Search Results (645)

Objective: To map and synthesize the published literature on the epidemiological burden of urinary tract infections (UTIs) in adults with spinal cord injury (SCI) or multiple sclerosis (MS) using intermittent catheterization (IC). Methods: We conducted a comprehensive literature review following PRISMA guidelines, searching PubMed, Scopus, and Web of Science for studies published since 2014. A total of 30 studies met the inclusion criteria. Results: Reported UTI incidence varied widely from 24% to 93.1%, highlighting significant heterogeneity across the evidence base. Annually, 15–17% of patients experienced 4–6 UTIs, and up to 16.4% required hospitalization for UTI-related complications. A critical evidence gap was exposed, with only one study focusing specifically on the MS population. Conclusions: Despite its clinical benefits, IC remains underutilized and inconsistently supported. Addressing systemic delivery gaps is essential. UTIs in neurogenic bladder care should be recognized as a modifiable public health issue requiring equity-driven interventions and strengthened implementation frameworks. This review underscores the urgent need for methodologically rigorous research to establish clear best practices. Full article

Canada was the first G7 country to legalize non-medical cannabis use, which rapidly expanded recreational cannabis consumption. This has implications for public health and land-use sustainability, particularly as agricultural systems face increasing pressure from land-use conflicts, which can cause food insecurity in a growing population. This study evaluates sustainability implications of recreational cannabis cultivation in Canada by integrating population-level health risk estimates with an agricultural land-use opportunity costs. Using published epidemiological studies, the population-attributable mortality associated with cannabis use across multiple health outcomes is estimated, including cardiovascular disease, neurocognitive disorders, cancer, injury-related mortality, suicide, and opioid-related poisoning. In parallel, counterfactual scenarios are modelled in which the >2 million m² of land used for recreational cannabis cultivation is reallocated to nutrient-dense food crops to assess potential caloric availability. Results of the land-use analysis indicate that reallocating existing cannabis cultivation areas to food production could supply annual nourishment for >3600 people. In addition, cannabis-associated health risks account for ~28,000–30,000 premature deaths annually when aggregated, with cardiovascular disease and dementia representing the largest shares. From a sustainability perspective, the results underscore the need for continued evaluation of cannabis policy and production systems in relation to public health externalities, food security, and land-use opportunity costs. Full article

Hypertriglyceridaemia is the third most common aetiology of acute pancreatitis and a leading cause of recurrence in specialized lipid clinics. The risk of acute pancreatitis rises steeply once triglycerides exceed approximately 10 mmol/L (≈885 mg/dL). Still, clinically meaningful risk may occur at lower levels in the presence of chylomicronaemia, metabolic stress, or pregnancy. This mini-review synthesizes contemporary evidence on epidemiology, mechanistic links between triglyceride-rich lipoproteins and pancreatic injury, and the practical distinction between secondary (acquired) and genetic drivers of severe hypertriglyceridaemia. We summarize acute management strategies aimed at rapid triglyceride reduction (including insulin-based approaches and therapeutic plasma exchange in selected scenarios) and focus on long-term prevention of recurrence through lifestyle interventions, correction of secondary contributors, and triglyceride-lowering pharmacotherapy. Finally, we discuss emerging RNA-targeted therapies against apolipoprotein C-III and angiopoietin-like 3, which are reshaping prevention strategies for familial and persistent chylomicronaemia and may reduce pancreatitis burden in the highest-risk phenotypes. Full article

