Hydrogen-rich water alleviates asthma airway inflammation by modulating tryptophan metabolism and activating aryl hydrocarbon receptor via gut microbiota regulation.

Hydrogen-rich water (HRW) is a beverage containing a high concentration of hydrogen that has been researched for its antioxidant, anti-apoptotic, and anti-inflammatory properties in asthma. This study investigates the potential therapeutic impact of HRW on the gut-lung axis. Using 16S rRNA and serum metabolomics, we examined changes in gut microbiota and serum metabolites in asthmatic mice after HRW intervention, followed by validation experiments. The findings revealed that HRW influenced gut microbiota by increasing Ligilactobacillus and Bifidobacterium abundance and enhancing the presence of indole-3-acetic acid (IAA), a microbially derived serum metabolite. Both in vivo and in vitro experiments showed that HRW's protective effects against airway inflammation in asthmatic mice may be linked to the gut microbiota, with IAA potentially playing a role in reducing asthmatic airway inflammation through the aryl hydrocarbon receptors (AhR) signaling pathway. In summary, HRW can modify gut microbiota, increase Bifidobacterium abundance, elevate microbial-derived IAA levels, and activate AhR, which could potentially alleviate inflammation in asthma.

Effectiveness of immediate appointment scheduling in smoking cessation clinics for patients with chronic airway diseases: Preliminary results from a randomized trial.

INTRODUCTION: Patients with airway diseases who bear the burden of smoking need access to smoking cessation support. We aimed to investigate the impact of immediately scheduled appointments on access to smoking cessation clinics compared with usual care in this patient group. METHODS: This multicenter, prospective, randomized, open-label study was conducted between November 2022 and June 2023 at pulmonary outpatient clinics. The study included adult patients who were current smokers and had a diagnosis of asthma, COPD, or bronchiectasis for at least six months. Sequentially randomization was used for the allocation of patients in a 1:1 ratio to two study arms: the usual support arm (representing the current standard care procedure) and the immediate support arm (involving intensive brief cessation advice followed by the immediate arrangement of an appointment at the same clinic's smoking cessation service). After one week, both patient groups were contacted by phone to assess their quit attempts and whether they had sought assistance from smoking cessation outpatient clinics (SCCs). RESULTS: A total of 397 patients were enrolled in the study, with 199 allocated to the usual support arm and 198 allocated to the immediate support arm. Within the first week, 18.1% of patients in the usual support arm and 77.3% of patients in the immediate support arm sought assistance from the smoking cessation clinic (p<0.001). The rate of smokers without an intention to quit was 56.7% in the usual support arm and 27.7% in the immediate support arm in the first week of follow-up. Immediate appointment scheduling was significantly associated with a 13-fold (OR=13.38; 95% CI: 8.00-22.38) increase in referral rates in the multivariate logistic regression model. CONCLUSIONS: Arranging instant appointments has increased access to SCCs by 13 times compared to the usual care, this group of patients should be given an immediate appointment to SCCs.

Exploring the pathogenicity of Mycoplasma pneumoniae: Focus on community-acquired respiratory distress syndrome toxins.

Community-Acquired Respiratory Distress Syndrome Toxin (CARDS TX) is a unique exotoxin produced by Mycoplasma pneumoniae (MP) and has been confirmed to possess ADP-ribosyltransferase (ART) and vacuolating activities. CARDS TX binds to receptors on the surfaces of mammalian cells followed by entry into the cells through clathrin-mediated endocytosis, and exerts cytotoxic effects by undergoing retrograde transport and finally cleavage on endosomes and cellular organelles. In addition, CARDS TX can trigger severe inflammatory reactions resulting in airway dysfunction, producing allergic inflammation and asthma-like conditions. As a newly discovered virulence factor of MP, CARDS TX has been extensively studied in recent years. As resistance to macrolide drugs has increased significantly in recent years and there is no vaccine against MP, the development of a vaccine targeting CARDS TX is considered a potential preventive measure. This review focuses on recent studies and insights into this toxin, providing directions for a better understanding of MP pathogenesis and treatment. IMPORTANCE: A serious hazard to worldwide public health in recent years, Mycoplasma pneumoniae (MP) is a prominent bacterium that causes community-acquired pneumonia (CAP) in hospitalized children. Due to their high prevalence and fatality rates, MP infections often cause both respiratory illnesses and extensive extrapulmonary symptoms. It has recently been shown that MP produces a distinct exotoxin known as Community-Acquired Respiratory Distress Syndrome Toxin (CARDS TX). Mycoplasma pneumoniae pneumonia (MPP)-like tissue injury is caused by this toxin because it has both ADP-ribosyltransferase and vacuolating properties. A better knowledge of MP etiology and therapy is provided by this review, which focuses on latest research and insights into this toxin.

