This research aimed to evaluate the prevalence of obstructive sleep apnea-hypopnea syndrome (OSAHS) in individuals with cystic fibrosis (CF) and to examine its relationship with sleep monitoring parameters and pulmonary function.

Five databases (EMBASE, PubMed, Web of Science, CNKI, and Cochrane Library) were searched for publications on the prevalence of OSAHS in CF. Two independent researchers assessed study quality using the Joanna Briggs Institute tool. Weighted mean differences were calculated for continuous variables, and the model choice (random vs fixed effects) was determined by whether I2 exceeded 50%.

Fourteen studies were included: 11 in the prevalence meta-analysis and 13 in the mean apnea-hypopnea index (AHI) analysis. Six studies compared sleep and pulmonary parameters between CF patients with and without OSAHS. The pooled prevalence of OSAHS in CF was 48% (I2 = 96.5%), slightly higher in pediatric than adult patients. The mean AHI was 3.47 in pediatric patients with CF and 6.19 in adult individuals with CF. Compared to OSAHS-negative patients, OSAHS-positive patients exhibited higher AHI and arousal index, lower mean and minimum oxygen saturation, and worse pulmonary function.

There is a significant prevalence of OSAHS among patients with CF, notably within the pediatric demographic. Patients with CF generally present with elevated AHI values and poorer pulmonary function in those with concurrent OSAHS. The findings advocate for earlier polysomnography screening in patients with CF to facilitate timely intervention.

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare, potentially life-threatening hypersensitivity reaction. Its occurrence during pregnancy, especially secondary to anti-tuberculous therapy (ATT), is exceedingly uncommon and presents major diagnostic and therapeutic challenges.

A 23-year-old pregnant woman (14 weeks gestation) presented with prolonged fever, jaundice, rash with desquamation, and respiratory symptoms while on first-line ATT for pulmonary tuberculosis.

Laboratory evaluation revealed severe eosinophilia, deranged liver function, hepatitis E virus co-infection, and autoimmune overlap (systemic lupus erythematosus with antiphospholipid antibody positivity). Based on clinical features and a Registry of Severe Cutaneous Adverse Reactions score of 6, a definite diagnosis of DRESS syndrome was established.

ATT was discontinued, and she was treated with systemic corticosteroids, antihistamines, and topical therapy. Sequential drug challenges confirmed hypersensitivity to all 4 first-line agents, necessitating initiation of bedaquiline, clofazimine, and delamanid.

The patient showed favorable clinical recovery with improvement in systemic manifestations and stabilization of pregnancy. She was discharged on modified ATT with multidisciplinary follow-up.

This case highlights the complexity of diagnosing and managing DRESS in pregnancy, particularly in tuberculosis-endemic regions. Coexisting viral hepatitis and autoimmune disorders may mimic or exacerbate the syndrome, underlining the importance of high clinical suspicion, timely drug withdrawal, and individualized therapy.

A 0/2-h algorithm for the i-STAT point-of-care (POC) high sensitivity troponin I (hs-cTnI) assay was recently derived in Australia. The objective of this study was to validate and optimize the performance of the 0/2-h algorithm in a multisite U.S. Emergency Department (ED) cohort.

A prospective cohort study was conducted at three U.S. EDs (February-September 2025). Adults without STEMI and at least one hs-cTnI ordered were accrued. Blood samples were collected simultaneously for POC hs-cTnI measurement on an i-STAT 1 analyzer (Abbott Laboratories) and central laboratory hs-cTnI measurement (Beckman Coulter). The primary outcome was index myocardial infarction (MI), adjudicated by experts using clinical hs-cTnI measures. Diagnostic performance of the Australian 0/2-h algorithm was assessed by calculating negative and positive predictive values (NPV, PPV) with associated 95% confidence intervals. Efficacy, defined as the proportion of patients classified into the rule-out zone, was calculated. Algorithm optimization tested modified cut points to increase efficacy while maintaining NPV ≥ 99% and achieving PPV ≥ 65%.

