Respiratory dysfunctions have been associated with Parkinson’s disease since the first observations of the disease in 1817. Patients with Parkinson’s disease frequently present respiratory disorders with obstructive ventilatory patterns and restrictive modifications, as well as limitations in respiratory volumes. In addition, respiratory impairments are observed due to the rigidity and kyphosis that Parkinson’s disease patients experience. Subsidiary pulmonary complications can also appear as side effects of medication. Silent aspiration can be the cause of pneumonia in Parkinson’s disease. Pulmonary dysfunction is one of the main factors that leads to the morbidity and mortality of patients with Parkinson’s disease. Here, we performed a narrative review of the literature and reviewed studies on dyspnea, lung volumes, respiratory muscle function, sleep breathing disorders, and subsidiary speech and swallow impairments related to pulmonary dysfunction in patients with Parkinson’s disease.

It is well known that rheumatoid arthritis (RA) patients are at an increased risk of developing non-infectious pulmonary complications, especially interstitial lung disease (ILD); however, the clinician must keep in mind that lung disease could not only be a manifestation of the underlying condition, but also a consequence of using disease-modifying therapies. New-onset ILD or ILD worsening has also been reported as a possible consequence of both conventional disease-modifying antirheumatic drugs (DMARDs) and biologic agents. This study is a narrative review of the current literature regarding the potential risk of developing interstitial lung disease along with the administration of specific drugs used in controlling rheumatoid arthritis. Its purpose is to fill knowledge gaps related to this challenging patient cohort by addressing various aspects of the disease, including prevalence, disease features, treatment strategies, and patient outcomes.

This review brings together the current knowledge regarding the risk factors and the clinical, radiologic, and histological features of both post-COVID-19 pulmonary fibrosis (PCPF) and idiopathic pulmonary fibrosis (IPF), describing the similarities and the disparities between these two diseases, using numerous databases to identify relevant articles published in English through October 2022. This review would help clinicians, pathologists, and researchers make an accurate diagnosis, which can help identify the group of patients selected for anti-fibrotic therapies and future therapeutic perspectives.

Inflammatory bowel diseases (IBDs) encompass Crohn’s disease and ulcerative colitis. They represent idiopathic and chronic inflammatory conditions. Mucosal immune dysfunction and compromised gastrointestinal barrier integrity are implicated in the pathophysiological mechanisms of inflammatory bowel diseases. Recent studies have identified endothelial dysfunction as a pivotal mediator in IBD pathogenesis. Through multiple cellular and molecular interactions, endothelial dysfunction orchestrates inflammatory responses. Objectives: This systematic review examines contemporary evidence (2019–2025), emphasising the role of endothelial dysfunction in intestinal inflammation mechanisms, focusing on vascular-epithelial crosstalk, molecular signalling pathways, and therapeutic implications. Methods and results: A comprehensive literature search was conducted using PubMed, Google Scholar, Europe PMC and DOAJ databases, focusing on peer-reviewed articles published between 2019 and 2025. Following the database search and screening process, a total of 53 studies met the eligible criteria and were included in the final analysis. Keywords included “endothelial dysfunction,” “inflammatory bowel disease,” “gut-vascular barrier,” “nitric oxide,” and “intestinal inflammation.” Contemporary research demonstrates that endothelial dysfunction in IBD manifests through decreased nitric oxide bioavailability, enhanced oxidative stress, aberrant cytokine networks, pathological angiogenesis, and compromised gut-vascular barrier integrity. The emerging concept of dual barrier dysfunction highlights the interdependent relationship between epithelial and endothelial barriers in maintaining intestinal homeostasis. Conclusions: Offering novel therapeutic targets for precision medicine approaches, endothelial dysfunction represents a central driver in the pathophysiological mechanism in IBD. Understanding vascular-epithelial interactions provides fundamental insights for developing targeted interventions to restore intestinal barrier function and resolve chronic inflammation.

Background: This is the first study that aims to define smoking, with obstructive sleep apnea (OSA), as a phenotype (SOSA). Moreover, we wanted to demonstrate the deleterious effects of the continuation of smoking on OSA. Methods: The cross-sectional study highlighted four dimensions of SOSA: the demographic and anthropometric features, the symptoms, the comorbidities, and the sleep study parameters. This study compared these characteristics between current smokers (CS), those who have never smoked (NS), and ex-smokers (ES) with OSA. Results: More men (83.95% in CS, versus 66.67% in NS) and an earlier onset of OSA (average age = 50.05 in CS, versus 52.26 in NS, p = 0.04) were recorded among CS. The distinguishing symptom of CS was daytime sleepiness, with an Epworth score that was significantly higher than in NS. Chronic obstructive pulmonary disease (COPD) was significantly more prevalent in CS (38.27%) than in NS (1.51%) (p < 0.001). The severity of OSA, consisting of a higher apnea-hypopnea index, a higher oxygen desaturation index, and a longer time spent below 90% oxygen saturation during sleep was significantly influenced by smoking. Conclusions: The SOSA phenotype includes younger male patients with a higher waist circumference, suggesting central obesity. They have a higher prevalence of COPD and a greater severity of OSA, in correlation with the number of pack-years of smoking.

Background and Aims: Gastroesophageal reflux disease (GERD) is a common condition present in daily practice with a wide range of clinical phenotypes. In this line, respiratory conditions may be associated with GERD. The Romanian Societies of Gastroenterology and Neurogastroenterology, in association with the Romanian Society of Pneumology, aimed to create a guideline regarding the epidemiology, diagnosis and treatment of respiratory conditions associated with GERD.Methods: Delphi methodology was used and eleven common working groups of experts were created. The experts reviewed the literature according to GRADE criteria and formulated 34 statements and recommendations. Consensus (>80% agreement) was reached for some of the statements after all participants voted.Results: All the statements and the literature review are presented in the paper, together with their correspondent grade of evidence and the voting results. Based on >80% voting agreement, a number of 22 recommendations were postulated regarding the diagnosis and treatment of GERD-induced respiratory symptoms. The experts considered that GERD may cause bronchial asthma and chronic cough in an important number of patients through micro-aspiration and vagal-mediated tracheobronchial reflex. GERD should be suspected in patients with asthma with suboptimal controlled or after exclusion of other causes, also in nocturnal refractory cough which needs gastroenterological investigations to confirm the diagnosis. Therapeutic test with double dose proton pump inhibitors (PPI) for 3 months is also useful. GERD induced respiratory conditions are difficult to treat; however,proton pump inhibitors and laparoscopic Nissen fundoplication are endorsed for therapy.Conclusions: This guideline could be useful for the multidisciplinary management of GERD with respiratory symptoms in current practice.