Reshaping respiratory care: potential advances in inhaled pharmacotherapy in asthma.

INTRODUCTION: Asthma is a common disease with a global burden of 358 million patients. Despite improvements in pharmacological and non-pharmacological treatments, many patients still do not achieve complete asthma control. Therefore, innovative pharmacotherapy is important. AREAS COVERED: Following a semi-structured search in Pubmed, an overview of advances in inhaled asthma therapy is provided, looking at innovations in digital inhalers, eco-friendly inhalers and novel inhaled biologic therapies, antibiotics and vaccines, as well as other potential novel asthma therapy targets. EXPERT OPINION: Digital inhalers, sending reminders and monitoring inhalation technique electronically, can support medication adherence and improve asthma control. To reduce the global warming potential of traditional aerosols used in pressurized metered-dose inhalers (HFA-134a, HFA-227ea), greener alternatives are under development (HFA-152a, HFO-1234ze) that are expected to be available by 2025. Current pharmacological advances in asthma therapy are mainly achieved by novel biologicals (anti-IgE, anti-IL5, anti-IL4/13, and anti-TSLP) targeting specific severe asthma phenotypes. While injection is the usual administration route for biologics and vaccines used in asthma, inhalation is an option being explored, although several (mainly formulation) challenges need to be overcome. Other potential novel future inhaled asthma therapies include anti-IL-33/ST2 biologicals and JAK inhibitors, all still requiring more clinical evidence.

Association of Dose of Inhaled Corticosteroids and Frequency of Adverse Events.

BACKGROUND: Inhaled corticosteroids (ICS) are the cornerstone of asthma treatment and significantly improve morbidity and mortality. Adverse effects of oral corticosteroids are well documented, but less is known about ICS. METHODS: We conducted observational studies in adults with asthma using two different UK nationwide datasets: Clinical Practice Research Datalink (CPRD) Aurum and CPRD GOLD. The exposure was incident ICS; the outcomes were major adverse cardiac events (MACE), arrhythmia, pulmonary embolism (PE) and pneumonia over 12-months. Our main analyses used a cohort method with stabilized inverse probability treatment weighting to balance confounding between exposed and unexposed patients. Secondary analyses included nested case-control studies, and self-controlled case series. ICS was treated both as a categorical and continuous variable. Absolute risk was estimated using weighted flexible parametric models. FINDINGS: From 162,202 patients in our main cohort, there was an association with all outcomes at medium daily ICS dose or higher (HR, 95%CI at 201-599mcg: MACE=2.63, 1.66-4.15, arrhythmia=2.21, 1.60-3.04, PE=2.10, 1.37-3.22, pneumonia=2.25, 1.77-2.85; at ≥600mcg: MACE=4.63, 2.62-8.17, arrhythmia=2.91, 1.72-4.91, PE=3.32, 1.69-6.50, pneumonia=4.09, 2.98-5.60). There were no associations with lower doses of ICS. Secondary analyses produced similar results. The number needed to harm (95%CI) using 12-months of ICS 201-599mcg: MACE=473 (344-754), arrhythmia=567 (395-1006), PE=1221 (744-3388) and pneumonia=230 (177-327) and using ICS ≥600mcg: MACE=224 (148-461), arrhythmia=396 (228-1523), PE=577 (309-4311), pneumonia=93 (69-141). INTERPRETATION: Short-term use of low dose ICS was not associated with adverse effects. Moderate-high daily ICS doses were associated with an increased risk, but low-frequency, of cardiovascular events, pulmonary embolism and pneumonia. It is important for clinicians to adhere to guideline recommendations to use the lowest effective ICS dose. This article is open access and distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).

