Annals of medicine最新文献

Background: Osteoporosis significantly impacts global morbidity. Recent evidence suggests anaemia may contribute to osteoporosis risk. This systematic review and meta-analysis investigates this association.

Methods: PubMed, Scopus, EBSCO, and ScienceDirect were searched for papers. Studies with definition of anaemia and assessing osteoporosis outcomes were included. Meta-analysis utilized random-effects models (DerSimonian-Laird method), and study quality was assessed via Newcastle-Ottawa Scale (NOS). Analyses were performed using R Studio.

Result: Eighteen studies (861,540 participants) were analyzed. Anaemia significantly increased osteoporosis risk in univariate analysis (OR 1.62; 95% CI 1.33-1.98; p < 0.001), despite high heterogeneity (I² = 92.7%). The results remain significant in studies that reported multivariate analysis (OR 2.01; 95% CI 1.26-3.21; p = 0.004). Sensitivity analyses confirmed the robustness of our result.

Conclusion: Anaemia significantly associated with osteoporosis, emphasizing the need for targeted screening in anaemic individuals. Further studies should consider incorporating anaemia into osteoporosis and fracture prediction tools.

Objective: This study aimed to identify risk factors associated with the development of VTE in patients admitted to the intensive care unit (ICU).

Methods: A systematic literature search was conducted via PubMed, Embase, Web of Science, and Cochrane databases up to 25 April 2025, to identify studies examining the association between risk factors and the occurrence of venous thromboembolism (VTE) in ICU patients. Data were pooled using odds ratios (ORs) and 95% confidence intervals (CIs).

Results: A total of 2465 relevant studies were identified through the systematic search, of which 30 were included in the meta-analysis. The pooled data showed that the following were significant risk factors for venous thromboembolism (VTE) in ICU patients: central venous catheterization (OR = 2.67, 95% CI: 1.67-4.28; I² = 28%), invasive mechanical ventilation (OR = 2.08, 95% CI: 1.46-2.96; I² = 0%), advanced age (OR = 2.06, 95% CI: 1.28-3.31; I² = 86%), length of ICU stay (OR = 4.24, 95% CI: 1.43-12.57; I² = 98%), malignancy (OR = 2.30, 95% CI: 1.03-5.12; I² = 67%), elevated D-dimer levels (OR = 2.46, 95% CI: 1.37-4.40; I² = 34%), and a history of VTE (OR = 2.84, 95% CI: 1.45-5.55; I² = 51%). According to the GRADE assessment, the quality of evidence was rated as moderate for invasive mechanical ventilation, low for central venous catheterization and D-dimer levels, and very low for the remaining factors.

Conclusion: Invasive mechanical ventilation, central venous catheterization, and elevated D-dimer levels are associated with VTE risk, supported by relatively high-quality evidence. These findings may help identify ICU patients at higher risk of VTE, inform the development of risk assessment models for patient stratification, and ultimately contribute to improved prognosis through optimal screening and management strategies.

Background: This study investigates clinical characteristics influencing post-progression survival (PPS) in locally advanced esophageal squamous cell carcinoma (ESCC) after definitive chemoradiotherapy (dCRT), aiming to develop individualized follow-up strategies using conditional PPS.

Methods: The correlation between PPS and overall survival (OS) using Spearman correlation analysis. LASSO regression, Cox regression, and machine-learning methods were employed to identify prognostic factors, and a prediction model was constructed. The Shapley additive explanations (SHAP) method was used to interpret the model. Conditional PPS survival rates and recurrence risks were analyzed.

Results: This study enrolled 741 patients, with a median follow-up of 27.2 months. PPS was positively correlated with OS. Prognostic factors included: N stage, tumor length, chemotherapy cycles, platelet-to-albumin ratio, lymphocyte-to-monocyte ratio, age, body mass index, radiotherapy dose, and neutrophil to monocyte to lymphocyte ratio. Calibration curves, decision curves, and ROC curves demonstrated the model's stability and predictive performance. Subgroup analyses suggested shorter PPS in high-risk patients. After adjusting for other confounders, multi-model analyses continued to show a positive association between the risk score and unfavorable PPS. Conditional PPS analyses across different risk groups revealed that, with increasing survival time, conditional PPS extended correspondingly, and the relapse risk gradually decreased. Finally, individualized follow-up strategies were proposed, indicating intensified monitoring for high-risk patients.

