Outcomes of Different Perioperative Management Strategies of Patients on Chronic Anticoagulation in Elective Total Hip and Knee Arthroplasty
Different anticoagulation-related perioperative management strategies achieve different outcomes following elective arthroplasty in patients with therapeutic chronic anticoagulation. There is contradictory evidence regarding the need for the discontinuation of therapeutic warfarin. Retrospective data showed that individual risk stratification with multi-modal prophylaxis resulted in minimal complications.
KEY FINDINGS: Different anticoagulation-related perioperative management strategies achieve different outcomes following elective arthroplasty in patients with therapeutic chronic anticoagulation. There is contradictory evidence regarding the need for the discontinuation of therapeutic warfarin. Retrospective data showed that individual risk stratification with multi-modal prophylaxis resulted in minimal complications.
BACKGROUND: There are currently different management guidelines for patients undergoing elective total hip arthroplasty (THA) or total knee arthroplasty (TKA) that are on long-term anticoagulation. The timing of discontinuation and restarting the anticoagulation is challenging during the postoperative care, which often involves general practitioners and physiotherapists.
DETAILS: The systematic review followed the PRISMA guidelines and included 3 databases: PubMed/MEDLINE, EMBASE, and Web of Science Core Collection. The risk of bias assessment was performed using the Methodological index for non-randomized studies (MINORS) criteria. Six retrospective studies involving 727 patients with therapeutic anticoagulation (1,540 controls) for elective THA, TKA and revision arthroplasty have been included. The follow-up ranged from 30 days to 1 year postoperatively. All studies evaluated outcomes of warfarin therapeutic anticoagulation versus prophylactic dosages of one or more of the following: warfarin, aspirin, low-molecular-weight heparin (LMWH) and unfractionated low-dose heparin (UFH). One study did not discontinue therapeutic anticoagulation. Two studies reported no significant differences in complications between groups, whilst 3 studies had significantly higher rates of superficial wound infections, revision surgeries, postoperative haematomas, and prosthetic joint infections (PJI).
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Source: Andronic, D., Andronic, O., Ammann, E., et al. (2024). Outcomes of Different Perioperative Management Strategies of Patients on Chronic Anticoagulation in Elective Total Hip and Knee Arthroplasty: A Systematic Review. Family Practice. 2024; 41(5): 629–637. Published: October, 2024. DOI: 10.1093/fampra/cmae020.
Re-envisioning the Lifespan Approach to Cardiovascular Disease Prevention and Treatment in Women
The anticipated life course of women supports a broadening focus on CVD toward that of lifelong care and emphasize key transitional stages for women - early risk factor onset, pregnancy, menopausal transition, and so on. This review is a call to action to re-envision a health system approach for lifespan prevention, detection, and treatment pathways to reduce CVD risk in women.
KEY FINDINGS:
- Mortality: CVD deaths in women exceed combined deaths from breast and lung diseases.
- Gap in Care: Insufficient sex-specific evidence continues to hinder lifesaving care.
- Call to Action: Transition from episodic care to a lifelong cardiovascular health system for women.
BACKGROUND: Despite the common misconception that respiratory or oncological diseases pose the greatest threat to women, Cardiovascular Disease (CVD) accounts for more female deaths than breast cancer, lung cancer, and chronic lung disease combined, with a comparable mortality to that of men. Historically, both the public and the medical community have underestimated CVD risks in women, leading to diagnostic delays and a scarcity of sex-specific evidence to guide clinical interventions. While advances have been made in the diagnosis, treatment and outcomes of CVD in women, there often remains insufficient evidence to guide effective, lifesaving care of women.
DETAILS: This review of sex-specific and traditional CVD risk and risk-enhancing factors in women identifies areas of knowledge gaps to consider for investigation. A focus on the coronary vasculature reveals physiological differences of clinical relevance which can be interrogated. Inspection of and addressing disadvantage and gender bias in both the medical and lay communities should continue to be addressed. As CVD results from traditional risk factors and emerging risk-enhancing factors, a focus on the detection of preclinical cardiovascular disease may be of particular importance for women. Unique risk markers originate early in pre-menopausal women, as this is considered a healthy period of life. Awareness and implementation of the existing knowledge of sex-specific risk factors and sex-specific thresholds to educate women and physicians are needed. The anticipated life course of women supports a broadening focus on CVD toward that of lifelong care and emphasize key transitional stages for women-early risk factor onset, pregnancy, menopausal transition, and so on. This review is a call to action to re-envision a health system approach for lifespan prevention, detection, and treatment pathways to reduce CVD risk in women.
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Hemochromatosis Proteins Hemojuvelin and Homeostatic Iron Regulator in Bone Morphogenetic Protein-Mediated Hepcidin Regulation and Iron Homeostasis
The findings suggest a model whereby BMP2 and BMP6 can signal to hepcidin induction independently of HJV and HFE and vice versa. In contrast, BMP5, HJV, and HFE are all required for iron-mediated hepcidin regulation in the absence of BMP2 and BMP6.