Solute Carrier Family 26 Member 4 (SLC26A4), A Potential Therapeutic Target for Asthma.

Asthma is a prevalent respiratory condition with multifaceted pathomechanisms, presenting challenges for therapeutic development. The SLC (Solute Carrier) gene family, encompassing diverse membrane transport proteins, plays pivotal roles in various human diseases by facilitating solute movement across biological membranes. These solutes include ions, sugars, amino acids, neurotransmitters, and drugs. Mutations in these ion channels have been associated with numerous disorders, underscoring the significance of SLC gene families in physiological processes. Among these, the SLC26A4 gene encodes pendrin, an anion exchange protein involved in transmembrane transport of chloride, iodide, and bicarbonate. Mutations in SLC26A4 are associated with Pendred syndrome. Elevated SLC26A4 expression has been linked to airway inflammation, hyperreactivity, and mucus production in asthma. Here, we review novel insights from SLC gene family members into the mechanisms of substrate transport and disease associations, with specific emphasis on SLC26A4. We explore triggers inducing SLC26A4 expression and its contributions to the pathogenesis of pulmonary diseases, particularly asthma. We summarize the inhibitors of SLC26A4 that have shown promise in the treatment of different phenotypes of diseases. While SLC26A4 inhibitors present potential treatments for asthma, further research is imperative to delineate their precise role in asthma pathogenesis and develop efficacious therapeutic strategies targeting this protein.

Omics approaches in asthma research: Challenges and opportunities.

Asthma, a chronic respiratory disease with a global prevalence of approximately 300 million individuals, presents a significant societal and economic burden. This multifaceted syndrome exhibits diverse clinical phenotypes and pathogenic endotypes influenced by various factors. The advent of omics technologies has revolutionized asthma research by delving into the molecular foundation of the disease to unravel its underlying mechanisms. Omics technologies are employed to systematically screen for potential biomarkers, encompassing genes, transcripts, methylation sites, proteins, and even the microbiome components. This review provides an insightful overview of omics applications in asthma research, with a special emphasis on genetics, transcriptomics, epigenomics, and the microbiome. We explore the cutting-edge methods, discoveries, challenges, and potential future directions in the realm of asthma omics research. By integrating multi-omics and non-omics data through advanced statistical techniques, we aspire to advance precision medicine in asthma, guiding diagnosis, risk assessment, and personalized treatment strategies for this heterogeneous condition.

[The silent correlate of rhinitis on lower airway]. / El impacto silencioso de la rinitis sobre la vía aérea inferior.

The respiratory tract, from the nose to the lung, behaves as an anatomical and pathophysiological unit under a holistic model. Lower airway abnormalities, such as bronchial hyperresponsiveness, reduced lung function and inflammation of the bronchial mucosa without clinical expression, have been observed in patients with rhinitis without asthma. These would be the consequence of a common systemic inflammatory phenomenon with simultaneous impact on the nose and lung. For unknown reasons, these patients do not exhibit a full clinical expression, which could mean an increased risk of developing asthma. In this review we address the frequency and characteristics of existing pulmonary abnormalities in children and adolescents with chronic rhinitis that derive from our previous research and, more recently, within the project "Allergic Respiratory Disease: The United Airway Concept" supported by the Universidad Católica de Córdoba, and a comparative analysis with the evidence provided by other authors in the medical literature.