Therapeutic inertia in lipid-lowering treatment remains a striking paradox of modern cardiovascular medicine: at a time when the causal role of LDL-cholesterol in atherosclerotic disease is unequivocal and potent therapies are widely available, a substantial proportion of high- and very-high-risk patients still fail to receive timely treatment intensification. Contemporary European and international data consistently show fewer than one in three patients in secondary prevention achieve guideline-recommended LDL-C targets, revealing a persistent and unacceptable gap between scientific evidence and clinical reality. This narrative review examines therapeutic inertia as a key explanatory framework for this gap, describing its epidemiology, mechanisms, and clinical consequences in secondary cardiovascular prevention. We summarize the main physician-, patient-, and system-level determinants and propose recurrent clinician “phenotypes” of inertia that may help explain why opportunities are missed even in the highest-risk patients. The consequences are profound: therapeutic inertia contributes to what we propose as the conceptual framework of an “avoidable atherosclerotic burden”, the cumulative vascular injury that accrues each period in which LDL-C remains above target, translating into higher rates of avoidable cardiovascular events, and increased healthcare costs. Emerging strategies such as upfront combination therapy, decision-support systems, structured lipid pathways, and the integration of artificial intelligence offer practical tools to shift lipid management from reactive to proactive care. Overcoming therapeutic inertia is therefore not merely a matter of improving process metrics, but a clinical and ethical imperative. Closing the gap between evidence and practice requires transforming optimal lipid management from an exception into a system-level default, ensuring that every patient receives the full benefit of therapies proven to save lives. This work proposes a novel characterization of clinician ‘phenotypes’ and the concept of ‘avoidable atherosclerotic burden’ as a framework to understand and address this gap. Full article

Background: Persistent pain following orthopaedic trauma is common, often disproportionate to structural healing, and increasingly interpreted as reflecting centrally mediated pain mechanisms. However, the mechanisms, clinical features, diagnostic approaches, prognostic indicators, and management strategies relevant to trauma-related central sensitisation (CS) remain poorly understood. Objective: To map and synthesise existing evidence on CS following orthopaedic trauma, addressing mechanistic pathways, clinical manifestations, epidemiology, assessment methods, management approaches, and health system implications. Methods: A scoping review was conducted in accordance with PRISMA-ScR. Twenty-one studies met the eligibility criteria, comprising nine primary trauma cohorts and 12 contextual mechanistic or review studies relevant to trauma-associated CS. Data were charted across six prespecified domains of mechanistic processes, clinical presentation and diagnostic features, epidemiology and prognosis, assessment tools and outcome measures, interventions, and health system and care delivery considerations. Results: Mechanistic studies demonstrated trauma-induced neuroimmune activation, altered cortical and spinal excitability, and molecular pathways consistent with sensitisation. Clinical studies have identified neuropathic features, widespread pain, and heightened sensory responsiveness following fractures and other injuries. Neurophysiological evidence has indicated early cortical disinhibition following upper limb trauma, whereas epidemiological cohorts have reported persistent pain and disability years after major trauma. Measurement studies have highlighted the limited reliability and specificity of current tools in trauma populations, including quantitative sensory testing and self-report instruments. Early predictors of adverse trajectories include severe acute pain, neuropathic descriptors, psychological distress, and opioid-dominant analgesia. Evidence regarding early intervention, rehabilitation strategies, and system-level screening pathways remains limited. Conclusions: Central sensitisation (CS)–consistent mechanisms after orthopaedic trauma are suggested by convergent mechanistic, neurophysiological, and clinical findings. However, trauma-specific diagnostic criteria, prognostic models, and management frameworks remain underdeveloped. High-quality longitudinal research is needed to clarify early trajectories, refine assessment methods, and establish targeted interventions to reduce long-term pain and disability. Full article

Background: Traumatic brain injury (TBI) is a leading cause of disability but one of the least recognized health problems in the world, affecting up to 69 million people annually. The associated lifelong disability in survivors, the loss of economic productivity, and being a risk factor for dementia consume 0.5% of global economic activity. Yet TBI is still largely invisible in national surveillance systems and not well represented in chronic disease frameworks. Consequently, governments are not equipped to provide proportional financing of acute care and long-term care of survivors, nor to build health care systems and resources for improving outcomes of TBI through policy frameworks targeting prevention, treatment, and equitable access. Objective: This commentary aims to provide a comprehensive picture of the global effort to formally recognize TBI as a notifiable and chronic condition, including the justifications for recognition, the formation of an international coalition of stakeholders, and the strategic plan for resolution at WHA79 of the World Health Assembly, one of the first concerted multinational efforts that occurred as a side event during the 78th World Health Assembly (WHA78) in May 2025. Methods: This commentary integrates information from epidemiological studies, global registries, and testimonies from people with lived experience of TBI. We analyze these data to develop policy needs and corresponding initiatives to address key needs. These include coordinated efforts to advocate change, such as technical briefings, consultations with stakeholders, and storytelling led by survivors, all of which informed and formed a part of the WHA78 side event. Our efforts have garnered wide, multi-sector support. Results: The WHA78 side event showed that ministries of health, neurosurgical, neurological, and rehabilitation societies, academic researchers, WHO representatives, and survivors all unprecedentedly support the recognition of the importance of TBI, facilitating national policies for its prevention and treatment via standardized surveillance. More than 30 non-governmental groups officially supported the campaign. A sponsoring member state made a public commitment to co-sponsor a WHA resolution, which set the stage for ongoing diplomatic progress and engagement across regions. Conclusion: To improve global brain health equity, access to long-term care, and the resilience of health systems, it is important to recognize TBI as a notifiable and chronic condition. A dedicated WHA resolution would make TBI a part of global health governance, making sure that it is counted, tracked, and dealt with as quickly and comprehensively as possible. It is both a technical necessity and a moral duty to help survivors and families and fight for justice in global health systems. Full article