During the study period, 578 patients with complete 0/2-h algorithm assessments were accrued. These patients were 48% (279/578) female, 40% (233/578) non-White, with a median age of 60 years (IQR: 50-70). Index MI occurred in 7.4% (43/578). Algorithm efficacy was 54.8% (317/578) and 8.8% (51/578) were classified to the rule-in zone. Among patients ruled-out, the NPV was 99.4% (95% CI: 97.7%-99.9%). The rule-in zone was associated with a PPV of 62.7% (95% CI: 48.1%-75.9%). Among 36.3% (210/578) patients classified to the observation zone, 4.3% (9/210) had an adjudicated index MI. An optimized 0/2-h algorithm increased efficacy to 60.0% (347/578) while achieving an NPV of 99.4% (95% CI: 97.9%-99.9%) and PPV of 74.4% (95% CI: 58.8, 86.5%) for index MI.

The original Australian and optimized 0/2-h algorithms for i-STAT POC hs-cTnI measurement had high NPV and efficacy in a multisite U.S.

Trial Registration: NCT06899776.

Cardiovascular disease (CVD) remains a major global health burden, with risk factors evolving alongside socioeconomic and lifestyle changes. The PREVENT equation provides race-free estimates of 10- and 30-year CVD risk, but its utility in Asian populations remains underexplored. This study assessed long-term trends in CVD risk among Korean adults and identified key contributing factors.

This cross-sectional analysis used nationally representative data from the Korea National Health and Nutrition Examination Survey (KNHANES), spanning 2001-2021. Adults aged ≥30 years with relevant clinical and laboratory data were included. The PREVENT equation was used to calculate 10- and 30-year CVD risk. Trends in risk estimates were examined by year and sex.

The estimated 10-year risk of total CVD increased from 4.6% ± 7.1% (mean ± SD) in 2001 to 7.9% ± 9.0% in 2021, and the estimated 30-year risk for total CVD climbed from 15.8% ± 14.6% to 22.9% ± 14.5% over the same period. Key contributors to this upward trend included worsening glycemic control (mean glucose: 97 ± 17 mg/dl in 2001 vs 103 ± 22 mg/dl in 2021) and increased antihypertensive medication use. In contrast, rising high-density lipoprotein cholesterol levels and declining male smoking rates (47.9% in 2001 to 28.9% in 2021) may have mitigated some risk.

Over two decades, estimated CVD risk has increased in the Korean population, highlighting the need for targeted prevention efforts. As countries undergo rapid economic and demographic transitions, long-term CVD risk estimation using the PREVENT equation may inform public health strategies to mitigate cardiovascular burden.

Supraventricular tachycardia (SVT) is a common arrhythmic disorder characterized by abnormal electrical impulses arising from supraventricular tissues, most commonly the atria or atrioventricular node. This study aimed to investigate the association between G protein-coupled estrogen receptor (GPER) levels and biomarkers of oxidative stress and neurodegeneration in the pathophysiology of SVT. This study included 51 patients diagnosed with SVT and 30 healthy controls. Plasma levels of the oxidative stress marker 8-iso-prostaglandin F2α (8-iso-PGF2α), the neurodegeneration-associated protein Tau, and GPER were measured using ELISA kits. Correlations between GPER and the studied biomarkers were analyzed, and the diagnostic performance of each biomarker was evaluated using ROC analysis. Pro-BNP levels were higher in patients with SVT compared to the control group (P = .05). GPER, Tau, and 8-iso-PGF2α levels were significantly higher in the SVT group compared to the control group (P < .001 for all 3 biomarkers). ROC analysis demonstrated that 8-iso-PGF2α had the highest diagnostic accuracy, while Tau (AUC = 0.986) and GPER (AUC = 0.981) also showed strong discriminative performance. GPER, a well-established marker of estrogen-mediated cellular signaling, emerges as a significant biomarker in patients with SVT. These findings suggest that GPER-mediated signaling pathways may be associated with systemic oxidative damage and neuronal effects in the pathophysiology of SVT.

