Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease; non-invasive biomarkers that accurately reflect the endoscopic and histological activity of UC require validation. Therefore, our study focused on exploring the potential of serum oncostatin M (OSM) as a biomarker for evaluating UC severity. A total of UC 89 eligible participants (≥18 years) underwent extensive clinical and paraclinical evaluation. Clinical, endoscopic, and histological activity were assessed using the partial Mayo score (pMS), the Mayo endoscopic score (MES), and the Nancy Histological Index (NHI), respectively. Serum OSM levels were determined by ELISA test and measured in pg/mL; fecal calprotectin (FC) was measured in µ/g. In our study, serum OSM was significantly associated with all four outcome measures: higher OSM levels predicted higher pMS (β = 0.471, p < 0.001, R² = 0.222), MES (β = 0.422, p < 0.001, R² = 0.178), NHI (β = 0.422, p < 0.001, R² = 0.256), and FC (β = 0.431, p < 0.001, R² = 0.186). Furthermore, ROC curve analyses demonstrated that OSM had excellent diagnostic accuracy for active disease, particularly in relation to histological inflammation (AUC = 0.967). In comparison, FC showed good but slightly lower accuracy (AUC = 0.875). Notably, OSM also outperformed FC in discriminating histological remission. Pairwise ROC curve analyses using DeLong’s test further confirmed the diagnostic accuracy of OSM, FC, and combined biomarker scores (OSM+FC) across clinical, endoscopic, and histological endpoints. The combined score PRE1 (OSM + FC based on NHI) achieved perfect discrimination (AUC = 1.000, p < 0.001). Composite models PRE2 and PRE3 (OSM+FC based on MES and pMS) improved diagnostic accuracy relative to OSM, confirming the value of combining OSM with FC. Although both outperformed OSM (p < 0.05), neither achieved a superior advantage over FC. Serum OSM is strongly associated with histological activity in UC and demonstrates superior performance compared with FC in assessing histological remission.

Introduction: Chronic inflammation in Crohn’s disease (CD) is associated with systemic alterations, including the loss of skeletal muscle mass. While nutritional deficits are known to impact clinical trajectories, the specific prognostic value of muscle wasting remains underutilised. The primary objective of this study is to construct a composite score integrating sarcopenia with paraclinical parameters to predict an unfavourable disease outcome (UO) more accurately. Materials and Methods: We conducted a retrospective study of patients with CD who were hospitalized at our institution between January 2020 and June 2024 and were treated with biologics or small molecules. Using previous CT scans, we measured skeletal muscle area (SMA) and skeletal muscle index (SMI) to assess their association with disease outcomes. Univariate and multivariate analyses were performed to identify significant predictors of UO, and Area Under the Curve (AUC) values were calculated to assess the predictive performance and to construct a composite prognostic score. Results: Multivariate analysis in the study group (52 patients) identified sarcopenia (low SMI), faecal calprotectin levels >129 μg/g, and complicated disease behaviour (Montreal B2/B3) as independent predictors of UO. Integrating these parameters into a composite risk score resulted in a promising predictive model with an Area Under the Curve (AUROC) of 0.864, significantly outperforming individual biomarkers. Conclusions: We performed a hypothesis-generating study suggesting that nutritional assessment in CD could provide an important benefit in stratifying patients for whom additional nutritional interventions may enhance the long-term outcomes.

Bariatric surgery (BS) and new pharmacological treatments cause significant neurometabolic changes. However, the pathways linking peripheral stress to central metabolic control remain poorly understood. This review highlights the GDF-15/GFRAL/RET complex as a key integrator of multiorgan-to-brain stress signals that shape systemic metabolic adaptation after surgical and pharmacological interventions. Based on a structured search across PubMed, Embase, Scopus, Google Scholar, and Web of Science covering 2020–2026 alongside foundational studies, we integrated translational evidence from peer-reviewed human trials and mechanistic animal models to map the GDF-15/GFRAL/RET axis across bariatric and incretin domains. We examined the neurobiology of the GDF-15/GFRAL axis to clarify variability in metabolic and behavioral outcomes after BS. This axis links metabolic stress signals from the gut, liver, and adipose tissue to the hindbrain and hypothalamic regulation of energy balance. Changes in the gut microbiome and SCFA–FFAR2/FFAR3 signaling after surgery interact with GDF-15 and incretin pathways. Future studies should critically compare BS with synergistic or alternative non-invasive neurometabolic approaches such as incretin mimetics, exogenous GDF-15 therapies, and high-protein diets.

