Cholecystocolonic fistula (CCF) is a rare type of cholecystoenteric fistula, which are sometimes diagnosed incidentally in patients undergoing cholecystectomy. They are usually a complication of chronic cholecystitis, often secondary to gallstones, and they are difficult to diagnose due to their rarity and vague clinical presentation. If untreated, they can lead to complications such as acute cholangitis, biliary peritonitis, and biliary cirrhosis. This highlights the importance of early recognition of CCF and timely treatment. While the generally accepted management is surgical, there are no consensus guidelines available. We present a case of a 79-year-old with a CCF, diagnosed preoperatively in the setting of workup for acute cholangitis and choledocholithiasis. She presented with four days of right-sided abdominal pain and one day of vomiting and new jaundice. She was initially hypotensive with elevated inflammatory markers, hyperbilirubinaemia, and deranged liver function tests. Contrast-enhanced CT revealed an 11 mm distal common bile duct calculus with hepatic biliary dilatation, gas in the gallbladder lumen, and a large gallstone in the hepatic flexure, which were suggestive of an underlying CCF. She underwent a laparoscopic converted to open cholecystectomy with transcystic bile duct exploration and choledochotomy, as well as right hemicolectomy due to extensive oedema and inflammation surrounding the CCF. This was later followed by endoscopic retrograde cholangiopancreatography (ERCP) and biliary sphincterotomy. Her CCF and acute cholangitis were thus successfully treated with surgical intervention, and she recovered well. The rare occurrence of CCF highlights the importance of having a high index of clinical suspicion preoperatively as well as maintaining surgical flexibility if it is encountered during an operation. Early recognition and surgical intervention of CCF are important to prevent life-threatening complications.

Objectives. This study assessed the health effects of occupational benzene exposure to inform preventive strategies. Methods. Occupational health surveillance data for benzene-exposed workers in Nanning (2020-2024) were obtained from the China Occupational Disease and Health Hazard Factors Monitoring Information System. Demographic, occupational and physical examination data were analyzed using χ[2] tests and multivariate logistic regression. Results. Abnormalities occurred in complete blood count (CBC) (4.47%), liver function (5.95%), electrocardiogram (ECG) (14.10%) and blood pressure (BP) (13.69%). Female workers had higher odds of CBC abnormalities (odds ratio [OR] 1.352) but lower odds of liver function (OR 0.362), ECG (OR 0.813) and BP (OR 0.572) abnormalities than males. Older age was associated with more ECG and BP abnormalities but fewer liver function abnormalities. Longer employment and manufacturing work (OR 1.735) increased the CBC abnormality risk. Conclusion. Occupational benzene exposure is associated with multifactorial health risks, warranting coordinated prevention by governments, enterprises and workers.

The present study aims to characterize the impact of Epstein-Barr virus (EBV) lytic replication on liver disease in patients with chronic hepatitis B virus (HBV) infection. We retrospectively enrolled 261 patients with HBeAg-negative chronic HBV infection who were admitted to Zhongnan Hospital between 2019 and 2025. Plasma levels of HBV-DNA, EBV-DNA, and liver function parameters were collected. Patients were grouped based on their viral DNA status, and the association between viral DNA status and liver function was evaluated. Compared to the HBV-DNA-negative group, HBV-DNA-positivity was significantly associated with aggravated hepatic injury, as evidenced by elevated ALT, AST, lymphocyte count, and fibrosis scores (APRI and FIB-4). Notably, regardless of HBV-DNA status or the stage of liver disease (CHB or LC), EBV-DNA-positivity was consistently associated with significantly lower plasma albumin (Alb) levels and albumin-to-globulin (A/G) ratio compared to EBV-DNA-negative patients. The reduction in the A/G ratio was attributable to decreased Alb levels rather than to elevated globulin (Glb) levels. These results suggest that EBV lytic replication was associated with hypoalbuminemia in this study. Circulating EBV-DNA status holds promise as a potential biomarker for monitoring disease progression, or assessing disease severity in patients with chronic HBV infection.