The significance of gut epithelial cell autoantibodies (GECAs), human leukocyte antigen (HLA) alleles, and other scientifically relevant factors has been largely overlooked, despite their potential importance in the medical management of HIV-infected individuals, in understanding the pathogenesis of AIDS, and in improving epidemiological and diagnostic approaches. This review may be considered as a hypothesis-driven narrative paper mostly considering GECAs and some easily detectable genetic markers. Thus, the aim is to highlight these neglected medical and scientific issues. Addressing them may contribute to a deeper understanding of HIV pathology at both the individual and population levels. Autoantibodies against enterocytes (GECAs) are present in the majority of HIV-positive patients. These intestinal epithelial cells are crucial for nutrient absorption and because of their role as antigen-presenting cells (APCs) within the immune system. Furthermore, the number of CD4-positive lymphocytes depends largely on daily antigenic stimulation rather than on thymic function, which becomes residual or inactive after puberty. The fall of CD4+ lymphocyte counts observed in HIV-infected patients may therefore be exacerbated by enterocyte dysfunction/damage, as indicated by the presence of GECAs. These autoantibodies either cause or reflect damage to these important antigen-presenting cells, which may impair intestinal antigen presentation by their surface HLA proteins to the clonotypic T-cell receptor of lymphocytes. Additionally, the association between specific HLA alleles and a CCR5 variant affects HIV disease progression or transmission and should be considered in both adults and mother–infant pairs. In particular, HLA-B35 and HLA-B57 allelic groups have been implicated in influencing both the transmission and progression of HIV infection. Moreover, several aspects of the natural history of HIV infection remain unresolved and controversial, and these issues warrant urgent clarification. For instance, diagnostic tests are not yet standardised globally, and viral abundance in HIV-infected individuals or AIDS patients’ cells may be relatively low. In summary, the neglected facets of HIV infection demand renewed investigation, particularly now that an HIV diagnosis is no longer the devastating prognosis it once was. The objective of this work is to emphasise additional factors that may influence the course of AIDS, such as enterocyte injury reflected by presence of GECAs. Ultimately, we propose that GECAs may impair enterocytes’ HLA (MHC II)-mediated antigen presentation by enterocytes to CD4+ T lymphocytes (through T-cell receptors), thereby diminishing T-cell proliferation, reducing CD4+ cell numbers, and impairing immune function. Full article

Background/Objectives: Severe traumatic brain injury (TBI) carries high mortality, and outcomes are particularly poor when prehospital cardiopulmonary resuscitation (CPR) is required. Because these patients are often excluded from research, epidemiological data and prognostic insights are limited. This study aimed to describe characteristics and outcomes of patients with suspected severe TBI who received prehospital CPR. Methods: We performed a sub-analysis of the prospectively collected multicenter BRAIN-PROTECT registry, including all patients with suspected severe TBI who underwent prehospital CPR and were transported to a participating trauma center. Results: A total of 256 patients with suspected severe TBI who received prehospital CPR were included. Early mortality was high, with 22.6% declared dead in the emergency department and an additional 28.9% within 24 h, resulting in 48.5% 24 h survival. Thirty-day mortality was 79.9%. Among survivors, 45.7% achieved moderate disability or good recovery at discharge. Outcomes, 30-day mortality, and neurological status at discharge did not differ between isolated and non-isolated TBI. Characteristics often seen in survivors included shockable initial rhythm, reactive pupils, and lack of anisocoria. All patients without prehospital return of spontaneous circulation died. Conclusions: Although overall 30-day mortality was high, survival among patients for whom resuscitation was attempted and who reached hospital care was not negligible, and a substantial proportion of the survivors achieved moderate to good neurological recovery. Prehospital ROSC and shockable rhythms were associated with better outcomes, suggesting that resuscitation may be valuable and warranted in selected patients with potentially reversible conditions. Further studies are needed to better define prognostic factors and guide management in this highly vulnerable population. Full article

