Background: Obstructive sleep apnea (OSA) is increasingly recognized as a chronic condition associated with systemic low-grade inflammation. Elevated levels of inflammatory markers such as C-reactive protein (CRP), fibrinogen, TNF-α, and IL-6 have been observed in OSA patients, independent of obesity. Tobacco use, a known pro-inflammatory factor, may further exacerbate this burden. This study aimed to evaluate whether smoking influences inflammatory markers and OSA severity in newly diagnosed patients. Methods: We conducted a retrospective, observational study on individuals newly diagnosed with OSA between 1 January 2024 and 31 December 2024 at the Clinical Hospital of Pulmonary Diseases Iași. All participants underwent overnight respiratory polygraphy using the SleepDoc Porti 9 system (Löwenstein Medical), with OSA severity classified according to the American Academy of Sleep Medicine (AASM) criteria. Inflammatory status was assessed using CRP and the erythrocyte sedimentation rate (ESR). Smokers were defined as individuals who had smoked within the past year; non-smokers had a lifetime history of fewer than 50 cigarettes. Statistical analysis was performed using IBM SPSS Statistics. Results: Smokers (n = 55) shoation Index (ODI) values, compared to non-smokers (n = 49): AHI 45.29 ± 20.94 vs. 38.40 ± 19.84 events/hour, ODI 45.69 ± 21.05 vs. 38.44 ± 19.40 events/hour (p < 0.05 for both). Mean CRP levels were approximately 3.5 times higher in smokers (10.32 ± 11.69 mg/dL) than in non-smokers (2.97 ± 2.45 mg/dL), indicating a significantly elevated inflammatory burden. Conclusions: The inflammatory burden and clinical severity of OSA may be influenced by smoking. Routine inflammatory marker screening, particularly CRP, may improve risk stratification and treatment planning in OSA patients, especially those who smoke or are obese. Routine assessment of CRP and other inflammatory markers may improve risk stratification and guide personalized treatment strategies, particularly in smokers and obese patients with OSA.

Background: Combined Pulmonary Fibrosis and Emphysema (CPFE) is a distinct syndrome characterized by upper-lobe emphysema and lower-lobe fibrosis, predominantly in older male smokers. Despite often preserved spirometric volumes, patients exhibit severely reduced diffusing capacity and high susceptibility to complications, including pulmonary hypertension (PH), acute exacerbations, and lung cancer, contributing to poor prognosis. Purpose: This review aims to synthesize current evidence on CPFE, focusing on clinical phenotype, functional impairment, differential diagnosis, complications, and emerging management strategies, highlighting distinctions from idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Methods: A narrative review of observational cohorts, retrospective series, and clinical studies examining CPFE patients was performed. Data on demographics, smoking history, symptomatology, pulmonary function, radiology, comorbidities, complications, and treatment approaches were extracted and integrated. Results: CPFE affects mainly males aged 65–70, with >90% reporting > 40 pack–years smoking history. Dyspnea is the cardinal symptom (>95%), often disproportionate to preserved FVC and TLC, accompanied by chronic cough in 30–70%. Exercise-induced desaturation is frequent, correlating with PH, observed in 47–90% of patients. Pulmonary function tests reveal preserved volumes, normal or near-normal FEV1/FVC, and severely reduced DLCO (35–45%), distinguishing CPFE from COPD and IPF. HRCT confirms the combined emphysematous and fibrotic pattern, critical for differential diagnosis. Acute exacerbations occur in 20–28% of cases, lung cancer in 22–46% (mostly squamous cell), and long-term oxygen therapy is required in >70%. Five-year survival is 35–55%, lower than emphysema alone and comparable or worse than IPF. Management focuses on smoking cessation, antifibrotics, oxygen therapy, and complication-specific treatments, and selected patients may undergo lung transplantation. Conclusions: CPFE is a clinically and functionally unique entity with a high burden of pulmonary and systemic complications. Accurate recognition using HRCT and DLCO, along with early intervention and tailored management, is essential to improve patient outcomes and guide prognostic stratification.

