Depression is a common comorbidity of chronic obstructive pulmonary disease (COPD) and is associated with worse prognosis. However, its association with lung health in individuals with pre-COPD remains unknown. We examined associations of increased depressive symptoms with respiratory symptoms, pre-COPD, and mortality.

We analysed data from the National Health and Nutrition Examination Survey (NHANES 2007-2012). Non-COPD individuals with available spirometry and Patient Health Questionnaire-9 (PHQ-9) data were included. Pre-COPD phenotypes included small airway dysfunction (SAD), preserved ratio impaired spirometry (PRISm) and nonobstructive chronic bronchitis (NOCB). Logistic and Cox regression models assessed associations of increased depressive symptoms with respiratory outcomes and all-cause mortality, respectively.

Among 10 941 participants, increased depressive symptoms were associated with higher risk of PRISm (adjusted OR (aOR) [95% CI] 1.41[1.07,1.85]), NOCB (aOR [95% CI] 1.90[1.49,2.42]), cough (aOR [95% CI] 2.17[1.72,2.73]), phlegm production (aOR [95% CI] 2.86[2.23,3.67]), exertional dyspnoea (aOR [95% CI] 2.53[2.04,3.13]) and wheeze (aOR [95% CI] 1.86[1.51,2.30]). A one-unit increase in PHQ-9 score was also associated with higher risks of respiratory symptoms and pre-COPD. Additionally, increased depressive symptoms were independently associated with higher all-cause mortality risk among participants with pre-COPD, including SAD (aHR [95% CI] 2.85[1.02,7.95]), PRISm (aHR [95% CI] 2.02[1.01,4.01]) and NOCB (aHR [95% CI] 2.45[1.24,4.84]). Similar associations were observed across depression scores and pre-COPD populations.

Increased depressive symptoms were associated with a higher risk of pre-COPD phenotypes, respiratory symptoms, and mortality. Increased depressive symptoms may be a treatable trait that can help mitigate adverse outcomes in participants with pre-COPD.

to analyze the symptoms of long COVID in patients treated in Primary Health Care, considering gender, age, and vaccination status.

this is a cross-sectional and analytical study conducted with a sample of 350 patients with long COVID treated in Primary Health Care services. Data were collected through the analysis of medical records and analyzed using the Poisson regression model.

older adults had an 88% higher prevalence of shortness of breath as a symptom of long COVID; females had a 13.5 times higher prevalence of hair loss; and unvaccinated individuals had a 3.64 times higher prevalence of reporting chest pain.

identifying the most prevalent symptoms of long COVID, taking into account age group, gender, and vaccination status, can contribute to clinical evaluation and the development of protocols to guide the appropriate management of these individuals.

Infectious and parasitic diseases remain a significant cause of mortality in the state of Amazonas, and are shaped by structural, environmental, and social vulnerabilities.

This descriptive, population-based study examines the temporal evolution and spatial distribution of mortality caused by infectious disease in Amazonas between 2013 and 2024. We analyzed monthly mortality rates using data from the Mortality Information System (SIM), focusing on International Classification of Diseases, 10th Revision (ICD-10) Chapter I (A00-B99) and selected codes from Chapter X (J09-J18).

Despite initial stability (2013-2018), mortality rates increased markedly from 2019 to 2021, associated with the direct and indirect impacts of the Coronavirus Disease (Covid-19) pandemic. After 2022, rates stabilized but remained elevated, indicating a shift toward a new endemic level. Spatial analysis revealed a persistent concentration of deaths in metropolitan areas and riverine municipalities, with recent expansion into medium-sized towns of the interior. Pneumonia, human immunodeficiency virus / acquired immunodeficiency syndrome (HIV/AIDS), septicemia, and tuberculosis accounted for most deaths, with a predominance of older adults and people identified as mixed race or Indigenous. High proportions of ill-defined causes and non-specific diagnoses, particularly in pneumonia and sepsis, highlight diagnostic limitations and the urgent need to strengthen death investigation services and expand etiological investigation.