The association between immunocyte phenotypes and dilated cardiomyopathy (DCM) has been explored, however the exact pathogenesis of the relationship between immune cells and DCM is unclear. This bidirectional two-sample Mendelian randomization (MR) research aims to further validate the causal link between 731 immunocyte phenotypes and DCM. Summary statistics from a genome-wide association study data of individuals with European ancestry were utilized, including 1444 DCM cases and 353,937 controls, as well as 3757 European adults for the 731 immunocyte phenotypes. Causal effects were estimated using inverse variance weighted, MR-Egger regression, weight median estimator, weighted mode, and simple mode. Sensitivity analysis was conducted to confirm data robustness and feasibility. Based on the inverse variance weighted findings, 14 immunocyte phenotypes were risk factors for DCM (P < .05, odds ratio [OR] > 1), while 15 immunocyte phenotypes exhibited a protective effect on DCM (P < .05, OR < 1). The results of reverse MR analysis suggested evidence that DCM occurrence might elevate the levels of 17 immunocyte phenotypes (P < .05, OR > 1) and decrease the levels of 9 immunocyte phenotypes (P < .05, OR < 1). Our research indicated that CD28 on secreting regulatory T cell could mitigate the occurrence of DCM, and reciprocally, the progression of DCM could reduce the level of CD28 on secreting regulatory T cell. This study confirmed the bidirectional genetic predictive relationship between immunocyte phenotypes and DCM, underscoring the complex interplay between DCM and the immune system.

This retrospective observational study aimed to identify clinical determinants of malnutrition in elderly patients with chronic heart failure. Elderly patients (≥65 years) with established chronic heart failure managed at a single tertiary hospital between January 2022 and December 2024 were included. Malnutrition was diagnosed according to the Global Leadership Initiative on Malnutrition criteria, using a 2-step approach combining risk screening and phenotypic and etiologic assessment. Demographic, anthropometric, comorbidity, laboratory, and heart failure-related data were extracted from electronic medical records. Univariate and multivariate logistic regression analyses were performed to explore factors associated with malnutrition, and model performance was evaluated using receiver operating characteristic analysis. Among 203 patients, 36 (17.7%) were classified as malnourished. Compared with non-malnourished patients, those with malnutrition were older and had a lower body mass index, lower serum albumin and prealbumin, higher C-reactive protein and neutrophil-to-lymphocyte ratio, poorer renal function, higher N-terminal pro-B-type natriuretic peptide levels, and a higher prevalence of New York Heart Association class III/IV and chronic obstructive pulmonary disease. In multivariate analysis, older age, lower body mass index, higher New York Heart Association class, elevated C-reactive protein, presence of chronic obstructive pulmonary disease, reduced estimated glomerular filtration rate, and higher N-terminal pro-B-type natriuretic peptide remained independently associated with malnutrition. The final model showed good discriminatory performance, with an area under the curve of 0.902, supporting its potential utility for nutritional risk stratification in this population.

The neutrophil percentage-to-albumin ratio (NPAR), calculated from neutrophil percentage and serum albumin levels, has been proposed as an inflammation-related indicator. Despite increasing interest in NPAR as an inflammatory marker, its prognostic relevance in rheumatoid arthritis (RA) remains insufficiently understood. The objective of this study was to investigate the prognostic relevance of NPAR in US adults with RA, particularly regarding all-cause and cardiovascular mortality, and to evaluate the prognostic performance of both NPAR and the neutrophil-to-lymphocyte ratio. Data were obtained from the National Health and Nutrition Examination Survey (NHANES) 2003-2018. RA status was identified according to participants' self-reported physician diagnosis, consistent with previous NHANES investigations. NPAR was calculated as neutrophil percentage × 100/albumin concentration (g/dL). Statistical analyses incorporated the NHANES complex survey framework, including weighting, stratification, and clustering procedures. Missing covariate data were addressed using multiple imputation. Associations between NPAR and mortality outcomes were examined using survey-weighted Cox regression models and restricted cubic spline analyses. The analysis included 2060 adults with RA, among whom 484 died during follow-up and 1576 remained alive. All-cause and cardiovascular mortality risks increased across NPAR levels and remained highest in the top quartile after multivariable adjustment. Kaplan-Meier analysis demonstrated significantly reduced survival probabilities among participants in the highest NPAR quartile, except for those with diabetes. NPAR exhibited a positive linear association with risks of all-cause and cardiovascular death in the restricted cubic spline models. Calculated AUCs reached 0.63 for the former and 0.66 for the latter, suggesting modest discriminatory power akin to neutrophil-to-lymphocyte ratio. NPAR was independently linked to mortality during follow-up in US patients with RA. As a routinely available biomarker, it may have prognostic relevance, although its predictive ability was relatively limited.

