Cirrhosis, a progressive condition characterized by hepatic fibrosis and functional decline, remains a significant global health burden. Despite advancements in understanding its pathophysiology, effective therapies to halt or reverse progression are limited, especially in advanced stages. Cirrhosis decompensation represents an inflection point in the disease course, with a substantial increase in mortality. Ascites is the most common decompensating event, associated with significant morbidity and healthcare burden, making it a key target in the management of decompensated cirrhosis. Sodium-glucose cotransporter 2 (SGLT2) inhibitors, widely used for type 2 diabetes mellitus, have demonstrated potential beyond glucose regulation. Evidence from clinical and preclinical studies suggests that SGLT2 inhibitors may improve hepatic parameters, reduce hepatic steatosis and fibrosis, and mitigate complications such as ascites. This review explores the multifaceted effects of SGLT2 inhibitors on cirrhosis, focusing on their mechanisms, clinical implications, and therapeutic potential in cirrhosis. By addressing current gaps in therapeutic strategies, SGLT2 inhibitors may represent a novel avenue for improving outcomes in patients with cirrhosis.

Acute kidney injury (AKI) is typically classified as prerenal, renal, or postrenal in etiology, with postrenal often referring to obstructive causes. However, certain uncommon conditions, such as intraperitoneal urinary leaks, may not fit clearly into these categories. In patients with a recent history of pelvic procedure, a complication such as intraperitoneal urinary leak can mimic AKI due to urine reabsorption across the peritoneum. When these leaks present beyond the immediate postoperative period, they can be challenging to diagnose, potentially leading to delayed management and complications. We report the case of a male patient who presented with lower abdominal pain and dysuria four weeks after undergoing radical prostatectomy. His initial evaluation, including urinalysis and imaging, suggested a urinary tract infection (UTI), and he was discharged with antibiotics. Three days later, he returned to the emergency room with persistent symptoms, new-onset diarrhea, and elevated creatinine compared to baseline. He was diagnosed with AKI, presumed to be secondary to dehydration, and received intravenous (IV) fluids. Despite undergoing treatment, his symptoms worsened, with further deterioration in renal function in the absence of a clear cause. An abdominal MRI ultimately revealed a fluid collection behind the bladder, indicative of a urinoma. His symptoms and renal function improved significantly after the Foley catheter placement. Intraperitoneal urinary leaks should be considered in post-pelvic surgery patients with unexplained serum creatinine elevations, as delayed recognition can lead to significant morbidity. This report underscores the importance of including intraperitoneal urinary leaks in the differential diagnosis for patients presenting with AKI following recent pelvic surgeries or procedures.

Foreign body ingestion (FBI) is a common clinical presentation, with most cases occurring in children. While accidental FBI in adults is less frequent, it is often associated with psychiatric conditions or substance use disorders. Magnet ingestion is particularly concerning due to the risk of pressure necrosis, perforation, and fistula formation, yet reports of magnet retention in adults are exceedingly rare.

Background and Aims: Sodium–glucose cotransporter-2 inhibitors (SGLT2i) may have favorable hepatic effects, but long-term outcomes in cirrhosis are uncertain. We investigated the relationship between SGLT2i exposure and 5-year outcomes among adults with cirrhosis. Methods: We performed a retrospective cohort study in the TriNetX US Collaborative Network (March 2013– January 2025). Adults (≥18 years) with cirrhosis were classified as SGLT2i users (first exposure on/after cirrhosis diagnosis) or non-users (no SGLT2i exposure) and propensity score matched 1:1. Outcomes were assessed over 5 years beginning 1 day after index. Primary outcomes were all-cause mortality and hospitalization burden (inpatient encounters per patient). Secondary outcomes included hepatic decompensation complications and prespecified adverse events; tertiary outcomes were the most recent liver- and kidney-related laboratory values during follow-up. Results: After matching, 24,559 patients were included per cohort. SGLT2i use was associated with lower all-cause mortality (11.8% vs 26.0%; OR=0.381, 95%CI: 0.363–0.399; p<0.001) and fewer hospitalizations (mean 3.6±10.7 vs 5.4±13.4; p<0.001). Composite hepatic decompensation was less frequent (OR=0.617, 95%CI: 0.580–0.656; p<0.001), including lower odds of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome; hepatic encephalopathy did not differ. Acute kidney failure and urinary tract infection were less frequent, while diabetic ketoacidosis did not differ. Laboratory profiles favored SGLT2i use (lower aspartate aminotransferase and bilirubin, higher albumin, lower international normalized ratio, and improved renal indices). Conclusions: In this matched real-world cohort, SGLT2i exposure after cirrhosis diagnosis was associated with an improved 5-year survival, fewer hospitalizations, and fewer decompensation events.

Background: Outcomes in chronic myeloid leukemia (CML) remain heterogeneous despite effective BCR::ABL1 tyrosine kinase inhibitors (TKIs). Somatic mutations in epigenetic regulators, particularly additional sex combs like 1 (ASXL1), have been implicated in adverse prognosis, but their clinical impact in CML has not been systematically defined. Methods: A systematic review was conducted using CINAHL, EMBASE, MEDLINE Ultimate, and PubMed from inception through August 2025. A total of 1,339 records were identified; after duplicate removal and screening, 11 studies met inclusion criteria and were included in qualitative synthesis and meta-analysis. Eligible studies included adult and pediatric patients with chronic and advanced phase (accelerated or blast) CML with ASXL1 mutation status assessed using validated molecular methods. Outcomes included molecular response, cytogenetic response, survival, and treatment resistance. Random-effects models were used to calculate pooled odds ratios (ORs) with 95% confidence intervals (CI). Statistical heterogeneity was assessed using the I² statistic. Results: Across included studies, ASXL1 mutations were detected in approximately 16% of patients. At 12 months, ASXL1-mutated patients had significantly lower odds of achieving major molecular response (MMR) compared with ASXL1–wildtype patients (OR 0.29; 95% CI 0.16–0.51; p< 0.0001; I²=30%). No statistically significant difference was observed in complete cytogenetic response (CCyR) (OR 0.30; 95% CI 0.02–5.31; p=0.41; I²=68%). Compared with patients harbouring other non-ASXL1 somatic mutations, ASXL1 mutation was not associated with a significant difference in MMR (OR 0.49; 95% CI 0.23–1.05; p=0.067; I²=0%). Conclusions: ASXL1 mutations are associated with inferior molecular response to TKI therapy in CML, supporting their role as an adverse prognostic biomarker. These findings highlight the potential value of incorporating myeloid mutation profiling into future CML risk-stratification strategies.