Our findings highlight persistent inequalities in health access and call for integrated public health strategies, including improved surveillance systems, expanded diagnostic capacity, and intersectoral approaches adapted to the Amazonian context.

Environmental factors may influence the severity of lower respiratory infections, a major cause of morbidity and mortality in infants. Sulfur dioxide (SO2) has biologically plausible pro-inflammatory and epithelial effects. This PRISMA 2020-compliant systematic review synthesized observational studies published between 2015 and 2025, selected to ensure methodological comparability and contemporary relevance, examining the association between atmospheric SO2 exposure and severity-related respiratory outcomes in infants. Thirteen studies met eligibility criteria. Most evaluated short-term exposure using daily lag structures (lag01 to lag03) or 1-2 week averages, whereas one birth cohort assessed annual exposure during the first year of life. All studies adjusted for meteorological variables, and most incorporated multipollutant regression models. Owing to substantial heterogeneity in exposure metrics, increments, lag structures, and effect scales, a meta-analysis was not performed. Across studies, short-term SO2 exposure was most consistently associated with increased hospitalization for ALRIs, longer length of stay, and progression to severe disease. Effect estimates per 10 µg/m3 were modest but statistically significant in specific lag windows. In one cohort, higher annual exposure was associated with severe ALRI (IRR 2.81; 95% CI 1.35-5.83), and one hospital-based study reported increased mortality (OR 2.04; 95% CI 1.33-3.13). Associations were less consistent in low-exposure settings or in models with strong multipollutant collinearity. Overall, the evidence suggests context-dependent associations between short-term SO2 exposure and increased severity of respiratory infections in infants, particularly hospitalization, longer length of stay, and progression to severe disease. Given the observational and heterogeneous nature of the data, findings should be interpreted cautiously.

Obstructive sleep apnea (OSA) affects the body due to repeated obstruction of the upper airways. Continuous positive airway pressure (CPAP) is a treatment that can influence muscle function. This nine-month longitudinal study evaluated the effects of CPAP on molar bite force and on the thickness and surface temperature of the masseter and temporal muscles in adults. The study included 12 adults aged 20-70 with moderate or severe OSA, confirmed by polysomnography, all using CPAP. Molar bite force was measured with dynamometer; muscle thickness was evaluated by ultrasound at rest and during maximum contraction; and temperature was assessed using infrared thermography. Measurements were taken before treatment and at 3, 6, and 9 months. Data were analyzed using repeated-measures ANOVA with Bonferroni correction (p<0.05). Although no significant differences in bite force were observed, only a non-significant tendency toward increased maximum molar force on both sides was noted after nine months. Ultrasound showed a significant increase in right temporal muscle thickness at rest and during contraction, and a left-side increase at rest. Nine months of CPAP therapy in adults with moderate to severe obstructive sleep apnea resulted may influence craniofacial muscle morphology without significantly altering stomatognathic function.

To determine the prevalence of oral alterations among critical patients within the first 48 hours of intensive care unit admission, and their association with hospital-acquired pneumonia, bloodstream infections, and sepsis.

This prospective cohort study was conducted from March 2018 to December 2021 in a Brazilian neurology intensive care unit. A single dental surgeon assessed oral conditions with follow-up until hospital discharge. Logistic regression analyzed the association between oral alterations and outcomes (hospital-acquired pneumonia, bloodstream infections, and sepsis), adjusting for confounders.

We enrolled 248 patients (55.6% male; mean age, 67.2 years), of whom 97.6% had oral abnormalities. The most common were visible dental plaque (61.7%), gingival inflammation (60.9%), and five or more missing teeth (49.2%). Carious teeth were linked to pneumonia (OR 1.10; 95%CI 1.00 - 1.20; p = 0.047). Destroyed teeth (OR 1.12; 95%CI 1.02 - 1.23; p = 0.02) and visible plaque (OR 1.08; 95%CI 1.00 - 1.17; p = 0.04) were associated with bloodstream infections. No factors were linked to sepsis.