Chronic kidney disease (CKD) is a global public health challenge associated with elevated all-cause and cardiovascular mortality, driven by chronic inflammation and malnutrition. The neutrophil percentage-to-albumin ratio (NPAR), integrating inflammatory, and nutritional markers, has shown prognostic value in other conditions but remains underexplored in CKD. This study aimed to evaluate the association between NPAR and mortality outcomes in CKD patients using a nationally representative cohort. Data from National Health and Nutrition Examination Survey 1999 to 2018 were analyzed, including 1990 adults with CKD. NPAR was calculated as neutrophil percentage divided by serum albumin and categorized into quartiles. Primary outcomes were all-cause and cardiovascular mortality, assessed via linkage with the National Death Index. Cox regression models adjusted for demographics, comorbidities, and laboratory parameters. Restricted cubic splines and mediation analyses explored dose-response relationships and underlying mechanisms. Higher NPAR quartiles were significantly associated with increased all-cause mortality (Q4 vs Q1: adjusted hazard ratio = 2.04, 95% confidence interval = 1.41-3.00, P < .001) and cardiovascular mortality (Q4 vs Q1: hazard ratio = 2.33, 95% confidence interval = 1.20-4.50, P = .012). Kaplan-Meier analysis revealed poorer survival in Q4 (P < .001). Subgroup analyses showed stronger NPAR-mortality associations in obese, hypertensive, and cardiovascular disease patients. Mediation analysis indicated no significant role of estimated glomerular filtration rat in these relationships. NPAR is an independent predictor of all-cause and cardiovascular mortality in CKD, particularly in high-risk subgroups. This biomarker may enhance risk stratification by reflecting combined inflammatory and nutritional dysfunction, supporting targeted interventions to improve outcomes. Further prospective studies are needed to validate its clinical utility.

Acute ischemic stroke remains a major cause of death and disability, and intravenous thrombolysis is central to early reperfusion; however, post-lysis thrombin activity may contribute to rethrombosis and incomplete reperfusion. We conducted a single-center retrospective cohort study of consecutive adults with acute ischemic stroke admitted between January 2023 and December 2024, comparing a control regimen of standard-dose recombinant tissue plasminogen activator (alteplase 0.9 mg/kg, maximum 90 mg) with an observation regimen of low-dose recombinant tissue plasminogen activator (0.6 mg/kg, maximum 60 mg) plus argatroban initiated after thrombolysis in clinically stable patients. Because treatment strategy was selected in routine care rather than randomly assigned, all comparative findings were interpreted as associations. Among 125 patients (control n = 67; observation n = 58) with comparable baseline characteristics, the observation regimen was associated with greater early neurological improvement on the National Institutes of Health Stroke Scale at 24 hours (median change, 4 vs 3; P = .001) and day 7 (6 vs 4; P < .001), with higher responder rates (National Institutes of Health Stroke Scale decrease ≥4) at 24 hours (67.2% vs 41.8%; P = .004) and day 7 (81.0% vs 59.7%; P = .010). Favorable 90-day functional outcomes on the modified Rankin Scale (mRS) were more frequent (mRS 0-1: 69.0% vs 47.8%, P = .017; mRS 0-2: 87.9% vs 70.1%, P = .016), with a more favorable ordinal mRS distribution (P = .001). Recanalization was more frequent (P = .028), infarct growth was lower (P = .001), and early neurological deterioration was less common (P = .037). Symptomatic intracranial hemorrhage and other adverse events were uncommon, without significant between-group differences. These real-world findings should be considered hypothesis-generating and require prospective randomized validation.