El aparato respiratorio, desde la nariz al pulmón, se comporta como una unidad anatómica y fisiopatológica bajo un modelo holístico. Se han observado alteraciones pulmonares sin traducción clínica en pacientes con rinitis sin asma, que se manifiestan como hiperreactividad bronquial, reducción de la función pulmonar e inflamación bronquial. Estas serían consecuencia de un fenómeno inflamatorio sistémico con impacto simultáneo en nariz y pulmón, que por razones desconocidas no tiene una expresión clínica completa, pero que podrían significar un mayor riesgo de desarrollo de asma. En esta revisión abordamos la frecuencia y características de las anormalidades pulmonares existentes en niños y adolescentes con rinitis crónica derivadas de nuestras investigaciones previas y, más recientemente, del proyecto "Enfermedad Alérgica Respiratoria: El Concepto de Unidad de la Vía Aérea", línea de investigación acreditada por la Universidad Católica de Córdoba y un análisis comparativo con las evidencias aportadas por otros autores en la literatura médica.

Pulmonary adaptation to repeated poly(I:C) exposure is impaired in asthmatic mice: an observational study.

BACKGROUND: While asthma exacerbations remain a major challenge in patient management, few animal models exist to explore the underlying mechanisms. Here, we established an animal model of asthma that can be used to study pathophysiological mechanisms and therapeutic strategies on asthma exacerbation. METHODS: Female BALB/c mice were sensitized and exposed to PBS or Dermatophagoides pteronyssinus (DerP) extract for 11 weeks. Asthmatic phenotype was assessed through lung inflammation, bronchial hyperresponsiveness and bronchial smooth muscle remodeling. Asthmatic and control mice were exposed once or three times to poly(I:C) to simulate virus-induced inflammation. RESULTS: Fourteen days after exposure to DerP, asthmatic mice showed resolution of inflammation with sustained bronchial hyperresponsiveness and bronchial smooth muscle remodeling compared to control. At this stage, when mice were subjected to a single exposure to poly(I:C), control and asthmatic mice were characterized by a significant increase in neutrophilic inflammation and bronchial hyperresponsiveness. When mice were repeatedly exposed to poly(I:C), control mice showed a significant decrease in neutrophilic inflammation and bronchial hyperresponsiveness, while asthmatic mice experienced worsening of these outcomes. CONCLUSIONS: This observational study report an asthmatic mouse model that can undergo exacerbation after repeated exposure to poly(I:C). Our findings on pulmonary adaptation in control mice may also pave the way for further research into the mechanism of adaptation that may be impaired in asthma and raise the question of whether asthma exacerbation may be a loss of adaptation.

Dietary antioxidant and inflammatory potential in asthmatic patients and its association with all-cause mortality.

BACKGROUND: The occurrence and progression of asthma can be influenced by the components in food. Our study aims to determine whether dietary antioxidant and inflammatory potential are associated with the risk of mortality in asthma patients. METHODS: Participants from the 2001-2018 National Health and Nutrition Examination Survey (NHANES) aged 20 years and older with a diagnosis of asthma were included. Mortality status was obtained according to death certificate records from the National Death Index. The antioxidant and inflammatory potential of the diet was assessed using two widely used and dependable indices, Composite Dietary Antioxidant Index (CDAI) and Dietary Inflammatory Index (DII). Restricted cubic spline (RCS) regression was used to analyze the non-linear relationship between the two indexes and mortality. Multivariable Cox proportional risk models were used to estimate hazard ratio and 95% confidence intervals for mortality. Finally, the relationship between CDAI and DII was analyzed. RESULTS: A total of 4698 NHANES participants represented 23.2 million non-institutionalized residents of the US were enrolled in our study. Patients with higher CDAI or lower DII exhibited longer survival times. RCS regression showed a linear relationship of CDAI or DII with mortality. In the Cox regression, both crude and adjusted models demonstrated that higher CDAI or lower DII was linked to a reduced risk of all-cause mortality. Similar associations were found in subgroup analysis. Finally, a negative relationship was found between CDAI and DII. CONCLUSION: Reducing pro-inflammatory or increasing antioxidant diets could reduce all-cause mortality among adult asthma patients.

Exploring the causal relationship between asthma in the metabolic syndrome: a Mendelian randomization study.

