This research focused on exploring the association between coagulopathy scores and the survival outcomes, both short-term and long-term, in individuals diagnosed with liver cirrhosis complicated by sepsis. This study retrospectively analyzed data from individuals with liver cirrhosis and sepsis who were admitted to the intensive care unit (ICU) at Beth Israel Deaconess Medical Center between 2008 and 2022. The main outcome of interest was all-cause mortality within 28 days post-admission, while the secondary outcome assessed mortality within 90 days. We used the Kaplan-Meier analysis to compare the mortality risk among the different groups. To evaluate the relationship between coagulopathy score and mortality risk in patients with liver cirrhosis and sepsis, a multivariate Cox proportional hazards regression analysis was performed. The predictive performance of the coagulopathy score for short- and long-term all-cause mortality was assessed using receiver operating characteristic (ROC) curve analysis, which included evaluation of its sensitivity, specificity, and area under the curve. Subgroup analyses were performed to evaluate the relationship between coagulopathy score and survival across different groups. The study included a total of 2,278 patients. Kaplan-Meier survival analysis demonstrated that individuals with elevated coagulopathy scores exhibited markedly higher rates of ICU mortality, in-hospital mortality, as well as 28-day and 90-day mortality, with all log-rank tests yielding P-values of less than 0.001. The results of the multivariate Cox regression analysis showed that an elevated coagulopathy score was independently linked to higher 28-day and 90-day all-cause mortality, both before and after controlling for potential confounders. ROC curve analysis showed that although the coagulopathy score was slightly less predictive of prognosis than the Model for End-stage Liver Disease score, it significantly outperformed the Sequential Organ Failure Assessment score and the Sepsis-induced Coagulopathy score. Subgroup analysis revealed no significant interaction between the coagulopathy score and survival across the different subgroups. Higher coagulopathy scores in critically ill patients with liver cirrhosis and sepsis were independently associated with poor prognosis. Due to its simplicity and potential predictive value, the coagulopathy score can serve as an effective complement to existing clinical tools for managing critically ill patients with liver cirrhosis and sepsis.

Objective: We investigated the association between serum uric acid (SUA) levels and gallstone (GS) prevalence in adult women.Methods: Participants' information were taken from the United States National Health and Nutrition Examination Survey (2017–2020). Logistic regression analysis and dose-response curve were used to assess the association between SUA levels and the prevalence of GS in adult women. Subgroup analyses were performed to investigate associations between SUA levels and age, ethnicity, body mass index, hypertension, and diabetes.Results: A total of 600 participants self-reported a history of GS. After adjusting for confounding, the prevalence of GS in adult women increased by 14% for every 1 mg/dL increase in SUA (odds ratio [OR]: 1.14, 95% confidence interval [CI]: 1.06, 1.22). Testing SUA as a categorical variable for sensitivity analyses indicated a 1.6-fold increase in the prevalence of GS in tertile 3 (OR=1.60, 95% CI: 1.25, 2.04) compared to tertile 1. Dose-response curves showed a nonlinear correlation between SUA levels and the prevalence of GS. Subgroup analyses indicated that SUA level was associated with an increased prevalence of GS in most subgroups, although subtle differences existed.Conclusion: SUA was positively and non-linearly associated with the prevalence of GS in adult females. Despite the inability to clarify the causal relationship between them, our results remain interesting.

Background: Benign tumors of the spleen are rare compared to those of other parenchymal organs, accounting for less than 0.007% of all tumors, and are often found incidentally. Splenolymphangiomas are much rarer, commonly occur in children, and tend to have multiple foci. Splenic lymphangiomas are rare in adults, and fewer than 20 adult patients with isolated splenic lymphangiomas have been reported. In this article, we report the case of a middle-aged female patient with isolated splenic lymphangioma who underwent laparoscopic anatomical hypophysectomy of the lower pole of the spleen. We also summarize the existing literature on splenic lymphangioma diagnosis and available treatment options.Case presentation: A 58-year-old middle-aged woman was found to have a mass approximately 60 mm in diameter at the lower pole of the spleen during a health checkup that was not accompanied by other symptoms or examination abnormalities. After completing a preoperative examination with no contraindications to surgery, the patient underwent laparoscopic anatomical splenectomy of the lower extremity of the spleen. The patient recovered well without complications and was discharged from the hospital on the 7th postoperative day. Histopathological and immunohistochemical results confirmed the diagnosis of splenic lymphangioma. Prompt surgical intervention is safe and necessary when splenic lymphangiomas are large or associated with a risk of bleeding.Conclusion: Splenic lymphangiomas are rare and require early surgical intervention in patients with large tumor diameters or those at risk of rupture and bleeding. After rigorous preoperative evaluation and preparation, laparoscopic anatomical partial splenectomy is safe and feasible for surgeons with experience in laparoscopic surgery.