Background: Mesenteric panniculitis (MP) is a chronic fibroinflammatory disorder of the mesenteric adipose tissue and is frequently considered an idiopathic condition. Its association with inflammatory bowel disease (IBD), particularly ulcerative colitis (UC), remains poorly characterized, with only limited evidence available in the literature. In addition to presenting a clinical case, we performed a narrative review of the literature regarding the relationship between MP and IBD, including epidemiology, pathophysiological mechanisms, diagnostic challenges, and therapeutic approaches. Case Presentation: We report the case of a 32-year-old woman with UC in deep clinical, endoscopic, and histological remission while receiving vedolizumab therapy, who developed symptomatic MP diagnosed by contrast-enhanced computed tomography. Infectious, neoplastic, and selected fibroinflammatory causes were excluded during the diagnostic work-up. Histological confirmation was not obtained. The patient was treated with prednisone and tamoxifen, resulting in complete clinical and radiological remission while vedolizumab therapy was continued. Conclusions: This case describes the rare co-occurrence of MP and UC in deep remission during ongoing vedolizumab treatment. Given the absence of histological confirmation and the frequently idiopathic nature of MP, a causal relationship with either UC activity or vedolizumab therapy cannot be established. The observation should therefore be regarded as hypothesis-generating. Further studies are required to clarify the potential relationship between MP, IBD, and biologic therapies.

Plasma Oncostatin M (OSM) has been proposed as a biomarker of disease activity in ulcerative colitis (UC). We evaluated OSM’s relationship with clinical, endoscopic, and histological activity across two follow-up visits, compared with fecal calprotectin (FC). One hundred UC patients were assessed at Visit 1 (baseline) and Visit 2 (12 months) for clinical (partial Mayo score), endoscopic (Mayo Endoscopic Score), and histological (Nancy Histological Index) activity, alongside plasma OSM, FC, CRP, and fibrinogen; 30 healthy controls were included for comparison. Given the marked right-skewness of OSM and FC, associations were assessed using both Pearson and Spearman correlations, and logistic regression effect sizes are reported as odds ratios per doubling of biomarker concentration (log2 scale). OSM correlated significantly with all activity measures at both visits, most strongly with histological activity (r = 0.521–0.602), but weakly or not with CRP/fibrinogen. OSM was significantly elevated versus controls at both visits (p < 0.001) and declined significantly with treatment response (Δ = −89.06 vs. +0.50 in controls, p = 0.006). FC was the dominant predictor of clinical (AUC = 0.788) and endoscopic (AUC = 0.926) remission at Visit 2, with OSM contributing little independent value; however, for histological remission, both baseline OSM and ΔOSM were independent, complementary correlates (OR = 8.43 and 9.64 per doubling, respectively; p < 0.001 for both), yielding the strongest model overall (AUC = 0.949). OSM’s discriminative accuracy improved markedly from Visit 1 to Visit 2 for endoscopic (AUC 0.695 → 0.897) and histological (AUC 0.738 → 0.927) activity. Across two follow-up assessments, OSM consistently reflected UC activity, with its strongest and most independent signal for histological inflammation, both as a concurrent correlate and—more modestly—as a genuine prospective marker independent of baseline treatment exposure. OSM’s incremental value over FC was most apparent for histological status and for stringent (MES 0) endoscopic remission, but not for conventional clinical or endoscopic remission thresholds.

Background and Clinical Significance: Neuroendocrine neoplasms (NENs) are a group of malignancies that may remain clinically silent for many years. The presence of hepatic metastases can be the first clue leading to diagnosis. Case Presentation: We report the case of a 67-year-old man with intermittent tiredness and suspicious hepatic nodules detected on routine abdominal ultrasound. Contrast-enhanced ultrasonography showed arterial hyperenhancement with early washout, suggestive of metastases. Synchronous high-grade neuroendocrine carcinomas (NECs) of the lung and cecum were identified. Although the liver lesions were initially presumed to arise from the cecal tumor, liver biopsy immunohistochemistry was TTF-1 positive/CDX2 negative, whereas the cecal lesion was TTF-1 negative/CDX2 positive. This mutually exclusive immunophenotype confirmed two separate primary carcinomas. Given the high-grade histology, the patient received platinum-based chemotherapy and achieved a partial response. Conclusions: This case illustrates the diagnostic complexity of synchronous lesions and highlights the “mirage of the first lesion” phenomenon, in which the initially detected tumor may not represent the true primary site. A comprehensive, multidisciplinary strategy is crucial for establishing the correct diagnosis and guiding optimal management.