BACKGROUND: Previous observational studies have indicated a potential association between metabolic syndrome (MetS) and asthma, though the causal nature of this connection is still uncertain. Our study used Mendelian randomization (MR) to examine the causal relationship between metabolic syndrome (MetS) and its components with asthma. METHODS: This study utilized single nucleotide polymorphisms (SNPs) related to MetS and its components, sourced from publicly available genome-wide association studies (GWAS) data, in combination with asthma data from the FinnGen database. Statistical analyses were conducted using the inverse variance weighted method (IVW), MR-Egger, and weighted median method. The robustness of the findings was confirmed through various sensitivity analyses. RESULTS: The IVW analysis indicated that MetS was associated with an increased risk of asthma (OR = 1.0781, 95% CI = 1.0255-1.1333, p = 0.0032). Among the components of MetS, waist circumference (WC) showed a strong association with asthma (OR = 1.4777, 95% CI = 1.3412-1.6281, p = 2.8707 × 10-15). Conversely, high-density lipoprotein cholesterol (HDL-C) was found to be inversely related to the risk of asthma (OR = 0.9186, 95% CI = 0.8669-0.9734, p = 0.0041). CONCLUSION: The findings of this study support that MetS and its specific components, particularly abdominal obesity, are linked to a higher risk of asthma, while HDL-C might offer protective effects against asthma. These findings provide a foundation both for further research and possible therapeutic interventions.

Exposure to agricultural pesticides and wheezing among 5-12-year-old children in the Imperial Valley, CA, USA.

Background: Exposure to pesticides has been linked to adverse respiratory health outcomes in children. Methods: We leveraged the Children's Assessing Imperial Valley Respiratory Health and the Environment cohort located in the rural community of Imperial Valley near the US-Mexico border. We calculated the kilograms of total pesticides applied within 400 m of children's residential addresses for the years 2016-2020. Estimated pesticide usage near homes was categorized into three groups (none vs. low vs. high [split at the median]). All health variables (i.e., asthma status and wheezing) were derived from a parent-reported questionnaire on respiratory health. We used generalized linear models, controlling for child sex, the language of survey, health insurance, respondents' highest education, and exposure to environmental secondhand smoking, to calculate prevalence differences between none versus low and high exposure to agricultural pesticides. Results: Approximately 62% of the 708 children (aged 5-12 years) lived within 400 m of at least one pesticide application within 12 months prior to survey administration. Exposure to pesticides within 400 m of children's residences was associated with 12-month prior wheeze. Those in the "high" exposure group had a prevalence of wheezing that was 10 (95% confidence interval: 2%, 17%) percentage points higher than among children not exposed to pesticide applications. Associations for high exposure to specific categories of pesticide applications, sulfur only, all pesticides except sulfur, chlorpyrifos, and glyphosate, also were observed with a higher prevalence of wheezing than among children not exposed to pesticide applications. Conclusions: We observed associations between living near pesticide applications and more wheeze symptoms among children.

The Sisyphean breath: role of anxiety sensitivity and distress tolerance in dyspnea among adults with asthma and COPD.

INTRODUCTION: Asthma and COPD are among the leading causes of morbidity and mortality, impacting over 260 million people and causing over 3 million deaths globally (Momtaz-Manesh, S. et al., 2023). Pulmonary symptoms can impair tolerance and increase the negative attribution of anxiety sensations. Reciprocally, anxiety associated with dyspnea can induce hyperventilation. This perpetuates a cycle of symptom exacerbation and poor treatment adherence. Managing labored breathing is challenging due to its subjective nature. Dyspnea is a sufferer's endless pursuit to breathe, rendering its experience as truly, "Sisyphean." AIM: This study explored the role of anxiety sensitivity and distress tolerance in dyspnea among adults with asthma and COPD (N = 107). A single-group cross-sectional research design was used. Data from pulmonologist-diagnosed adults with asthma and COPD were collected across various clinics in Delhi-NCR. RESULTS: It was found that anxiety sensitivity, distress tolerance and dyspnea were strongly correlated. Also, an increase in anxiety sensitivity was strongly predictive of dyspnea severity. Further, distress tolerance acted as a partial mediator between anxiety sensitivity and dyspnea. CONCLUSIONS: Improving distress tolerance can act as an adjuvant in effective dyspnea management.