Problem Statement: Upper crossed syndrome (UCS), as first described by Janda, refers to a group of muscle imbalances in which tightness in the upper trapezius and levator scapulae dorsally cross with tightness in the pectoralis major and minor muscles, and weakness of deep cervical flexors cross ventrally with weakness of the middle and lower trapezius. Postural alterations from this dysfunction, including forward head, rounded shoulders, and scapular dyskinesis, contribute to upper-back and shoulder pain, particularly among office workers who spend long periods of the workday on a computer. Upper crossed syndrome is a significant contributor to both neck pain and shoulder pain among computer users, which have been rated at 55–69%, and 15–52%, respectively. Despite its prevalence, knowledge about UCS and its treatment remains spotty among primary care physicians. In addition, improvements in workstation ergonomics along with hourly work breaks may be considered as primary prevention strategies for UCS. Objectives: This narrative review examines and synthesizes evidence about the epidemiology and diagnosis of UCS, along with clinical recommendations for physiotherapeutic approaches to treatment. Ergonomic measures in the workplace, including changes in the design of computer workstations so that both the keyboard and monitor are at the proper heights to minimize the risk of long-term musculoskeletal disorders, are also critical. Methods: The first author, a Doctor of Behavioral Health, performed the initial literature search, which was reviewed by the second author, a PhD in sports injury epidemiology. The third author, a chiropractor and practice owner, provided clinical recommendations for stretching and strengthening exercises, which were also described in the literature. Discussion: While easily treatable when caught early, UCS may become resistant to noninvasive approaches over time, and more severe pathologies of the neck and shoulder, including impingement, thoracic outlet syndrome, and cervicogenic headaches may result. Because there is no specific ICD code for UCS, it is important for physicians to recognize the early signs, consider them in the context of workplace-related injuries, and understand physiotherapeutic strategies for symptom resolution. Full article

This study explores the relationship model among the dark triad traits, non-suicidal self-injury (NSSI) behavior in adolescents, negative life events, and depression. A moderated mediation model was tested among 224 middle school students with left-behind experience in Inner Monolgia. These students were surveyed using the Dirty Dozen Dark Triad Measure, the Adolescent Self-Harm scale, the Adolescent Self—Rating Life Events Checklist, and the Center for Epidemiologic Studies Depression Scale. The dark triad traits had a significant positive predictive effect on NSSI behavior among adolescents with left-behind experience and indirectly influenced NSSI behavior through negative life events. The second half of the mediation path of “the dark triad traits → negative life events → NSSI behavior” was moderated by depression. The influence of the dark triad traits on NSSI behavior is exerted through negative life events, and the relationship between negative life events and NSSI behavior is moderated by depression. Full article

Background: Lung adenocarcinoma in non-smoking women represents a distinct clinical entity that cannot be fully explained by traditional exposure-centered carcinogenic models. Although ambient air pollution is a recognized risk factor, sex-specific vulnerability suggests the involvement of additional biological modulators shaping inflammatory, immune, and proliferative responses. Main body: In this conceptual review, we integrate epidemiological, experimental, and mechanistic evidence to propose a multisystem framework of lung carcinogenesis in non-smoking women. We delineate a central carcinogenic spine encompassing lung epithelial injury, chronic inflammation, growth factor signaling activation—particularly epidermal growth factor receptor (EGFR) pathways—and tumor microenvironment remodeling. Within this framework, three interacting domains function as biological modulators that amplify carcinogenic processes: chemosensory–neural–immune modulation, hormonal–endocrine signaling including estrogen–EGFR crosstalk, and psychosocial stress–hypothalamic–pituitary–adrenal (HPA) axis dysregulation. These domains converge through feedback mechanisms that reinforce systemic dysregulation and tumor-promoting microenvironments. Implications: This integrative model provides a biologically grounded perspective on female-specific vulnerability to lung adenocarcinoma and informs precision prevention, risk stratification, and ESG-informed public health strategies beyond conventional exposure reduction. Full article

Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) increasingly co-occur in low- and middle-income countries and aging populations. Prior pulmonary TB is a robust, smoking-independent determinant of COPD and is linked to persistent systemic inflammation, endothelial dysfunction, dyslipidemia, and hypercoagulability axes that also amplify cardiovascular disease (CVD) risk. We conducted a targeted narrative non-systematic review (2005–2025) of PubMed/MEDLINE, Embase, Scopus, and Web of Science, selecting studies for clinical relevance across epidemiology, clinical phenotypes, pathobiology, biomarkers, risk scores, sleep-disordered breathing, and management. No quantitative synthesis or formal risk-of-bias assessment was performed. Accordingly, findings should be interpreted as a qualitative synthesis rather than pooled estimates. Prior TB is associated with a distinctive COPD phenotype characterized by mixed obstructive–restrictive defects, reduced diffusing capacity (DLCO), radiographic sequelae, and higher exacerbation/hospitalization burden. Mechanistic insights: Convergent mechanisms chronic immune activation, endothelial injury, prothrombotic remodeling, molecular mimicry, and epigenetic reprogramming provide biologic plausibility for excess CVD, venous thromboembolism, and pulmonary hypertension. Multimarker panels spanning inflammation, endothelial injury, myocardial strain/fibrosis, and coagulation offer incremental prognostic value beyond clinical variables. While QRISK4 now includes COPD, it does not explicitly model prior TB or COPD-TB outcomes, but data specific to post-TB cohorts remain limited. Clinical implications: In resource-constrained settings, pragmatic screening, prioritized PAP access, guideline-concordant pharmacotherapy, and task-shifting are feasible adaptations. A history of TB is a clinically meaningful modifier of cardiopulmonary risk in COPD. An integrated, multimodal assessment history, targeted biomarkers, spirometry/lung volumes, DLCO, 6 min walk test, and focused imaging should guide individualized care while TB-aware prediction models and implementation studies are developed and validated in high-burden settings. Full article

This review explores the interplay between SARS-CoV-2 and HIV-1 infections within the human brain, highlighting the significant neurological implications of these viral infections. SARS-CoV-2 can infect the central nervous system (CNS), with evidence of the virus detected in various brain regions, including the hypothalamus, cerebellum, and olfactory bulb. This infection is linked to microglial activation and neuroinflammation, which can lead to severe neurological outcomes in affected individuals. Autopsy studies revealed microglial changes, including downregulation of the P2RY12 receptor, indicating a shift from homeostatic to inflammatory phenotype. Similar changes in microglia are found in the brains of people with HIV-1 (PWH). In SARS-CoV-2, the correlation between inflammatory cytokines, such as IL-1, IL-6, and MCP-1, found in cerebrospinal fluid and brain tissues, indicates significant neurovascular inflammation. Astrogliosis and microglial nodules were observed, further emphasizing the inflammatory response triggered by the viral infections, again in parallel to those found in the brains of PWH. Epidemiologic data indicate that although SARS-CoV-2 infection rates in PWH mirror those in People without HIV (PWoH) populations, Long-COVID prevalence is markedly higher among PWH. Evidence of overlapping cognitive impairment, mental health burden, and persistent neuroinflammation highlights diagnostic complexity and therapeutic gaps. Despite plausible mechanistic synergy, direct neuropathological confirmation remains scarce, warranting longitudinal, biomarker-driven studies. Understanding these interactions is critical for developing targeted interventions to mitigate CNS injury and improve outcomes. Full article