BackgroundHepatic dysfunction is increasingly recognized as a contributor to adverse outcomes in patients with pulmonary arterial hypertension (PAH). However, current prognostic models for PAH do not incorporate hepatic function parameters.ObjectivesTo develop and validate a novel risk prediction model that integrates hepatic function indicators with established PAH severity markers, and to compare its performance against the COMPERA 2.0 model.DesignProspective cohort study.MethodsThree liver fibrosis scores (LFSs)-FIB-4, NFS, and HUI-were evaluated for their prognostic significance. A total of 715 PAH patients from Fuwai Hospital were used to develop the FW-HP model. The model's predictive performance was assessed and compared with COMPERA 2.0. Risk stratification of the PAH cohort was subsequently conducted based on model scores.ResultsAll three LFSs were independently associated with mortality in PAH. The FW-HP model, incorporating albumin, total bilirubin, N-terminal pro-B-type natriuretic peptide, and World Health Organization functional class, provided superior risk prediction with area under the receiver operating characteristic curve of 0.86, 0.89, and 0.83 at 1-, 2-, and 3-year intervals, respectively-markedly exceeding COMPERA 2.0. The FW-HP score demonstrated higher net clinical benefit and enabled earlier identification of non-low-risk patients requiring more aggressive management.ConclusionsThe FW-HP model offers improved prognostic accuracy by incorporating hepatic function into PAH risk stratification. It represents a practical tool for early risk identification with potential to guide clinical decision-making in PAH patients.

Pre-eclampsia is a pregnancy complication that involves the development of high blood pressure in a pregnant woman and other features such as protein in the woman's urine, kidney or liver problems, or poorer growth for the baby. It can also have long-term health impacts for the mother after pregnancy. Pre-eclampsia typically occurs after 20 completed weeks of pregnancy (either mid-pregnancy known as 'early onset pre-eclampsia' or, more commonly, later in pregnancy, at or after 34 weeks, known as 'late onset' pre-eclampsia). Different blood pressure medications can be used to treat this condition, but not all women respond in the same way to the same medication. This is probably due to variables in the function of the maternal heart and blood vessels. Over the past 20 years, technological developments have meant it is now possible to measure important individual aspects of maternal cardiovascular function, using simple non-invasive tests. These tests can establish whether the mother's heart and circulatory system have any unusual features that may place her at higher risk of complications. They can also be used to monitor whether the mother's health and circulatory system is adapting in the right way to the pregnancy. For example, it is now possible to measure cardiac output (volume of blood pumped out by the heart) and vascular resistance (the physical resistance to the flow of blood), as well as the mother's blood pressure. It is also possible to monitor if and how changes in the above follow the patterns of change that are usually seen during pregnancy. Testing, and repeat testing as necessary, can identify individual measurements, or patterns of measurements, of concern and can identify whether the mother's heart and blood flow are adapting to the pregnancy in the typical and expected way. Studies in these areas have shown two distinct patterns of abnormal measurements of blood circulation and heart health in the pregnant woman that can occur with pre-eclampsia. Some changes and abnormalities can be detected before the symptoms of pre-eclampsia become obvious. Some features associated with pre-eclampsia can also be detected early in pregnancy or even before pregnancy. For example, we understand that some pregnant women who have a lower volume of blood being pumped out of their hearts per minute (low cardiac output), are more at risk of being affected by pre-eclampsia earlier in pregnancy, and more likely to have a baby with a low birth weight. Women that develop pre-eclampsia later in pregnancy typically have more circulating blood and babies of normal or larger size. The distinct measurable features of maternal heart health and blood flow can be used to identify those women at risk of developing pre-eclampsia at an early stage. Recognising the features of maternal heart health and the patterns of blood flow associated with pre-eclampsia provides an opportunity to individualise treatment plans for pregnant women, such as a personalised plan of monitoring and review, and using the most appropriate drugs that are tailored to address specific difficulties and likely to be most effective in restoring balance to the circulatory system of that individual. Early recognition, before the onset of symptoms, also allows timely reviews, and appropriate treatment to be started sooner. This, in turn, can lower the incidence of serious manifestations of pre-eclampsia for the mother, such as the development of seizures or a stroke. There is clear evidence that the management of pre-eclampsia can be improved by more detailed cardiovascular evaluation and tailored monitoring. The drugs that lower blood pressure work in different ways and the opportunity exists to target therapy to the underlying problem, however at the time of writing, many of the non-invasive tests and assessments able to identify women at risk of pre-eclampsia are typically only being used in a research setting. Routine clinical use of the available tests, and the establishment of clear care pathways and defined parameters for risk assessment based on those maternal heart and circulation test results, would allow targeted treatment and assist in preventing avoidable harm.

