Postnasal drip (PND) is a common symptom associated with upper respiratory tract disorders. It occurs without other symptoms or combined with chronic rhinosinusitis. However, the pathophysiology of PND is debated to this day, and an objective definition of PND has not been established. Therefore, we aimed to elucidate whether the viscosity and volume of nasal secretions as well as the mucociliary clearance and sensitivity of the nasopharynx, or atopy could play a role in the pathophysiology of PND.

COPD has a substantial burden seen in both patient quality of life and health-care costs. One method of minimizing this burden is the implementation of clinical pathways (CPWs). CPWs bring the best available evidence to a range of health-care professionals by adapting guidelines to a local context and detailing essential steps in care.

COPD increases susceptibility to sleep disturbances, which may in turn predispose to increased respiratory symptoms. The objective of this study was to evaluate, in a population-based sample, the relationship between subjective sleep quality and risk of COPD exacerbations.

Common variable immunodeficiency disorders refer to a relatively common primary immune deficiency group of diseases that present with infectious and inflammatory complications secondary to defects in antibody production and sometimes in cellular immunity. The disorder often presents in middle age or later with recurrent sinopulmonary infections, bronchiectasis, or a plethora of noninfectious complications such as autoimmune disorders, granulomatous interstitial lung disease, GI diseases, malignancies (including lymphoma), and multisystem granulomatous disease resembling sarcoidosis. Infusion of immunoglobulin by IV or subcutaneous is the mainstay of therapy. Management of complications is often difficult as immune suppression may be necessary in these conditions and entails the use of medications and biologicals which may further increase the risk for infections. Specifically, bronchiectasis, granulomatous lymphocytic interstitial lung disease, repeated sinopulmonary infections, and malignancies are sequelae of antibody deficiency that may present to the pulmonologist. This review will provide an updated understanding of the molecular aspects, differential diagnosis, presentations, and the management of common variable immunodeficiency disorders.

Dyspnea is prevalent among hospitalized patients but little is known about the experience of dyspnea among inpatients. We sought to characterize the multiple sensations and associated emotions of dyspnea in patients admitted with dyspnea to a tertiary care hospital.

The relationship between OSA and glucose metabolism remains controversial. This retrospective study investigated the relationship between OSA and incident type 2 diabetes (T2D) in a clinic cohort of Chinese adults in Hong Kong, and the effect of long-term CPAP treatment.

Evidence regarding the association between sarcopenia (skeletal muscle depletion) and outcomes in patients with lung cancer varies across studies. We aimed to systematically review the prognostic value of sarcopenia in lung cancer.

Abundant epidemiologic evidence supports an association between idiopathic pulmonary fibrosis (IPF) and lung cancer. Lung tumors in patients with IPF develop preferentially in the periphery immediately adjacent to fibrotic areas, with different histologic distribution and immunohistochemical features compared with non-IPF-associated lung tumors. In this context, evidence indicates that IPF and lung cancer share many pathogenic similarities including genetic and epigenetic markers. It has been suggested that specific germline mutations predispose toward both IPF and lung cancer, leading to imbalance between oncogenes and tumor suppressor genes and ultimately carcinogenesis within fibrotic lungs. Aberrant epigenetic regulation due to methylation, histone modifications, and mainly deregulation of common noncoding RNAs represents a possible pathogenic link between the two disease paradigms. Genetic and epigenetic alterations lead to abnormal activation of common transduction pathways, including Wnt/β-catenin and phosphoinositide 3-kinase/protein kinase B, mediating metaplasia and hyperproliferation in alveolar type II epithelial cells. Cellular transformations in the mesenchymal phenotype represent a common link between lung fibrosis and carcinogenesis. In this review we summarize current data on common cellular and molecular pathogenic mechanisms between IPF and lung cancer and highlight promising therapeutic targets for this disease combination.

Exercise stress testing of the pulmonary circulation may uncover decreased pulmonary vascular (PV) distensibility as a cause of impaired aerobic exercise capacity and right ventricular (RV)-pulmonary arterial (PA) uncoupling. As such, it may help in the differential diagnosis of unexplained dyspnea, including pulmonary hypertension (PH) and/or heart failure with preserved ejection fraction (HFpEF). We investigated rest and exercise invasive pulmonary hemodynamics, ventilation, and gas exchange in patients with unexplained dyspnea, including 44 patients with HFpEF (of whom 20 had a normal pulmonary vascular resistance [PVR] during exercise [ie, passive HFpEF] and 24 had a higher than normal exercise PVR), 22 patients with exercise PH, 19 patients with pulmonary arterial hypertension (PAH), and 24 age- and sex-matched normal control subjects.