Most patients exhibited oral alterations upon admission to the intensive care unit. Carious teeth may increase pneumonia risk, while destroyed teeth and visible plaque may raise bloodstream infection risk.

Respiratory distress syndrome (RDS), or hyaline membrane disease, is a common condition in preterm infants (< 37 weeks' gestation) and a leading cause of neonatal morbidity and mortality. The risk is highest in extremely preterm (< 28 weeks) and very preterm (28 to < 31 weeks) infants due to immature lung and cardiovascular development. RDS results from a deficiency or dysfunction of pulmonary surfactant, which lines the alveoli to reduce surface tension, prevent atelectasis, and protect the lungs. Surfactant is primarily composed of dipalmitoylphosphatidylcholine (DPPC), other phospholipids, and four proteins that support its function, recycling, and innate lung defense. Surfactant replacement therapy improves lung compliance, reduces the need for ventilator support, and decreases the risk of pneumothorax, death, and the combined outcome of death or bronchopulmonary dysplasia. Its widespread use has substantially improved survival among preterm infants without increasing long-term neurological or developmental disability. Various surfactant preparations, including animal-derived, synthetic, and protein or peptide-containing formulations have been evaluated. Surfactant can be administered prophylactically immediately after birth or selectively once RDS develops. Both strategies are effective, with theoretical advantages and disadvantages. Prophylactic surfactant may prevent respiratory insufficiency, reduce the need for ventilator support, and distribute surfactant more evenly in fluid-filled lungs, lowering the risk of lung injury. Selective treatment targets only infants with clinical RDS, avoiding unnecessary therapy, potential risks, and costs for those who would not benefit. Administration methods include endotracheal tube, intubation with rapid extubation, thin catheter, laryngeal mask, hypopharyngeal deposition, and, more recently, aerosolized or nebulized approaches, though the effectiveness of the latter remains unproven. For this review, a prophylactic strategy refers to intubation and bolus surfactant administration immediately after birth, while selective therapy refers to administration once evidence of RDS is present. The effect of surfactant may differ in infants stabilized early on continuous positive airway pressure (CPAP) and those whose mothers received a complete course of antenatal corticosteroids. In these infants, the benefits of prophylactic surfactant appear less pronounced than in neonates who did not receive early CPAP or antenatal steroids. In this update, we explored these factors in subgroup analyses, as in the previous version of the review. Additionally, we examined how the threshold of FiO₂ (fraction of inspired oxygen) used to initiate selective treatment, as well as the method of surfactant administration, might influence the effect of the surfactant replacement strategies.

To compare the effect of prophylactic surfactant administration versus selective surfactant administration on morbidity and mortality in preterm infants at risk of respiratory distress syndrome (RDS).

We searched CENTRAL, MEDLINE, Embase, and CINAHL on 31 January 2025. To identify any studies not captured by our search of bibliographical databases, we also searched clinical trial registers, conference proceedings, and reference lists of included studies and surfactant reviews.

We included randomized controlled trials (RCTs) and quasi-RCTs comparing the effects of prophylactic surfactant administration in preterm infants at risk of RDS versus surfactant treatment of preterm infants with established RDS.

We used standard Cochrane methods. Our main outcomes were mortality, neurodevelopmental disability, and complications of preterm birth including pneumothorax and chronic lung disease. We performed meta-analysis and expressed our results using mean difference (MD), standardized mean difference (SMD), or risk ratio (RR), with 95% confidence intervals (CIs). We used GRADE to assess the certainty of the evidence.

