Acute kidney injury (AKI) is a serious clinical condition that is linked to markedly higher rates of morbidity and mortality in cirrhosis patients. Its diagnosis is challenging due to overlapping clinical and laboratory features among causes such as hepatorenal syndrome (HRS), acute tubular injury (ATI), and prerenal hypovolemia. In order to address the distinct pathophysiology and clinical context of cirrhosis, the definitions and classification of AKI have changed over time, moving from RIFLE and AKIN to KDIGO and ICA-AKI. Because cirrhosis patients have altered muscle mass and fluid retention, traditional markers like serum creatinine (sCr) and urine output have significant limitations. Neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and cystatin C (CysC) are some of the new biomarkers that have shown promise in early AKI detection and in differentiating structural from functional kidney injury. NGAL and KIM-1 are sensitive indicators of tubular damage with potential prognostic implications. IL-18 reflects inflammatory injury, and CysC offers a more reliable measure of glomerular filtration. Incorporating these markers may improve early diagnosis, risk stratification, and treatment decisions, representing a key direction for future research in managing AKI in cirrhosis.

Spontaneous bacterial peritonitis (SBP) is the most common bacterial infection in cirrhotic patients. Historically, the bacterial spectrum was dominated by Gram-negative bacteria. However, recent studies showed that fluoroquinolone (FQ)-based prophylaxis promotes the intestinal overgrowth of Gram-positive bacteria and contributes to the selection of quinolone-resistant Gram-negative bacteria, increasing multidrug-resistant (MDR) organism infections. FQ resistance rates reach up to nearly one-third in community-acquired cases and 50% in hospital-acquired cases, raising concerns about FQ efficacy. Moreover, rare but serious side effects further limit FQ use. Predictive factors of FQ treatment failure have been identified, guiding management strategies. Rifaximin has emerged as a promising alternative for SBP prophylaxis, with encouraging results. This review aims to explore the shifting role of FQ-based SBP prophylaxis, focusing on the emerging concerns, side effects, and alternative strategies. While norfloxacin remains a first-line prophylactic in cirrhotic patients with low ascitic protein levels, its efficacy appears to be reduced in those with advanced liver failure or additional risk factors for MDR organisms. In these subgroups, alternative prophylactics, such as trimethoprim–sulfamethoxazole or rifaximin, may be preferable. We propose a risk-stratification approach to guide treatment selection, with further studies needed to refine these criteria.

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.

Backwash ileitis (BWI) refers to inflammation in the distal ileum in patients with extensive ulcerative colitis (UC) that is thought to be caused by a “reflux” or “backwash” of colonic contents. In the absence of well-defined diagnostic criteria for BWI, more recently, the term UC-associated ileitis was proposed in favor of the backwash theory, which questions the existence of backwash ileitis as a distinct disease-specific subset of patients. Moreover, distinguishing UC-associated BWI from terminal ileitis of Crohn’s disease or other conditions could be a diagnostic challenge and significantly affect treatment management. Therefore, clinical, endoscopic, histologic, and imagistic diagnostic features may aid in making this distinction. This literature review related to BWI outlines the hypothesis that the ileum may also become involved in UC as a primary manifestation of UC based on recent findings. This study also highlights the possibility that associated ileitis in UC patients may represent a potential risk factor for neoplasia, a positive association with primary sclerosing cholangitis, and a higher risk for the subsequent development of pouchitis after restorative proctocolectomy. It synthesizes recent key findings and highlights areas for further research.

Inflammatory bowel diseases (IBD) represent chronic conditions with etiopathogenic mechanisms incompletely elucidated despite extensive research efforts. Therefore, it is essential for clinical monitoring of the implementation of personalized medicine, enabling risk stratification and the selection of therapies with the highest likelihood of a favorable response. Multi-omics approaches have emerged as an excellent opportunity for the prevention, clinical phenotype differentiation, and prediction of IBD development. Proteomics has gained significant enthusiasm in medical practice, primarily due to its focus on studying the composition and dynamic expression of various cellular and tissue structures. This approach provides critical insights into their impact on signaling pathways, post-translational modifications, and the development of sequence variations. Hence, it could provide the foundation for developing biomarkers with the potential to assess mucosal healing and predict prognostic variability among patients, facilitating the implementation of a personalized therapeutic approach. This review focuses on the recent research regarding the possibility of implementing proteomics technologies into clinical practice, given the challenges and limitations, and the advantages of increasing the quality of life in patients with IBD.

Background: Early rebleeding after endoscopic variceal ligation (EVL) represents a serious complication in patients with cirrhosis and is associated with poor short-term outcomes. This study aimed to identify independent predictors of early rebleeding after EVL, with a particular focus on distinguishing factors associated with variceal rebleeding from those related to post-banding ulcer (PBU) bleeding, and to assess predictors of six-week mortality. Methods: We conducted a retrospective cohort study including 217 cirrhotic patients who underwent first emergency EVL for an index episode of esophageal variceal bleeding at a tertiary referral center. Early rebleeding was defined as recurrent upper gastrointestinal bleeding occurring between days 6 and 42 after the index EVL. Results: Early rebleeding occurred in 38/217 patients (17.5%): 27/38 (71.1%) variceal rebleeding and 11/38 (28.9%) PBU rebleeding. In multivariable logistic regression analysis, lower hemoglobin (OR = 0.19, 95% CI: 0.067–0.539, p = 0.002) and a higher albumin–bilirubin (ALBI) grade (OR = 24.94, 95% CI: 1.134–548.342, p = 0.041) were independently associated with increased odds of early variceal rebleeding, whereas a higher number of bands applied during index EVL (OR = 0.52, 95% CI: 0.302–0.896, p = 0.019) was independently associated with reduced odds of rebleeding, with excellent model discrimination (area under the curve [AUC] 0.981; 95% CI: 0.959–1.000). For PBU rebleeding, lower fibrinogen level was the only independent predictor (OR = 0.957, 95% CI: 0.916–1.000, p = 0.047), with strong discriminative performance (AUC 0.945; 95% CI: 0.909–0.982). Model for End-Stage Liver Disease (MELD) score, serum albumin, platelet count, and PBU rebleeding independently predicted six-week mortality. Conclusions: Markers of liver function, along with endoscopic parameters, predict early rebleeding after EVL, emphasizing the importance of the complete assessment of cirrhotic patients for refined risk stratification and tailored post-EVL management.