Conclusion: This study fills the research gap in the influencing factors of PPS and personalized follow-up strategies for patients with locally advanced ESCC after dCRT, and provides important clinical evidence for promoting the transformation of post-recurrence management from 'experience-driven' to 'data-driven'.

Objective: Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has recently emerged as a promising therapeutic strategy for cervical cancer, particularly in tumors resistant to conventional radiotherapy and chemotherapy. This review aims to systematically summarize the current understanding of ferroptosis mechanisms in cervical cancer and its potential therapeutic implications.Methods: We comprehensively reviewed the literature focusing on key regulators of ferroptosis in cervical cancer, including system Xc- (SLC7A11), glutathione peroxidase 4 (GPX4), iron metabolism, and lipid peroxidation pathways. The interactions between ferroptotic processes and cervical cancer-specific cellular redox homeostasis and metabolic adaptations were analyzed. Additionally, the crosstalk between ferroptosis and oncogenic signaling pathways such as p53 and NRF2 was examined.Results: Accumulating preclinical evidence indicates that induction of ferroptosis sensitizes resistant cervical cancer cells to standard therapies by disrupting cellular redox balance and metabolic mechanisms. The intricate interplay between ferroptotic pathways and established tumorigenic signaling networks highlights the complexity of ferroptosis regulation in cervical cancer progression. Nonetheless, translational challenges remain, including the lack of robust ferroptosis-specific biomarkers for clinical application, potential off-target toxicity, and the need for optimized combination regimens.Conclusion: Future research should prioritize elucidating ferroptosis modulators within the tumor microenvironment, refining combinatorial therapeutic strategies, and developing targeted delivery systems. Integrating ferroptosis-based approaches with existing treatments holds significant potential to overcome therapeutic resistance and improve outcomes in advanced or recurrent cervical cancer. This review provides new insights and strategic directions for leveraging ferroptosis as a novel and actionable vulnerability in cervical cancer therapy.

Introduction: Endoscopic retrograde cholangiopancreatography (ERCP) is associated with significant discomfort and necessitates adequate sedation. This study aims to determine the effect of dexmedetomidine nasal spray adjunct to propofol sedation for patients undergoing ERCP procedures.

Patients and methods: This randomized, double-blind, placebo-controlled trial will be conducted at a tertiary teaching hospital in eastern China. Approximately 15 min before sedation, 160 adult patients will be randomly assigned (1:1) to either the dexmedetomidine group (dexmedetomidine nasal spray; n = 80) or the control group (normal saline nasal spray; n = 80). Sedation will be achieved with a target-controlled infusion of propofol, titrated to Modified Observer's Assessment of Alertness/Sedation scores of 1 and 2. The primary endpoint is the total propofol consumption during sedation. Secondary endpoints include the composite incidence of hypotension and hypoxemia during the procedures and recovery; and fatigue scores 15 min after emergence from sedation. An independent Data and Safety Monitoring Committee will conduct an ongoing review of study implementation.

Discussion: We anticipate that preoperative dexmedetomidine nasal spray will decrease total propofol requirements, reduce sedation-related adverse events, and enhance recovery for patients undergoing ERCP.

Trial registration: Chinese Clinical Trial Registry (ChiCTR2400093656) on December 10, 2024.

Background: Inflammation has been implicated in numerous diseases. The treatment of inflammation-related diseases is a significant global burden. Recent studies have found that lactic acid and its signalling pathway can inhibit inflammatory responses through macrophage polarization without any toxic side effects.

Objective: This study aimed to develop a rational drug delivery system that can release lactic acid into the desired area.

Methods: We extracted the macrophage-derived apoptotic bodies (ABs) to prepare the AB-encapsulated nanoparticles (ABNs) and evaluated the amount of lactic acid released and the safety of ABNs. Then, we observed the anti-inflammatory effect of ABNs and the phenotypic distribution of macrophages in vitro and in vivo.