We identified 10 relevant individually randomized controlled trials (involving 3151 preterm infants). All trials were conducted in North America and Europe. Eight were conducted in the 1990s, and two were published more recently, at a time of greater use of antenatal steroids and nasal continuous positive airway pressure (CPAP). Nine trials were at risk of performance and detection bias. When all studies are considered, prophylactic surfactant probably results in little to no difference in the risk of chronic lung disease (CLD) at 36 weeks' postmenstrual age compared to selective use of surfactant (RR 1.13, 95% CI 1.00 to 1.28; I² = 0%; RD 0.04, 95% CI 0.00 to 0.08; NNTH 25 95% CI 13 to > 1000; I² = 0%; 5 trials, 1874 infants; moderate-certainty evidence). There may be little to no difference between the prophylactic and selective approaches in moderate to severe neurodevelopmental impairment (RR 0.83, 95% CI 0.57 to 1.21; 1 trial, 976 infants; I² not applicable; low-certainty evidence). Prophylactic surfactant may result in a slight reduction in pneumothorax compared to selective surfactant administration (RR 0.76, 95% CI 0.56 to 1.04; I² = 12%; 8 trials, 3094 infants; low-certainty evidence). In studies in which infants were stabilized on CPAP, the use of prophylactic surfactant, compared with selective surfactant administration, may make little to no difference to the risk of chronic lung disease and probably slightly increases mortality, while the evidence remains uncertain regarding the effect of prophylactic surfactant on all other outcomes, including pneumothorax. In contrast, in settings without routine use of CPAP, prophylactic surfactant reduces mortality and may reduce pneumothorax slightly, with very uncertain evidence for CLD. In our view, these findings support managing neonates at risk of respiratory distress syndrome with initial stabilization using CPAP and then selective surfactant administration. We were not able to draw conclusions about our subgroup analyses conducted according to receipt of antenatal steroids, threshold used to apply selective treatment, and method of surfactant administration, which provided evidence of low to very low certainty. There were insufficient data to carry out subgroup analysis by gestational age.

Studies of prophylactic surfactant administration in infants at risk of developing RDS that were conducted prior to widespread use of maternal prenatal steroids and routine early stabilization on CPAP demonstrated a decreased risk of mortality and slight reduction in pneumothorax compared with selective surfactant use in infants with established RDS. However, larger trials that reflect current neonatal care practices do not support this finding. Instead, they show that, compared with selective surfactant administration in infants stabilized on CPAP, prophylactic surfactant likely results in little to no difference in the risk of chronic lung disease and slightly increases mortality.

Eosinophilic granulomatosis with polyangiitis (EGPA) is an anti-neutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis characterized by asthma, eosinophilia and inflammation of small-tomedium vessels. Although respiratory and neurological manifestations are predominant, cardiovascular involvement and ischemic complications may significantly affect the prognosis.

We report a case of a 37-year-old woman, diagnosed with EGPA based on a history of bronchial asthma, marked eosinophilia, mononeuritis multiplex progressing to sensorimotor polyneuropathy, nasal polyps and vasculitic lesions of the toes and feet associated with MPO-ANCA positivity. Despite treatment with high dose corticosteroids, cyclophosphamide, anticoagulation, and plasmapheresis, the disease progressed with development of digital necrosis and ischemic lesions in the spleen, kidney, and cerebrum. Transesophageal echocardiographic examination confirmed Loeffler endocarditis of the mitral and aortic valve. Due to the fulminant and therapeutically challenging disease course, treatment with rituximab (375mg/m²) was initiated, with positive clinical and biochemical response. After clear demarcation, amputation of the affected toes was successfully performed. Maintenance therapy included corticosteroids, methotrexate (later discontinued due to hepatotoxicity), and antimalarials, with sustained remission during a three-year follow-up.