To reconnoitre the mechanism of Abietic acid (AA) in diabetes by in-silico and in-vivo experiments. Using GeneCards, diabetes gene targets were obtained. The protein-protein interaction and network topology analysis were performed using the String platform and Cytoscape 3.7.2. The enrichment analysis was done by Shiny GO. The docking was by Autodeck. Diabetes was induced by injecting STZ (55 mg/kg, i.p once) in Sprague-Dawley rats. The parameters included glucose, lipids, blood pressure, ECG, OGTT, kidney and cardiac markers, liver enzymes, AMPK, Nrf2, PPAR-γ, TLR-4, oxidative markers, LVF tests, and histopathology. AA interacts with 15 important targets (PIK3CD, MAPK1, NF-κB, mTOR, STAT3, GRIN1, ITGB3, ACACA, HSP90AB1, SERPINE1, ADRB1, ULK1, TLR4, CTSD, CDK5). The signalling pathways, like insulin, MAPK1, TLR, AMPK, JAK-STAT, are associated with these proteins. In docking, the highest affinity of AA was observed for ITGB3 (- 8.1), TLR4 (- 7.8), and ACACA (- 7.3). In rats, AA(40 and 80 mg/kg) decrease hyperglycaemia and hyperinsulinemia, improves glucose tolerance, normalize blood pressure, combat dyslipidaemia (decrease triglyceride, total cholesterol, LDL, increase HDL), preserves myocytes and ventricular function (decrease troponin-I, LDH, CK-MB, LVEDP, normal ECG), hepatoprotective (decrease AST, ALT), reno-protective (decrease creatinine, urea, uric acid) and combat oxidative stress (decrease MDA, increase SOD, catalase). Nrf2, AMPK, and PPAR γ levels were increased while TLR-4 levels were decreased after AA treatment. The study is supported by the preserved histopathological architecture of pancreatic, renal, hepatic, and cardiac cells. The present study preliminarily clarifies that AA exhibits therapeutic potential in preclinical models through multitargets and multi-pathways (Nrf/TLR4/PPAR γ), which points out a new direction for further research and clinical application.

Background: Butyrophenone neuroleptics are used in veterinary practice-haloperidol in the capture and translocation of wild ungulates, azaperone in swine-and antipsychotics prescribed to owners are a recognised cause of accidental toxicosis in dogs and cats. Organ-level toxicity data for this drug class are nonetheless almost absent in any species. Intravenous lipid emulsion (ILE) is an established antidote in small-animal emergency medicine for lipophilic intoxications, but the veterinary evidence base consists of case reports with clinical endpoints, and no controlled study has examined what ILE does to the tissues themselves. This study used an acute rodent overdose model to provide that organ-level assessment. Methods: Forty male Wistar albino rats were randomised to four groups of ten: control (saline 2 mL/kg oral gavage), HP (17.5 mg/kg oral gavage), HP + ILE (17.5 mg/kg HP plus 20% ILE 7.5 mL/kg intravenously at 0.5 h and 8 h, an empirical regimen) and ILE alone. Endpoints were assessed at 24 h. Seventeen histopathological parameters across seven organs were scored semi-quantitatively by a blinded pathologist (n = 10 per group), with independent re-scoring of a stratified random 30% subsample by a second blinded pathologist. Serum total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI) and routine biochemistry were measured in animals with adequate serum (n = 34 and n = 35). Comparisons used Kruskal-Wallis and Mann-Whitney U tests with Benjamini-Hochberg false discovery rate (FDR) control. Results: Haloperidol produced significant injury in the liver, kidney, brain and testis (all p < 0.001 vs. control) and mild histological cardiac changes (degeneration p = 0.014; congestion p = 0.034); lung and eye were unaffected. Serum urea was markedly elevated in HP (67.4 ± 13.2 vs. 46.5 ± 8.8 mg/dL; p = 0.001, d = 1.82) and HP + ILE (61.5 ± 8.7 mg/dL; p = 0.003), with unchanged creatinine, and correlated strongly with renal histopathology (renal inflammation vs. urea ρ = 0.74, p < 0.001). ILE significantly attenuated histopathological injury in 8 of the 12 haloperidol-associated parameters after FDR correction (renal congestion q = 0.032, r = 0.70; testicular Johnsen score q = 0.032, r = 0.66); the testicular score improved significantly relative to HP (q = 0.032) but remained statistically indistinguishable from control (p = 0.072), which does not establish equivalence. ILE did not reduce serum urea (HP + ILE vs. HP, p = 0.26) and did not modify the mild histological cardiac changes (p ≥ 0.40); no functional or electrophysiological cardiac endpoint was assessed. No group difference was detected in serum TOS or OSI (p = 0.43 and p = 0.51), whereas TAS was significantly reduced in the ILE-alone group (p = 0.011); the biological interpretation of this TAS finding remains uncertain, because interference of residual lipaemia with the spectrophotometric assay could not be excluded and would also propagate to the derived OSI. No tissue oxidative marker was measured. Transaminases were not elevated by haloperidol and showed no correlation with hepatic histopathology (|ρ| ≤ 0.17, all p > 0.34). ILE alone caused no histopathological abnormality at this dose and time point. Inter-observer agreement was high (95.6% exact agreement; median weighted κ = 0.893). Conclusions: In this acute overdose model, ILE is associated with a differential and structurally incomplete histopathological response: microscopic injury improves in four organs while renal function does not, and the mild histological cardiac changes are unaltered. Serum transaminases did not reflect concurrent organ-level injury at 24 h. Serum TOS and OSI showed no detectable group differences, while TAS was reduced in the ILE-alone group with an uncertain biological interpretation. Given the analytical uncertainty and the limited sample size, these indices provided no usable surrogate information about organ-level injury in this model. These findings define which organ systems respond and require confirmation in target veterinary species before informing clinical practice.