Results: ABNs were specifically taken up by activated macrophages in vitro and in vivo. The levels of reactive oxygen species and inflammatory signalling proteins significantly decreased in activated macrophages after ABN treatment. ABNs relieved the inflammation of the colon and liver tissue, reduced the expression of TNF-α and IL-1β in serum, and inhibited the expression of TLR4/NF-κB proteins. The immunofluorescence images revealed that ABNs promoted the transformation of M1 macrophages (CD86+) into the M2 phenotype (CD206+). The expression of CD86 and iNOS decreased, whereas the expression of CD206 and Arg-1 significantly increased in the ABN-treated group. The cytotoxicity test revealed no obvious cytotoxic effect of ABNs.

Conclusions: ABNs can regulate the phenotypic transformation of macrophages through the local release of lactic acid and improve inflammation and injury of the liver and colon in mice. Our study demonstrated that the proposed nanosystem could serve as a promising delivery platform for the release of lactic acid to effectively reduce inflammation.

Background: Atopic dermatitis (AD), a common chronic inflammatory skin disease, has been extensively studied using single-cell genomics. However, keratinocytes, as key effector cells in AD, have underlying mechanisms remain incompletely understood and require further investigation.

Methods: We integrated single-cell transcriptomic data from skin tissues of healthy controls, chronic active AD patients, spontaneously healed AD (SHAD) patients, and an ovalbumin-induced AD mouse model. The study particularly emphasized the gene expression and cellular dynamics of keratinocytes across the different groups, as well as their interactions with immune cells.

Results: Compared to healthy controls, we observed significant changes in the keratinocyte transcriptome, cellular state, and keratinocyte-immune cell ligand-receptor interactions in AD skin, particularly the marked activation of genes involved in antigen processing and presentation. Interestingly, such gene activation was not observed in keratinocytes from the ovalbumin-induced AD mouse model, despite its phenotype closely resembling human AD. Furthermore, in SHAD, we identified a recovery of both the ligand-receptor interaction patterns and antigen processing and presentation genes, accompanied by a notable shift in the transcriptome. This involved a significant downregulation of genes related to cytoplasmic transcription and oxidative phosphorylation. Notably, this pattern was not observed in the self-healing mouse model following the removal of ovalbumin stimulation.

Conclusion: Our results suggest that the persistent activation of antigen processing and presentation pathways in keratinocytes may be a key driver of chronic inflammation in AD. Therefore, redirecting anti-allergic therapeutic strategies from solely targeting immune cells to targeting of keratinocyte-mediated antigen presentation may offer a more effective approach. Furthermore, we raise concerns about the use of ovalbumin-induced mouse models to recapitulate human chronic AD, as the underlying mechanisms may differ significantly.

Background: Micro/nanoplastics (MNP) have emerged as ubiquitous environmental contaminants with demonstrated bioaccumulation potential in organisms through multiple exposure pathways, posing substantial health risks globally. While mounting evidence indicates that MNP exposure adversely affects various organ systems including the nervous, reproductive, and digestive systems, the specific mechanisms underlying MNP-induced thyrotoxicity remain enigmatic.

Methods: 4-week-old male C57BL/6 mice were administered microplastics (MP, 5 μm) or nanoplastics (NP, 50 nm) via intragastric gavage at 30 mg/kg for 4 and 8 weeks. The thyroid architecture and endocrine function were evaluated by histological staining and thyroid hormones ELISA kit. The expression of apoptosis indicators (BCL2, BAX, CASPASE3), inflammatory factors (IL-1β, IL-18, TNF-α) and pyroptosis related-proteins (NLRP3, CASPASE1 and GSDMD), as well as the activity of NF-κB signaling were determined by immunofluorescence.

Results: We found that MNP exposure induces significant thyrotoxicity characterized by disrupted thyroid follicular architecture, comprised endocrine function, heightened apoptosis, and excessive inflammatory cytokines production, with NP exhibiting a more pronounced effect than MP. Mechanistically, MNP exposure stimulated thyroid follicular cell pyroptosis by upregulation of key pyroptotic mediators including NLRP3, CASPASE1, and GSDMD, driven by NF-κB signaling pathway activation.