Whether four direct oral anticoagulants (DOACs) are superior to warfarin in Asian patients with nonvalvular atrial fibrillation (NVAF) remains unclear.

Historically, COPD has been considered to affect mostly older men with a history of smoking; however, in recent times, its prevalence and mortality rates have steadily increased among women.

Right ventricular (RV) dysfunction is associated with shortened life expectancy in heart failure with preserved ejection fraction (HFpEF). The contribution of pulmonary vascular dysfunction to RV dysfunction in HFpEF is not well understood.

Results of previous studies examining associations between cigarette smoking and sleep-disordered breathing (SDB) are inconsistent. We therefore investigated this association in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL).

Moderate to severe depressive symptoms occur in up to one-third of patients at 1 year following ICU discharge, negatively affecting patient outcomes. This study evaluated patient and caregiver factors associated with the development of these symptoms.

Burnout syndrome is an increasingly common phenomenon that threatens our critical care workforce and the well-being of its members. Burnout syndrome can be conceived of as a workforce manifestation of chronic workload and workforce capacity imbalance. This study explores the role of workload management tools that can address workload as a complement to the resilience-based countermeasures that seek to increase worker capacity. We were able to use step-wise increments in the volume of documentation-related tasks that occurred at the time of electronic health record (EHR) implementation to investigate the relation of workload and burnout. Specialty-specific increases in the prevalence of self-reported burnout during the era of EHR adoption were compared with increases of the length of documentation created by the corresponding specialists observed prior to and following EHR implementation; a robust direct association was reported. To connect ICU workload to burnout, the number of tasks performed was extracted from the EHR, and we measured the average time that our ICU team members required to complete these tasks. Our ICU workforce efficiency was calculated as the ratio of mandatory task time to scheduled time. Comparing this ratio vs a well-established industrial standard for equipment efficiency made us realize that our average workload seemed excessive and placed our staff at risk of burnout syndrome. It is difficult to conceive that our resilience-based countermeasures to prevent and treat burnout would not be more effective when combined with measures that reduce the time our staff members spend on mandatory ICU tasks.

Medical malpractice data can be leveraged to understand specialty-specific risk.

Group 2 innate lymphoid cells (ILC2s) are increasingly recognized as a key controller of type 2 inflammation, and are well known to be highly elevated in human airway type 2 inflammatory diseases including allergic rhinitis, chronic rhinosinusitis with nasal polyps, and asthma. ILC2-mediated production of type 2 cytokines initiates and amplifies airway inflammation via activation of eosinophils, B cells, mast cells, macrophages, fibroblasts, and epithelial cells in these diseases. ILC2s require at least three major signals to fully activate and robustly produce type 2 cytokines. IL-1 family cytokines (IL-1β, IL-18, IL-33), IL-25, and TNF superfamilies (TNF, TL1A, GITR-L, RANK-L) activate the NF-κB and AP-1 pathways that initiate production of IL-5 and IL-13. Lipid mediators (LTC4, LTD4, PGD2) and neuropeptide NMU promote production of IL-4 through the NFAT pathway. IL-2 and IL-7 family cytokines (IL-2, IL-7, IL-9, TSLP) activate the STAT5 pathway that induces survival of ILC2s and enhances cytokine production. The activation of STAT5 is necessary to potently induce cytokine- and lipid mediator-mediated production of type 2 cytokines. Inhibitory pathways for ILC2s have also become clearer. Type I and II interferons and IL-27 inhibit ILC2 functions through the activation of STAT1. Suppression mediated via β2-adrenergic receptor agonists, PGE2, and PGI2 occurs through cAMP and PKA. Glucocorticoid, testosterone, IL-10, and TGF-β are also able to inhibit ILC2-mediated production of type 2 cytokines. Blockage of ILC2 activators, activation of inhibitory pathways of ILC2s, and suppression of ILC2-mediated pathways including type 2 cytokines (IL-5, IL-13, IL-4Ra) may become therapeutic strategies for airway type 2 inflammatory diseases.

To guide rational antibiotic selection in community-onset pneumonia, we previously derived and validated a novel prediction tool, the Drug-Resistance in Pneumonia (DRIP) score. In 2015, the DRIP score was integrated into an existing electronic pneumonia clinical decision support tool (ePNa).