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.

Background: Autonomic dysfunction, including orthostatic hypotension and postural tachycardia syndrome, has emerged as a COVID-19 complication. This nationwide propensity score-matched cohort study investigated COVID-19's impact on subsequent prescriptions of autonomic dysfunction in Japan.

Patients and methods: Using a claims database covering 16 million residents identified between 2020 and 2022, propensity-score matching (PSM) created comparable groups of COVID-19 patients and controls. PSM used age, sex, calendar month, comorbidities, and baseline medications, with nearest-neighbor 1:1 with replacement. The primary composite outcome was the first outpatient prescription of midodrine, fludrocortisone, amezinium methylsulfate, and droxidopa. Cox proportional hazards models yielded hazard ratios (HRs) with 95% confidence intervals (CIs). Effect modifications were examined by subgroups.

Results: Among 3,074,329 matched pairs, over a median follow-up of 8 months, 13011 composite outcome were observed, and COVID-19 infection was associated with a 36% relative increase in prescriptions (HR 1.36, 95%CI 1.32-1.41). The risk persisted beyond one year, with the strongest association observed for fludrocortisone (576 events, HR 1.71, 95%CI 1.44-2.02), although the frequency was the highest in midodrine prescription (7009 events, HR 1.28, 95%CI 1.22-1.34). Subgroup analysis revealed higher risks among older individuals, males, those with myocardial infarction, heart failure, and antihypertensive medications.

Conclusions: COVID-19 infection is significantly associated with increased initiation of pharmacotherapy for autonomic dysfunction, with sustained risk beyond one year. These findings highlight the to manage autonomic dysfunction among COVID-19 survivors and informing clinical care and public health planning.

Background: The maxillary sinus (MS) exhibits interindividual anatomical variation influenced by sex, age, and craniofacial morphology. Understanding these variations is essential for surgical, endodontic, and implant planning. However, morphometric data for Saudi subpopulations, particularly from northern regions such as Ha'il, remain limited.

Objective: To assess MS morphometric dimensions using cone-beam computed tomography (CBCT) in a Saudi subpopulation from the Ha'il region and to evaluate variations according to sex, age, and laterality.

Methods: A retrospective CBCT-based cross-sectional study analysed 1,018 scans of Saudi adults aged 18-70 years. Sinus width, length, area, and perimeter were measured bilaterally on standardised coronal sections. Statistical analyses included Mann-Whitney U, Wilcoxon signed-rank, Kruskal-Wallis, and repeated-measures ANCOVA tests, with significance set at p < 0.05.

Results: Males demonstrated significantly larger MS dimensions than females, particularly for area (p = 0.043), perimeter (p = 0.045), and width after covariate adjustment (p = 0.007). No significant age-related differences were observed across adult groups. Although right-left differences were statistically significant for all parameters (p < 0.01), the magnitude of asymmetry was minimal and clinically insignificant. Overall, MS dimensions remained stable throughout adulthood with a slight right-sided laterality predominance.

Conclusion: CBCT-based morphometric assessment of the MS in a Saudi subpopulation from the Ha'il region revealed significant sex-related differences, minimal laterality-related asymmetry, and stable dimensions across adult age groups. These region-specific normative data enhance anatomical understanding and support improved diagnostic accuracy and procedural safety in implantology, oral surgery, maxillofacial practice, and forensic applications.

Background: Many patients with hypertensive nephropathy progress to chronic kidney disease (CKD). Targeting the core pathophysiological pathway of endothelin-1 activation, this study aimed to elucidate response patterns to the endothelin receptor type A/B (ETA/ETB) antagonist bosentan and construct a personalized prediction model.

Methods: This single-centre retrospective cohort study enrolled 166 patients with hypertension-related nephropathy confirmed by renal biopsy. Risk stratification was performed based on a pathological injury scoring. Three efficacy trajectories were identified using latent variable growth mixture models. Efficacy drivers were screened via random forest algorithms. Finally, early response thresholds were established using receiver operating characteristic (ROC) curves.

Results: Patients in the high-damage group exhibited significantly lower creatinine reduction than those in the low-damage group. Trajectory analysis revealed three patterns: sustained improvement (65.1%), with a 12-month creatinine reduction of 110.8 μmol/L, and deterioration (12.0%), with a deterioration inflection point at 5.3 ± 1.7 months and a subsequent creatinine increase of 40.2 μmol/L. Pathological injury score was the primary determinant of efficacy and was significantly negatively correlated with creatinine reduction (r = -0.61). Early response threshold analysis indicated that ΔCr_3M ≥ 42.3 μmol/L predicted 12-month efficacy, with an area under the curve (AUC) of 0.79. The early target-achievement group demonstrated significantly greater creatinine reduction than the nonachievement group. Compared with the non-sodium-glucose cotransporter-2 inhibitor (SGLT2i) group, the SGLT2i group demonstrated a 59% reduction in creatinine, while the diabetic subgroup showed a 47.1% smaller reduction than the nondiabetic subgroup.

Conclusions: Bosentan may improve glomerular haemodynamics in patients with hypertensive nephropathy. We propose pathological and early-response thresholds that could guide dynamic, precision interventions before critical inflection points, potentially paving the way for an upgrade from static to proactive management. These findings require validation in larger cohorts.

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.