Background and Objective: Ultrasound has become more popular and useful over the last few years in improving healthcare. While handheld devices offer portability and convenience, their diagnostic accuracy and clinical utility require further scrutiny. This study attempted to evaluate the non-inferiority of handheld portable ultrasound devices compared to standard ultrasound devices for common lung pathologies. Materials and Methods: Videos of various common lung pathologies from 20 patients were recorded by a single operator using both portable handheld and standard ultrasound devices in a single setting. These videos were then assessed via online questionnaires by clinicians of various levels of experience from respiratory and non-respiratory departments. A Likert scale was used, ranging from strongly disagree to strongly agree (ranging from 1 to 5) in terms of overall image quality, clear anatomical visualization, similar clinical interpretations/decisions, and the perception of non-inferiority. Median values with interquartile ranges were reported; a rating of 3 or above was defined as indicating non-inferiority. Results: Thirty participants completed the questionnaires, of which the majority were at trainee level (n = 20, 73%) and from a respiratory department (n = 20, 67%). The participants had mixed levels of experience in terms of the years and frequency of use of the ultrasound. Overall median ratings were 4.0 for overall image quality, clear anatomical visualization, and similar clinical interpretations/decisions, with slight variations in interquartile ranges. No significant differences were observed between subgroups. The portable ultrasound device was rated similarly for the overall perception of non-inferiority, but clinicians from respiratory departments and clinicians with less experience showed statistically significant variability in their assessments. Conclusions: The portable handheld device demonstrated potential as a reliable alternative to standard models in standard clinical settings without compromising clinical decision. Further evaluation is needed that includes a direct comparison of various types of handheld ultrasound devices, across different operators’ levels of experience, to further solidify their suitability in patient care.

Severe asthma imposes a significant burden on public health worldwide, mainly due to its morbidity and high cost. The management of severe asthma has dramatically changed in the past few years with the introduction of biologics. Zero exacerbations, zero systemic corticosteroids, better asthma control, and better lung function are the outcomes that the era of biologics has made attainable in a large proportion of severe asthmatics, ending up in a better quality of life. Still, even today, the changes at the tissue level that reflect these outcomes are not that clear. As a chronic inflammatory disease, asthma often involves airway remodeling in its severe forms; endobronchial biopsies may provide critical insights into these tissue-level changes before and after biologic treatment. However, bronchoscopy is an invasive tool for severe asthma, thus limiting its use in daily clinical practice. This review focuses on summarizing the changes that biologics exert in biopsies obtained from severe asthmatics under biological treatment, providing an opportunity to shed light on what really happens there where it is not easy to see, and especially on what does not happen in patients under biologics who fail to respond as expected. Moreover, the armamentarium of biomarkers used for making the proper choice in patients eligible for more than one biologic needs to be enriched. Biopsy-related markers could be an ideal adjunct to the current ones—blood eosinophils, FeNO, and IgE—to assist the clinician to choose the right biologic for the right patient with severe asthma to achieve disease remission.

Central airway obstruction is of major clinical importance since it is a major cause of morbidity and mortality and is usually clinically diagnosed late. Pulmonary function tests, with the recent incorporation of oscillometry, can have a crucial role in earlier diagnosis. In this review, we summarize all recent advances in that view, including the crucial role of oscillometry.

EBUS-TBNA is the most common interventional pulmonology procedure performed globally and remains the cornerstone of the diagnosis and staging not only of lung cancer but also for other neoplastic, inflammatory, and infective pathologies of the mediastinum. Infective complications of EBUS-TBNA are underreported in the literature, but the constantly rising incidence of lung cancer is leading to an increasing number of EBUS-TBNA procedures and, therefore, to a significant number of infective complications, even 4 weeks following the procedure. In this review we attempt to summarize the risk factors related to these infective complications, along with useful biomarkers that can be used to identify patients that might develop infective complications, to facilitate the prediction or even prompt treatment of these.

Small cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy defined by a number of genetic and molecular features, including near-universal TP53 and RB1 inactivation, MYC amplifications, Notch pathway disruption, and hyperactivated PI3K/AKT/mTOR signaling. The subtypes of SCLC, SCLC-A/N/P/I, are primarily based on four transcription regulators (ASCL1, NeuroD1, YAP1, POU). This review provides a concise overview of the molecular landscape of SCLC and then focuses on the subset displaying epidermal growth factor receptor (EGFR) alterations. EGFR-positive SCLC presents either as rare primary (de novo) disease (2.6–19.3%) or as transformed SCLC originating from EGFR-mutant non-small cell lung cancer (NSCLC) in 3–14% of cases following EGFR tyrosine kinase inhibitor (TKI) therapy. In both cases, the tumors harbor EGFR mutations with the most frequent one being exon 19 deletions. A number of pathways have been identified regarding the lineage transformation with the co-occurring TP53 and RB1 loss predominating, while a number of other molecular mechanisms have been explored, including activation of epithelial-to-mesenchymal transition factors (ZEB1, SLUG), MDM4 or BCL2L2/NFKBIA co-amplifications, and newly postulated genetic variants such as FBN1 and PALLD, alongside emergent surface expression of DLL3, B7-H3, and PTK7. Once SCLC transformation occurs, tumors tend to drop EGFR dependence and display profound resistance to EGFR-TKIs, necessitating a shift to standard platinum–etoposide chemotherapy, with or without immunotherapy. The value of EGFR-TKIs has been explored, as an add-on treatment, in several cases and its efficacy has not so far provided satisfactory outcomes. An update of the literature, within this particular field, is being provided along with the value for routine serial re-biopsy (tissue or liquid) upon disease progression, especially when EGFR-TKIs have been used. Early identification of neuroendocrine transformation can prevent futile EGFR-TKI monotherapy, capture mixed histologies, and recognize potential re-transformation back to adenocarcinoma.

Zinc may mitigate platinum-induced toxicity through antioxidant, anti-inflammatory and anti-apoptotic effects. We systematically reviewed preclinical in vivo evidence on zinc-based interventions, focusing on organ protection, mechanisms and antitumour efficacy. PubMed, Scopus, Web of Science and supplementary sources were searched for studies in rats and mice. Risk of bias was assessed using SYRCLE, and the findings were synthesised narratively. Database searches identified 1552 records; 25 studies were included following database and supplementary screening. The risk of bias was frequently unclear for sequence generation, allocation concealment and blinding. Most studies investigated cisplatin; fewer evaluated carboplatin, oxaliplatin or combination chemotherapy. Zinc interventions included salts, dietary supplementation, organic complexes and nanoformulations, predominantly administered before platinum exposure. Protective findings were reported across renal, reproductive, nervous, hepatic, haematopoietic and cardiovascular systems. Proposed mechanisms included metallothionein induction, enhanced antioxidant defences and modulation of inflammation and apoptosis. Heterogeneity precluded conclusions about formulation superiority. Limited tumour-bearing evidence indicated that zinc-induced metallothionein may reduce cisplatin activity, whereas bismuth zinc citrate preserved tumour control within the tested model. Methodological weaknesses, heterogeneity and scarce tumour-bearing evidence limit confidence in efficacy and oncological safety. These findings support further preclinical investigation rather than clinical implementation.