infection rates. Discussion: The management of CDI is evolving rapidly with the integration of precision diagnostics, targeted therapies, and microbiome-based interventions. Preventive strategies are critical, particularly in healthcare settings where C. difficile persists in the environment. Continued research and coordinated public health efforts are essential to reduce disease burden, improve outcomes, and limit transmission. Conclusions: Clostridioides difficile infections remain a major healthcare challenge with rising incidence and recurrent cases. Fidaxomicin has become the preferred first-line therapy. Microbiota-based therapies (like FMT, Rebyota, and Vowst) and Lipopolysaccharide Binding Protein (LBP) are highly effective for recurrent CDI prevention. Diagnostic strategies have improved with multi-step testing, enhancing accuracy and reducing overtreatment. Future focus lies in vaccines, targeted antimicrobials, and stricter prevention through antibiotic stewardship and hygiene.