Background: Depression and Metabolic Dysfunction-Associated Steatotic Fatty Liver Disease (MASLD) are common chronic diseases, respectively. However, the causal and molecular links between them remain unclear. In order to explore whether depression contributes to an increased risk of MASLD and whether inflammation mediates this effect, we integrated multi-level evidence from the epidemiology of the National Health and Nutrition Examination Survey (NHANES), the genetics of GWAS, the transcriptomes of GEO, and single-cell RNA sequencing datasets. Methods: A multi-level integrative analysis strategy was used to validate this pathway. First, a cross-sectional epidemiological analysis based on NHANES data was used to reveal the association between depression and MASLD, and to explore the mediating role of inflammation and liver injury markers. Secondly, a two-sample Mendelian randomization analysis was used to infer the causal direction of depression and MASLD, and to verify the mediating effect of systemic inflammation and liver injury indicators at the genetic level. Then, the transcriptome co-expression network analysis and machine learning were used to screen the common hub genes connecting the two diseases. Finally, single-cell transcriptome data were used to characterize the dynamic expression of potential key genes during disease progression at cellular resolution. Results: Depression significantly increased the risk of MASLD, especially in women (OR = 1.39, 95%CI [1.17–1.65]). Parallel mediation analysis showed that high-sensitivity C-reactive protein (hs-CRP) (p < 0.001), γ-glutamyltransferase (GGT) (p < 0.001), and alkaline phosphatase (ALP) (p < 0.001) mediated this relationship. Mendelian randomization analysis confirmed the unidirectional causal effect of depression on MASLD, and there was no reverse association (β = 0.483, SE = 0.146, p = 0.001). Weighted gene co-expression network analysis and machine learning identified CD40LG as a potential molecular bridge between depression-associated immune modules and MASLD. In addition, single-cell data analysis revealed a stage-specific trend of CD40LG expression in CD4⁺ T cells during MASLD progression, while its receptor CD40 was also activated in B cells. In the female sample, CD40LG maintained an upward trend. However, the stability of this result is limited by the limited sample size. Conclusions: This study provides converging multi-omics evidence that depression plays a causal role in MASLD through inflammation-mediated immune signaling. The CD40LG-CD40 axis has emerged as an immune mechanism that transposes depression into the pathogenesis of MASLD, providing a potential target for the intervention of gender-specific metabolic liver disease. Full article

Background: Acinetobacter baumannii (AB), particularly carbapenem-resistant strains (CRAB), is a major cause of difficult-to-treat infections associated with substantial mortality. Contemporary data from Central and Eastern Europe remain scarce. We aimed to characterize the epidemiology, clinical features, and survival of patients with AB bloodstream infection in a multicenter Polish cohort. Methods: We conducted a retrospective multicenter study including consecutive adults with microbiologically confirmed AB bloodstream infection. Clinical and demographic data, comorbidities, infection origin, and antimicrobial treatments were collected. Outcomes included all-cause in-hospital mortality and infection-attributed mortality. Survival was assessed using Kaplan–Meier curves and log-rank tests, while factors associated with death were examined with univariable and multivariable Cox regression. Results: Among 245 patients with CRAB bloodstream infection, overall mortality was 69.4%, and infection-attributed mortality reached 51.8%. Most infections (75.1%) were hospital-acquired. In univariable analyses, male sex (HR = 0.66; p = 0.008) and colistin-based therapy (HR = 0.71; p = 0.037) were associated with improved survival. Conversely, hospital-acquired infection (HR = 0.43; p < 0.001) and acute kidney injury (HR = 1.40; p = 0.038) were linked to higher mortality. In the multivariable model, male sex remained protective (HR = 0.61; p = 0.006), while hospital-acquired infection (HR = 0.35; p < 0.001) and COVID-19 (HR = 1.64; p = 0.049) independently predicted death. After adjustment, no other comorbidities or antimicrobial regimens showed significant associations. Conclusions: In this multicenter cohort of patients with CRAB bloodstream infection, mortality remained extremely high. Hospital-acquired infection, acute kidney injury, and COVID-19 were strong independent predictors of poor outcomes, whereas male sex was associated with better survival. Although colistin-containing therapy appeared beneficial in univariable analysis, this effect did not persist after adjustment, underscoring potential confounding. These findings highlight the urgent need for early recognition, optimized antimicrobial strategies, and prevention of healthcare-associated spread to improve outcomes in CRAB bacteremia. Full article