
Malignant pleural effusion (MPE) and malignant pleural disease (MPD) are common complications of cancer. Although they may significantly affect the quality of life, treatment options remain limited. Official guidelines recommend effusion drainage and pleurodesis, and, while they may achieve symptomatic relief, their impact on disease progression is limited. Intrapleural therapy has been studied for several decades due to its theoretical (and proven) superior local drug retention, maximising drug exposure. Recent works on intrapleural administration include exploring novel therapeutic agents and administration methods, such as hyperthermic intrathoracic chemotherapy (HITHOC) and pressurised intrathoracic chemotherapy (PITAC). These therapies directly modulate the tumour environments. Promising intrapleural candidates include targeted and immunotherapies such as CAR (chimeric antigen receptor)-T cells, PD-1 (programmed death protein 1) inhibitors, and IL-6 (interleukin-6) inhibitors. However, the level of evidence remains mixed, requiring further studies and quantitative synthesis.
Tobacco cigarette smoking is a leading preventable cause of morbidity and mortality worldwide. Pharmacological treatment can substantially increase cessation rates among daily smokers who wish to quit. Cytisine is a long-established smoking-cessation medication that has recently attracted renewed interest. We conducted a narrative review of cytisine, focusing on its pharmacological properties, clinical efficacy, safety profile, and role relative to other recommended smoking-cessation therapies. The literature search was updated to June 2026. Cytisine (cytisinicline) is a plant-derived partial agonist of nicotinic acetylcholine receptors that reduces nicotine withdrawal symptoms and attenuates the rewarding effects of cigarette smoking. It has good oral bioavailability, undergoes minimal hepatic metabolism, and is mainly eliminated unchanged by the kidneys. Randomized trials show that cytisine has greater smoking-cessation efficacy than placebo. Evidence also suggests greater efficacy than single-form nicotine replacement therapy (NRT), whereas comparisons with varenicline indicate broadly comparable efficacy but remain limited by heterogeneity and imprecision. Cytisine is generally well tolerated and has been associated with fewer reported adverse events than varenicline in direct comparative trials. Cytisine is an effective and generally well-tolerated pharmacological treatment for smoking cessation. The World Health Organization recommends cytisine, alongside varenicline, NRT, and bupropion, as an effective tobacco-cessation treatment, and cytisine was added to the WHO Model List of Essential Medicines in 2025. Further studies should define the optimal dose and treatment duration and clarify its role in populations for whom evidence remains limited. Differences in study design, behavioral support, outcome assessment, and treatment duration should be considered when comparing cytisine with other smoking-cessation therapies.
Long COVID is a heterogeneous post-infectious condition following acute severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection. Ongoing uncertainty around its definition, burden, diagnosis and management complicates clinical recognition and care in Southeast Asia. A modified Delphi consensus study was conducted with twelve experts from six Southeast Asian countries to develop regional guidance on long COVID. Consensus was predefined as ≥ 80
Inhaled maintenance therapy (long-acting β2-agonists [LABA], long-acting muscarinic antagonists [LAMA], and inhaled corticosteroids [ICS], used alone or in combination) is the cornerstone of chronic obstructive pulmonary disease (COPD) management. This study described contemporary real-world COPD treatment patterns in the USA. Retrospective data for patients aged ≥ 40 years with COPD were obtained from Komodo Research Data (01/01/2016–06/30/2024). The index date was January 1, 2022 for patients with a prior COPD diagnosis (i.e., prevalent patients) or the first observed COPD diagnosis for incident patients. Continuous health insurance enrollment was required for ≥ 12 months pre-index (i.e., baseline) and ≥ 6 months post-index, unless death occurred (i.e., follow-up). A claims-based algorithm identified lines of therapy for inhaled maintenance treatments. Treatment patterns were described during follow-up, overall and among subgroups of interest, including at-risk patients (i.e., ≥ 1 severe or ≥ 2 moderate exacerbations during baseline). A total of 1,421,278 patients with COPD were identified (incident 153,390; prevalent 1,267,888). Over a mean follow-up of 16.6 and 24.7 months, 33.0
Pulmonary fibrosis comprises a heterogeneous group of interstitial lung diseases characterized by progressive extracellular matrix deposition and structural remodeling. Although currently available antifibrotic therapies can slow disease progression, additional biological pathways remain under investigation. Incretin-based therapies, including glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors, have attracted increasing interest because their biological effects extend beyond glucose regulation and may involve pathways relevant to pulmonary fibrogenesis. Preclinical studies suggest that incretin-related pathways may modulate transforming growth factor-β signaling, fibroblast activation, extracellular matrix deposition, mesenchymal transition, inflammation, oxidative stress, and metabolic mechanisms involved in fibrosis. However, these findings remain predominantly experimental, and evidence of antifibrotic efficacy in patients with fibrotic interstitial lung disease is currently lacking. A complementary aspect is represented by the profound effects of incretin-based therapies on body weight and composition. This is particularly relevant in pulmonary fibrosis, where excess adiposity may contribute to metabolic and functional burden, whereas low body mass index, unintentional weight loss, and skeletal muscle depletion are associated with adverse outcomes. Incretin-induced weight loss predominantly reflects reduction in adipose tissue, but is accompanied by variable reductions in lean or fat-free mass, whose implications for skeletal muscle and functional reserve remain incompletely defined. This narrative review integrates current preclinical evidence on the potential antifibrotic effects of incretin-related pathways with clinical evidence on body weight, adiposity, and skeletal muscle in pulmonary fibrosis. Future clinical and translational studies are required to determine whether the potential pulmonary and metabolic effects of incretin-based therapies translate into meaningful clinical benefits in fibrotic interstitial lung disease.