KEY FINDINGS: Together with other published data, these findings suggest a model whereby BMP2 and BMP6 can signal to hepcidin induction independently of HJV and HFE and vice versa. In contrast, BMP5, HJV, and HFE are all required for iron-mediated hepcidin regulation in the absence of BMP2 and BMP6.
BACKGROUND: The bone morphogenetic protein (BMP)-SMAD signaling pathway is central to regulating hepcidin, the master regulator of systemic iron homeostasis. Authors have previously demonstrated that BMP6, BMP2, and, to a lesser extent, BMP5 are the major ligands contributing to hepcidin and iron homeostasis regulation in vivo.
DETAILS: Hemojuvelin (HJV) and homeostatic iron regulator (HFE) are hepcidin modulators that are mutated in hereditary hemochromatosis. Although both HJV and HFE regulate hepcidin, at least partly, by functionally interacting with the BMP–SMAD pathway, the mechanisms are incompletely understood. Notably, both HJV and HFE can regulate hepcidin in a BMP6-independent manner. To understand whether HJV and HFE influence hepcidin regulation by BMP2 and/or BMP5, authors investigated the iron phenotype of mice with combined mutations in endothelial Bmp2/Hjv and Bmp5/Hfe. Authors found that endothelial Bmp2/Hjv double knockout (KO) mice exhibit more severe hepcidin deficiency and iron overload than single endothelial Bmp2 or Hjv KO mice, similar to previous findings in mice with double endothelial Bmp2/Hfe KO and Bmp6/Hjv KO, or a functional loss of both Bmp6 and Hfe. Moreover, authors found that iron completely fails to induce hepcidin in both endothelial Bmp2/Hjv and Bmp2/Hfe double KO mice. In contrast, a functional loss of BMP5 does not worsen hemochromatosis in Hfe KO mice.
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Source: Xiao, X., Moschetta, G. A., Chowdhury, S. B., et al. Hemochromatosis Proteins Hemojuvelin and Homeostatic Iron Regulator in Bone Morphogenetic Protein-Mediated Hepcidin Regulation and Iron Homeostasis. American Journal of Hematology. 2025; 100(12): 2175-2184. Published: December, 2025. DOI: 10.1002/ajh.70055.
Efficacy and Safety of Time-Restricted Eating in Metabolic Dysfunction-Associated Steatotic Liver Disease
This 16-week RCT compared TRE, CR, and standard of care in patients with MASLD. It effectively reduced steatosis, with similar benefits on weight loss, body composition, and metabolic parameters as CR. TRE is a practical dietary strategy for MASLD and warrants further long-term study. TRE's effectiveness in MASLD remains unclear despite its potential metabolic benefits.
KEY FINDINGS: TRE effectively reduces hepatic steatosis in MASLD, with comparable benefits on weight loss, body composition, and metabolic parameters as CR. This approach may serve as a practical dietary strategy for MASLD management.
BACKGROUND: Time-restricted eating (TRE) may improve weight loss, insulin resistance, and body composition, which are key factors in the pathophysiology of metabolic dysfunction-associated steatotic liver disease (MASLD). However, evidence on the efficacy of TRE in patients with MASLD is limited. This study aimed to evaluate the potential benefits of TRE in patients with overweight or obesity and MASLD.
DETAILS: In this 16-week randomized controlled trial, patients with overweight or obesity and MASLD were randomized into three groups in a 1:1:1 ratio: standard of care (SOC), calorie restriction (CR), and TRE. The primary endpoint was an improvement in hepatic steatosis, measured using MRI-proton density fat fraction. Changes in liver fibrosis, body composition, lipid profiles, glucose homeostasis, and sleep quality were also analyzed. Among the 337 participants randomized, 333 were included in the full analysis set (113 in SOC, 110 in CR, and 110 in TRE). After the 16-week intervention, hepatic steatosis significantly decreased in the TRE group (-25.8%) compared to the SOC group (0.7%, p <0.001), with no significant difference between TRE and CR (-24.7%, p >0.999). The TRE group also showed greater reductions in body weight, waist circumference, and body fat mass compared to the SOC group, while changes were comparable between TRE and CR. Liver stiffness, glucose homeostasis, and sleep quality were similar between the TRE and CR groups. No serious adverse events were reported.
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Source: Oh, J. H., Yoon, E. L., Park, H., et al. Efficacy and Safety of Time-Restricted Eating in Metabolic Dysfunction-Associated Steatotic Liver Disease. Journal of Hepatology. 2025; 83(6): 1256-1265. Published: December, 2025. DOI: 10.1016/j.jhep.2025.06.005.
Effects of Sodium Glucose Cotransporter 2 Inhibitors by Diabetes Status and Level of Albuminuria
Within the studied participants, there were clear absolute benefits of SGLT2 inhibitors on kidney, hospitalization, and mortality outcomes irrespective of diabetes status and level of UACR.
KEY FINDINGS: Within the studied participants, there were clear absolute benefits of SGLT2 inhibitors on kidney, hospitalization, and mortality outcomes irrespective of diabetes status and level of UACR.