To our knowledge, this rare form of EGPA presenting as a combination of digital gangrene and Loeffler endocarditis associated with MPO-ANCA positivity and cryofibrinogenemia has not previously been reported. The case highlights the potential immunopathogenic interplay between eosinophilic inflammation, ANCA-mediated vasculitis, and cryofibrinogenemia-associated thrombosis leading to severe ischemic complications. Early recognition and timely initiation of B-cell-targeted therapy with rituximab resulted in sustained remission and functional recovery.

Anti-glomerular basement membrane (anti-GBM) disease is not a distinct, isolated entity but rather a condition that frequently overlaps with other autoimmune serological profiles. Most notably, it can coexist with antineutrophil cytoplasmic antibodies (ANCA), alongside a diverse spectrum of additional autoantibodies. Despite the occurrence of such antibody overlap in a subset of patients, their specific clinical manifestations and prognostic implications remain poorly defined and largely elusive.

This study retrospectively enrolled patients diagnosed with anti-GBM disease at the First Affiliated Hospital with Nanjing Medical University between January 2017 and January 2024. Based on serological profiles, enrolled patients were stratified into three cohorts: the classic anti-GBM group (anti-GBM antibodies positive alone), the ANCA-anti-GBM double-positive group, and the anti-GBM-non-ANCA autoantibody overlap group. Clinical, pathological, treatment, and outcome characteristics were systematically compared across the three groups. Additionally, landmark analysis was conducted to assess prognostic discrepancies across distinct time intervals.

A total of 67 patients with anti-GBM disease were enrolled in this study, with 30, 18, and 19 cases allocated to the classic anti-GBM group, ANCA-anti-GBM double-positive group, and anti-GBM-non-ANCA autoantibody overlap group, respectively. The ANCA-anti-GBM double-positive group presented with the highest mean age at onset among the three cohorts. A statistically significant difference was detected in baseline anti-GBM antibody titers across the groups (median: 141.20 vs. 104.25 vs. 181.70; interquartile range: 102.90-257.70 vs. 52.15-137.07 vs. 121.05-555.40; p = 0.044). By contrast, no significant differences were noted in terms of other clinical characteristics, renal pathological findings, and therapeutic regimens. Although the overall survival rates showed no statistical discrepancy among the three groups, distinct trends were observed in early survival outcomes: the ANCA-anti-GBM double-positive group had the poorest early survival, followed by the anti-GBM-non-ANCA autoantibody overlap group, while the classic anti-GBM group exhibited the most favorable early survival profile.

This study identifies the distinct phenotypic traits of anti-GBM disease with concurrent other autoimmune antibodies, underscoring that sole reliance on anti-GBM antibody titers is inappropriate for prognostic judgment and treatment decision-making. For patients with anti-GBM disease overlapping with non-ANCA autoantibodies, intensive treatment regimens may be justified to achieve more favorable clinical prognosis.

Public health implementation of wastewater-based disease surveillance (WBDS) increased dramatically during the COVID-19 pandemic. WBDS raises unique ethical considerations because of its community-scale method of disease surveillance. However, the perspectives of community members regarding the ethics of WBDS are absent from the literature.

We explored ethical considerations of WBDS by interviewing community members and professionals across the United States using vignettes and a semi-structured interview process. Vignettes highlighted ethical opportunities and concerns noted in the literature, and interview questions solicited information relevant to Kass's Public Health Ethics Framework. Professional interviewees were identified from their contributions to the field of WBDS, and community interviewees were recruited through a national survey panel firm. We recorded, transcribed, and qualitatively analyzed interview data using a blended inductive and deductive approach.

We interviewed 8 community members and 13 professionals from February to November of 2023. Interviewees broadly supported WBDS and collectively identified a variety of conditions needed for the ethically acceptable conduct of WBDS, such as transparency, effective communication, data privacy, legitimate purpose, responsible data use, public oversight, equity, and community engagement. Ethical concerns and suggested protective measures were similar between the two interviewee groups with few notable differences.

This exploratory study found interviewees were receptive to WBDS when accompanied by transparency, safeguards against data misuse, and clear public health purpose.