Background: To evaluate the feasibility, safety, and short-term clinical outcomes of robot-assisted partial splenectomy (RAPS) in the treatment of benign splenic lesions (BSLs). Methods: A retrospective analysis was conducted on nine patients with BSLs who underwent RAPS in the Department of Hepatobiliary, Pancreatic, and Splenic Surgery at Mianyang Central Hospital between January 2024 and September 2025. Clinical data, including demographic characteristics, lesion features, intraoperative parameters, postoperative recovery, and complications, were collected. All patients underwent preoperative contrast-enhanced abdominal computed tomography, magnetic resonance imaging, and three-dimensional (3D) reconstruction to delineate the anatomical relationship between the lesion and splenic vasculature. All procedures were performed by the same surgical team. Results: All nine procedures were successfully completed without conversion to open surgery. The cohort comprised three men and six women, with a mean age of 49.0 ± 10.3 years. Lesions were located in the lower pole in seven cases and in the upper pole in two, with a mean diameter of 4.34 ± 0.8 cm. The mean operative time was 179.4 ± 15.5 min, the mean intraoperative blood loss was 71.1 ± 19.6 mL, and the mean postoperative hospital stay was 6.4 ± 0.9 days. No cases of splenic infarction, pancreatic fistula, hemorrhage, or severe infection were observed. Pathological diagnoses included splenic hemangioma ( n = 3), non-parasitic splenic cyst ( n = 5), and splenic lymphangioma ( n = 1). During follow-up, no recurrence, new lesions, or splenic dysfunction were detected, and hematologic parameters remained within normal ranges. Conclusion: RAPS is a safe, feasible, and minimally invasive spleen-preserving procedure. Preoperative 3D reconstruction facilitates precise surgical planning, and when combined with the high-precision maneuverability of robotic technology, enables complete lesion removal while preserving functional splenic tissue. This approach aligns with the principles of modern precision and minimally invasive surgery.

Idiopathic mesenteric phlebosclerosis (IMP) is an extremely rare disease with an unclear pathogenesis and risk factors. The clinical manifestations of IMP are mostly non-specific, mainly consisting of digestive symptoms such as abdominal pain, bloating and diarrhea. The diagnosis of IMP mainly relies on abdominal computed tomography (CT) and colonoscopy. Pathological changes associated with IMP often involve fibrous degeneration of the venous wall, which results in the thickening of the colonic wall and longitudinal calcification of the mesenteric arteries. Currently, there is no standard treatment protocol for IMP, and nonsurgical treatment is the mainstay of most medical centers. In this study, we reported a case of a 55-year-old female patient with IMP whose main clinical presentation was recurrent abdominal pain. The patient’s initial diagnosis was considered an incomplete intestinal obstruction and received non-surgical treatments; however, the efficacy of the treatment was unsatisfactory. After completing abdominal CT and colonoscopy, we excluded common diseases of the digestive system (e.g., tumors, Crohn’s disease), and finally considered that this patient had a high likelihood of IMP. This patient eventually underwent laparoscopic enlarged right hemicolectomy due to recurrent symptoms and poor outcomes of non-surgical treatment. Postoperative pathological results confirmed the diagnosis of IMP. During the follow-up period, the patient recovered well without recurrence of IMP. Furthermore, we have reviewed the literature related to IMP and summarized the etiology, risk factors, diagnostic methods, treatment options and prognosis of IMP.

KMT2C (lysine methyltransferase 2C), also known as mixed-lineage leukemia 3 (MLL3), is a member of the KMT2 family of histone methyltransferases that catalyzes histone H3 lysine 4 monomethylation (H3K4me1), a hallmark of active enhancer elements. Operating within COMPASS-like complexes (Complex of Proteins Associated with Set1) and in association with the ASCOM coactivator complex (ASC-2–containing complex), KMT2C plays a central role in maintaining enhancer and super-enhancer integrity, thereby sustaining lineage-specific transcriptional programs. Across gastrointestinal malignancies, KMT2C is recurrently altered, predominantly through truncating loss-of-function variants, splice-disrupting events, and structural alterations that impair protein function. Importantly, the biological impact of KMT2C alteration is highly context dependent, shaped by mutation class, co-occurring genomic lesions, and tissue-specific transcriptional circuitry. Rather than inducing linear dysregulation of individual signaling pathways, KMT2C deficiency preferentially destabilizes enhancer and super-enhancer networks, leading to large-scale transcriptional rewiring. Disruption of enhancer modules that enforce cellular identity and homeostasis is frequently accompanied by activation of stress-adaptive and metabolic programs. Concurrently, defects in homologous recombination and replication-stress responses promote genomic instability, while attenuation of cell-cycle checkpoints and senescence barriers facilitates epithelial–mesenchymal transition, stem-like plasticity, and invasive or metastatic behavior. Beyond tumor-intrinsic effects, KMT2C dysfunction can reshape the tumor immune microenvironment through altered antigenic burden, inflammatory signaling, senescence-associated secretory programs, and dynamic stromal interactions, ultimately giving rise to heterogeneous therapeutic vulnerabilities. Clinically, KMT2C alteration has been linked to tumor mutational burden (TMB), microsatellite instability (MSI), immune infiltration patterns, and outcomes following immune checkpoint blockade (ICB). In parallel, KMT2C-associated DNA repair deficiencies provide a mechanistic basis for synthetic-lethal strategies involving poly(ADP-ribose) polymerase (PARP) inhibitors and inhibitors of ataxia telangiectasia and Rad3-related protein (ATR) or checkpoint kinase 1 (CHK1), including rational combinations with epigenetic therapies. In this review, we integrate evidence from hepatocellular carcinoma, pancreatic ductal adenocarcinoma, cholangiocarcinoma, colorectal cancer, gastric cancer, esophageal cancer, and gallbladder cancer within a unified framework that links KMT2C domain architecture to enhancer-network destabilization, phenotypic state transitions, and clinical manifestations. We further propose a functional evaluation paradigm that reframes discrete KMT2C variants as graded states of epigenetic deficiency, coupled with a closed-loop validation strategy integrating tissue-based profiling, liquid biopsy monitoring, and spatial multi-omics analyses.