BACKGROUND: There is uncertainty about the effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors in participants with chronic kidney disease, with guidelines offering different strengths of recommendation based on diabetes status and urine albumin to creatinine ratio (UACR). Study was conducted to assess the relative and absolute effects of SGLT2 inhibitor use across efficacy and serious safety outcomes in participants stratified by diabetes status and UACR (>=200 mg/g or <200 mg/g). Included 8 randomized clinical trials that studied an SGLT2 inhibitor with a label indication for use in kidney disease and recorded longitudinal kidney outcomes and baseline data on albuminuria. Assessed the effects of SGLT2 inhibitor use on clinical efficacy and safety outcomes. Heterogeneity by baseline level of UACR was assessed separately by diabetes status.
DETAILS: A total of 58,816 participants (mean age, 64 [SD, 10] years; 35% were female; 48,946 with diabetes and 9870 without diabetes) were included from trials comparing an SGLT2 inhibitor vs placebo. Allocation to an SGLT2 inhibitor produced a lower rate of kidney disease progression (33 vs 48 for placebo per 1000 patient-years; hazard ratio [HR], 0.65 [95% CI, 0.60-0.70] in those with diabetes and 32 vs 46 per 1000; HR, 0.74 [95% CI, 0.63-0.85] in those without diabetes), a lower rate of acute kidney injury (14 vs 18 per 1000 [HR, 0.77; 95% CI, 0.69-0.87] with diabetes and 13 vs 18 per 1000 [HR, 0.72; 95% CI, 0.56-0.92] without diabetes), a lower rate of any hospitalization (202 vs 231 per 1000 [HR, 0.90; 95% CI, 0.87-0.92] with diabetes and 203 vs 237 per 1000 [HR, 0.89; 95% CI, 0.83-0.95] without diabetes), and a lower rate of any death (42 vs 47 per 1000 [HR, 0.86; 95% CI, 0.80-0.91] with diabetes and 42 vs 48 per 1000 [HR, 0.91; 95% CI, 0.78-1.05] without diabetes). Diabetes-specific HRs were similar in participants (with a UACR >=200 mg/g vs with a UACR <200 mg/g) considered separately. Higher absolute risk at a UACR of 200 mg/g or greater meant larger estimated absolute benefits on kidney disease progression were evident in this subgroup. Clear absolute benefits were evident for other efficacy outcomes, and particularly hospitalization, in participants with a UACR less than 200 mg/g. Net absolute benefits remained in the analyses of non–heart failure populations and when estimated glomerular filtration rate was less than 60 mL/min/1.73 m2.
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Source: Staplin, N., Roddick, A. J., Neuen, B. L., et al. Effects of Sodium Glucose Cotransporter 2 Inhibitors by Diabetes Status and Level of Albuminuria: A Meta-Analysis. JAMA. . 2025; Published online: November 7, 2025. DOI: 10.1001/jama.2025.20835.
Prenatal PM2.5 Exposure Induces Offspring Hypertension via Nrf2/NLRP3 Pathway
Overall, prenatal fine particulate matter exposure induces excessive inflammation and oxidative stress in paraventricular nucleus microglia through the Nrf2/NLRP3 signaling pathway, resulting in central and peripheral sympathetic overactivation, leading to hypertension and left ventricular hypertrophy.
KEY FINDINGS: Overall, prenatal fine particulate matter exposure induces excessive inflammation and oxidative stress in paraventricular nucleus microglia through the Nrf2/NLRP3 signaling pathway, resulting in central and peripheral sympathetic overactivation, leading to hypertension and left ventricular hypertrophy.
BACKGROUND: Adverse factors during pregnancy can significantly increase the incidence of hypertension in adult offspring. Activation of the sympathetic nervous system is closely associated with the development and progression of hypertension.
DETAILS: Authors established a model of offspring hypertension induced by prenatal fine particulate matter exposure to evaluate the role of the sympathetic nervous system activation. Quantitative immunofluorescence and Western blot analysis were used to assess the levels of activated and inhibitory sympathetic neurons. The effects of the central and peripheral sympathetic nervous systems were evaluated using clonidine and renal sympathetic denervation. In addition, the activation of microglia in the lateral ventricle region and the expression of the Nrf2 (nuclear factor E2-related factor)/ NLRP3 (NLR family pyrin domain-containing 3) signaling pathway were analyzed. The adult offspring showed increased neuronal hyperactivity and sympathetic nervous system activity. Specific inhibition of the central sympathetic nervous system and renal denervation effectively reversed the prenatal fine particulate matter-induced blood pressure elevation in adult offspring. In addition, overactivation of oxidative stress and microglia-mediated inflammation in the paraventricular nucleus was responsible for increased central sympathetic activity in the adult offspring exposed to prenatal fine particulate matter. Furthermore, authors confirmed the critical role of the Nrf2/NLRP3 signaling pathway in oxidative stress and inflammation activation in the paraventricular nucleus of adult offspring.
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Source: Zhang, X., Yang, B., Li, M., et al. Prenatal PM2.5 Exposure Induces Offspring c via Nrf2/NLRP3 Pathway. Hypertension. 2025; 82(11): 1841-1843), Published: November, 2025. DOI: 10.1161/HYPERTENSIONAHA.125.2487.
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