Conclusion: Collectively, these findings provide novel mechanistic insights into MNP-induced thyroid toxicity and highlight the critical role of follicular cell pyroptosis, contributing to our understanding of the adverse health consequences associated with environmental plastic pollution.

Background: While dexamethasone is proven to enhance single-shot erector spinae plane block (ESPB), its role as an adjuvant in continuous ESPB catheters is unclear. This randomised controlled trial evaluated whether adding dexamethasone to ropivacaine improves analgesia after video-assisted thoracoscopic surgery (VATS).

Methods: 85 patients undergoing VATS with continuous ESPB were randomised to receive postoperative infusion of either 0.2% ropivacaine(C-ESPB group) or ropivacaine with 10 mg dexamethasone(D + C-ESPB group). The primary outcome was resting pain visual analog scale (VAS)at 12 h postoperatively, while secondary outcomes included QoR-15 scores, tramadol consumption, time to first analgesic requirement, postoperative adverse events, 3-month incidence of chronic pain, catheter-related complications, pain intensity at other times, and hospital stay.

Results: The D + C-ESPB group had significantly lower resting pain at 12 h [2.56 (1.03) vs 3.24 (1.21), mean difference -0.680, p = 0.006]; and lower coughing pain at 12 h [4.60 (1.48) vs 5.69 (1.35), mean difference 1.086, p < 0.001], with analgesic superiority sustained through 72 h. Quality of Recovery-15 scores were higher at 12 h [124.70 (12.48) vs 117.26 (12.24); mean difference -7.436, p = 0.007] and 48 h [141.60 (5.51) vs 138.98 (6.64); mean difference -2.628, p = 0.050]; Total tramadol consumption over 72 h was markedly reduce [0 (0,100) vs 100 (75,100), z = -3.807, p < 0.001], and hospital stay was shorter [Mean (SD) 6.09 (1.34) d vs 6.93 (1.55)d, p < 0.001]. The intervention did not, however, alter the 3-month incidence of chronic postsurgical pain (31% vs 34%, p = 0.756).

Conclusion: Dexamethasone significantly enhances the analgesic efficacy of continuous ESPB, improving early pain control, recovery quality, and opioid-sparing after VATS, but does not reduce the incidence of chronic persistent surgical pain.

Background: Many factors can influence the occurrence of postoperative pulmonary complications (PPCs) in the perioperative period, but it is unclear whether chronic high-altitude exposure (CHAE) affects the occurrence of PPCs.

Methods: This retrospective study included 235,128 surgical patients aged 18 years and older from January 2013 to December 2022. The occurrence of PPCs, such as pneumonia, atelectasis, and respiratory failure, was determined based on the admission and discharge diagnoses. To reduce the confounding effects caused by imbalances in demographic and clinical characteristics at baseline, we employed a 1:1 propensity score matching (PSM) to match the CHAE and non chronically high-altitude exposed (NCHAE) patients. Statistical analyses were conducted from January 1, 2025, to March 1, 2025.

Results: A total of 235,128 cases were included, with 11,075 (4.7%) patients experiencing PPCs. There were 8,565 patients with CHAE, of whom 484 (5.7%) developed PPCs. In contrast, there were 226,562 patients NCHAE, with 10,591 (4.7%) experiencing PPCs. After 1:1 PSM, 8,564 CHAE were matched with 8,564 NCHAE. In the CHAE group, 484 (5.7%) experienced PPCs, while 394 (4.6%) in the NCHAE group shoewd a statistically significant difference (p = 0.002). Adjusted multivariable conditional logistic regression analysis indicated that CHAE increased the incidence of PPCs (odds ratio [OR], 1.25; 95% CI, 1.02-1.53). Furthermore, the length of hospitalization and postoperative hospitalization duration of patients in the CHAE group were longer than those in the NCHAE group.

Conclusions: This retrospective study suggests an association between CHAE and PPCs within 30 days after surgery. However, the undefined exposure duration highlight the need for prospective studies to definitively establish causality.