Imagining the severe asthma decision trees of the future.

INTRODUCTION: There are no validated decision-making algorithms concerning severe asthma (SA) management. Future risks are crucial factors and can be derived from SA trajectories. AREAS COVERED: The future severe asthma-decision trees should revisit current knowledge and gaps. A focused literature search has been conducted. EXPERT OPINION: Asthma severity is currently defined a priori, thereby precluding a role for early interventions aiming to prevent outcomes such as exacerbations (systemic corticosteroids exposure) and lung function decline. Asthma 'at-risk' might represent the ultimate paradigm but merits longitudinal studies considering modern interventions. Real exacerbations, severe airway hyperresponsiveness, excessive T2-related biomarkers, noxious environments and patient behaviors, harms of OCS and high-doses inhaled corticosteroids (ICS), and low adherence-to-effectiveness ratios of ICS-containing inhalers are predictors of future risks. New tools such as imaging, genetic, and epigenetic signatures should be used. Logical and numerical artificial intelligence may be used to generate a consistent risk score. A pragmatic definition of response to treatments will allow development of a validated and applicable algorithm. Biologics have the best potential to minimize the risks, but cost remains an issue. We propose a simplified six-step algorithm for decision-making that is ultimately aiming to achieve asthma remission.

Inhaled tea polyphenol-loaded nanoparticles coated with platelet membranes largely attenuate asthmatic inflammation.

BACKGROUND: Tea polyphenols (TPs), prominent constituents of green tea, possess remarkable antioxidant and anti-inflammatory properties. However, their therapeutic potential is limited due to low absorption and poor bioavailability. To address this limitation and enhance their efficacy, we developed a biomimetic nanoplatform by coating platelet membrane (PM) onto poly-lactic-co-glycolic acid (PLGA) nanoparticles (NPs) to create targeted delivery vehicles for TPs (PM@TP/NPs) to the inflamed tissues in asthma. METHODS: After synthesizing and characterizing PM@TP/NPs, we assessed their biocompatibility and biosafety through cell viability assays, hemolysis tests, and inflammation analysis in vivo and in vitro. The therapeutic effect of PM@TP/NPs on asthma was then evaluated using a mouse model of HDM-induced asthma. Additionally, PM@TP/NPs-mediated reactive oxygen species (ROS) scavenging capacity, as well as the activation of signaling pathways, were analyzed in HBE cells and asthmatic mice via flow cytometry, RT-qPCR, and western blotting. RESULTS: Compared with free TPs, PM@TP/NPs demonstrated excellent biocompatibility and safety profiles in both in vitro and in vivo, as well as enhanced retention in inflamed lungs. In HDM-induced mouse asthma model, inhaled PM@TP/NPs largely attenuated lung inflammation and reduced the secretion of type 2 pro-inflammatory cytokines in the lungs compared to free TPs. The therapeutic effects of PM@TP/NPs on asthma might be associated with an enhanced ROS scavenging capacity, increased activation of the Nrf2/HO-1 pathway, and decreased activation of the CCL2/MAPK and TLR4/NF-κB pathway in the lungs. CONCLUSIONS: Our findings demonstrate that inhalation of PM@TP/NPs largely attenuated lung inflammation in HDM-induced asthmatic mice. These results suggest that PM@TP/NPs might be a novel therapeutic strategy for asthma.

How early life respiratory viral infections impact airway epithelial development and may lead to asthma.