Background: Liver injury (LI) is frequently observed in patients with COVID-19, particularly in severe forms of disease. However, its prognostic significance remains incompletely defined. Aim: To evaluate the association between LI at admission and clinical outcomes in hospitalized patients with moderate, severe, and critical COVID-19. Methods: This single-centre retrospective cohort study included 816 adults hospitalized with moderate-to-critical COVID-19 at a tertiary care hospital in Romania. LI was defined as elevations ≥ 2× the upper limit of normal (ULN) in alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), or total bilirubin (TB) at admission. Clinical, laboratory, imaging, and outcome data, including intensive care unit (ICU) admission, invasive mechanical ventilation (IMV), and mortality, were analysed. Results: LI was present in 34.9% of patients. Compared with patients without LI, affected patients more frequently exhibited inflammatory syndrome (98.7% vs. 95.2%, p = 0.017), elevated interleukin-6 (IL-6) levels (65.3% vs. 44.3%, p = 0.007), and extensive pulmonary involvement (>75% on chest computed tomography; 38.2% vs. 27.3%, p = 0.003). They were also more likely to require ICU admission (44.2% vs. 36.2%, p = 0.025) and IMV (30.9% vs. 23.5%, p = 0.011). Seven-day mortality (25.9% vs. 16.1%, p = 0.001) and overall mortality (49.8% vs. 36.8%, p < 0.001) were significantly higher among patients with LI. In multivariable analysis, LI remained independently associated with both 7-day and overall mortality. The association between admission LI and mortality remained consistent across pandemic waves, with no significant interaction between liver injury and wave (p = 0.731). Conclusions: LI at admission may help identify patients with COVID-19 at increased risk of adverse outcomes and represents a simple and widely available tool for early risk stratification and clinical management.

Malaria is still a pressing global health challenge, especially in sub-Saharan Africa, where behavioural factors such as alcohol consumption may exacerbate its impact. The present study is aimed at investigating the pathogenesis of alcohol-exacerbated malaria in Plasmodium berghei-infected an animal model (mice). Mice were separated into four treatment groups: control, alcohol control, P. berghei and P. berghei plus acute alcohol treatment groups. Animals were infected with malaria through intraperitoneal injection of P. berghei and an acute dose of ethanol (20% v/v, oral) was introduced 48 h post-infection. Parasitaemia was monitored using the Giemsa-stained thin blood smears. Haematological parameters were assessed using an automated blood analyser. Liver function was evaluated by measuring serum levels of AST and ALT; oxidative stress biomarkers (MDA, SOD, CAT, GSH) were evaluated, and cytokine profiles (TNF-α, IFN-γ, IL-6, IL-1β) were quantified using ELISA kits. Results show that acute alcohol intake led to a significant increase in parasitaemia in the P. berghei group (p < 0.01). Haematological analysis revealed a significant (p < 0.001) reduction in RBC count, haemoglobin levels, haematocrit percentage, platelet count and others in the P. berghei plus acute alcohol treatment group. Liver enzyme assays revealed elevated AST and ALT levels (p < 0.001) in the P. berghei group, due to acute alcohol. Cytokine analysis revealed a significant (p < 0.01) upregulation of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1β and IL-6), due to acute alcohol. Oxidative stress was significantly (p < 0.001) increased, evidenced by significant elevation of MDA and significant depletions in GSH, SOD and CAT, due to acute alcohol. These results suggest that alcohol exacerbates malaria pathogenesis by increasing parasitaemia, promoting immune dysregulation, liver injury and oxidative stress, in a murine model.