Childhood asthma is a common chronic disease of the airways that results from host and environment interactions. Most risk factor studies of asthma point to the first year of life as a susceptibility window of mucosal exposure that directly impacts the airway epithelium and airway epithelial cell development. The development of the airway epithelium, which forms a competent barrier resulting from coordinated interactions of different specialized cell subsets, occurs during a critical time frame in normal postnatal development in the first year of life. Understanding the normal and aberrant developmental trajectory of airway epithelial cells is important in identifying pathways that may contribute to barrier dysfunction and asthma pathogenesis. Respiratory viruses make first contact with and infect the airway mucosa. Human rhinovirus (HRV) and respiratory syncytial virus (RSV) are mucosal pathogens that are consistently identified as asthma risk factors. Respiratory viruses represent a unique early life exposure, different from passive irritant exposures which injure the developing airway epithelium. To replicate, respiratory viruses take over the host cell transcriptional and translational processes and exploit host cell energy metabolism. This takeover impacts the development and differentiation processes of airway epithelial cells. Therefore, delineating the mechanisms through which early life respiratory viral infections alter airway epithelial cell development will allow us to understand the maturation and heterogeneity of asthma and develop tools tailored to prevent disease in specific children. This review will summarize what is understood about the impact of early life respiratory viruses on the developing airway epithelium and define critical gaps in our knowledge.

A Case Report of Central Bronchiectasis in a Poorly Controlled Asthmatic Adolescent With Allergic Bronchopulmonary Aspergillosis and Secondary Spontaneous Pneumothorax.

Allergic bronchopulmonary aspergillosis (ABPA) is a multifaceted immune hypersensitivity reaction occurring in the lungs and bronchi, triggered by exposure and colonization of Aspergillus species, commonly Aspergillus fumigatus (A. fumigatus). It typically affects individuals who are immunocompetent but predisposed, such as those with bronchial asthma and cystic fibrosis. Diagnosis involves various methods including chest radiography, computed tomography, identification of eosinophilia, elevated serum IgE (immunoglobulin E) levels, and immunological tests for Aspergillus antigen. Left undiagnosed and untreated, ABPA can advance to bronchiectasis and/or pulmonary fibrosis, leading to significant morbidity and mortality.

Integrating Pulmonary Health and Maternal Care: Bridging Gaps for Optimal Respiratory Outcomes in Pregnancy and Beyond.

The integration of pulmonary health and maternal care is critical for ensuring optimal respiratory outcomes for both mothers and their infants. Pregnancy induces significant physiological changes in the respiratory system, increasing the risk of pulmonary complications and exacerbating conditions such as asthma. This editorial emphasizes the necessity for collaborative care between pulmonologists and midwives to manage these challenges effectively. By working together, healthcare providers can develop comprehensive care plans that address potential respiratory issues early, monitor and manage chronic conditions, and provide vigilant postpartum care. Enhanced education and interdisciplinary training for both professions are essential for bridging the gaps in care and improving maternal and neonatal health outcomes. This integrated approach is supported by research demonstrating the benefits of coordinated care models in reducing complications and promoting better health outcomes.

Drug-Induced Acute Eosinophilic Pneumonia With Pneumomediastinum: An Unusual Presentation.

A 27-year-old female, with no significant past medical history, presented to the casualty department with a two-week history of progressive dyspnea, cough, and fever. She reported that she had recently started taking a non-conventional alternative medication for her irregular menstrual cycles. Chest radiography demonstrated bilateral alveolar opacities, and computed tomography (CT) of the chest revealed bilateral ground-glass opacities and pneumomediastinum. Laboratory testing showed peripheral blood eosinophilia, and bronchoscopy with bronchoalveolar lavage confirmed an elevated eosinophil count. Based on the clinical presentation, radiographic and laboratory findings, and exclusion of other etiologies, a diagnosis of drug-induced eosinophilic lung disease with pneumomediastinum was made. The alternative non-conventional drug was immediately discontinued and the patient was treated with systemic corticosteroids, leading to a rapid improvement in her symptoms and radiographic abnormalities. A repeat CT of the chest after 15 days revealed significant resolution of the ground-glass opacities and complete resolution of pneumomediastinum. This case highlights the importance of thorough medication history and vigilance for potential adverse effects of non-conventional treatments.