Background: Obstructive sleep apnea (OSA) impacts daytime alertness, mood, cognition, and quality of life (QoL). Initial alterations in these patient-reported outcomes (PROs) following CPAP therapy, along with their association with adherence and residual respiratory events, are only partially understood. Materials and methods: We conducted a retrospective, observational study from January 2024 to May 2025 involving adult patients with OSA. Standardized assessments were performed at baseline and at six months following the initiation of CPAP: Epworth Sleepiness Scale (ESS), WHOQOL-BREF, MoCA, DASS-21, GAD-7, and PHQ-9. The primary endpoint was the change in Patient-Reported Outcomes (PROs) and cognitive performance. The second was to identify associations between these improvements and the degree of adherence to CPAP therapy and residual AHI. Results: Seventy-two patients (median age, 57; 65.3% male) with moderate to severe OSA had a baseline median AHI of 34.5/h, ODI of 35.5/h, and a mean nocturnal SpO₂ of 92.4%. The initial burden was high: median ESS was 14, indicating excessive daytime sleepiness (EDS), present in 68.9%; median MoCA was 24, with 98.6% scoring below 26; median PHQ-9 was 7; median GAD-7 was 5; and 56.8% and 47.9% scored below 50 in physical and psychological domains of WHOQOL-BREF, respectively. After 6 months, group averages showed improvement: ESS decreased to 8.6 ± 3.7, with a 27.0% residual EDS; PHQ-9 was 7.1 ± 4.5; GAD-7 was 6.2 ± 4.1; and MoCA increased to 25.3 ± 2.7, although 48.6% still showed impairment. WHOQOL-BREF scores improved across domains: physical 58.7 ± 14.2, psychological 61.5 ± 13.6, social 63.2 ± 15.4, and environmental 59.8 ± 14.7, with fewer scores below 50 (physical 23.0%, psychological 18.9%). CPAP adherence was high, with a mean of 87.7% and a median of 95%, predicting a greater ESS reduction (p = 0.027) and showing a trend toward improvement in PHQ-9 scores (ρ = 0.218; p = 0.066). Residual respiratory indices at 6 months (AHI, ODI, SpO₂) did not correlate with PRO or cognitive scores at the same time point (all p > 0.16), nor with their change scores. Conclusions: Over the course of six months, CPAP therapy led to notable improvements in sleepiness, mood, anxiety, cognition, and overall quality of life. Nonetheless, many patients continued to face residual problems, mainly excessive daytime sleepiness (EDS) and cognitive challenges. The positive effects were more closely associated with how well patients adhered to the treatment than with remaining levels of residual AHI or ODI.

Introduction: COPD-OSA overlap syndrome (OVS) is defined by the coexistence of chronic obstructive pulmonary disease and obstructive sleep apnea syndrome in the same patient; it affects 28.3% of patients evaluated for either condition and is associated with significantly higher mortality compared to either pathology in isolation. Current therapeutic approaches, involving PAP therapy and bronchodilation, treat this syndrome as a homogeneous entity and ignore the biological heterogeneity of this patient population. Objectives: This review proposes a systematic framework for the endotypic classification of biological interactions between COPD and OSA, integrating current literature on the pathophysiological mechanisms underlying the OVS, clinically accessible biomarkers, and emerging therapies. Methods: A narrative review based on available literature, focusing on studies published between 2010 and 2026 identified via searches in PubMed, PMC, and Dove Medical Press using the terms: COPD-OSA overlap syndrome, endotype, precision medicine, phenotype, biomarker, dupilumab, and incretin-based therapies. Results: Four clinical phenotypes (obese-metabolic, emphysematous, bronchitic-hypoxemic, and hypercapnic) and three molecular endotypes (Th2/eosinophilic, neutrophilic/oxidative, and metabolic-adipokine) are proposed, each with distinct pathophysiological mechanisms and specific therapeutic implications. The interaction between the two conditions generates a unique, pronounced hypoxemic profile. We propose the “double-hit hypoxemia” model as a conceptual framework characterized by amplified systemic inflammation and increased cardiovascular risk compared to either pathology in isolation. This proposed model has not yet been prospectively validated. Dupilumab (approved for an inflammatory phenotype in COPD patients characterized by eosinophil counts ≥ 300 cells/μL) represents a promising option, though currently unsupported in the OVS population, that could nonetheless be relevant to the Th2/eosinophilic endotype of this syndrome and tirzepatide (which reduced the AHI by up to 23.8 events/hour versus placebo in the SURMOUNT-OSA trial, conducted in patients with obesity and moderate-to-severe OSA, rather than in patients with confirmed OVS) could represent a promising therapy for the metabolic-adipokine endotype of obese patients with OVS. A minimal biomarker panel, comprising blood eosinophils, FeNO, daytime PaCO₂, BMI, and T90, allows for a practical approach to identifying the dominant endotype. Conclusions: Endotyping of OVS may provide a framework for moving beyond a uniform therapeutic approach toward more individualized management based on the dominant underlying biological mechanism. Randomized clinical trials focusing on endotypic stratification and OVS cohorts remain research priorities.

A thoracic finding in a patient with hepatocellular carcinoma (HCC) may represent metastatic disease, vascular extension, treatment-related injury, or a complication of cirrhosis, and each carries different implications for staging and care. The mechanism behind the finding therefore matters as much as the finding itself. We searched the PubMed/MEDLINE database for articles published up to August 2026 and screened the reference lists of retrieved articles for additional relevant publications. The narrative review is organised into four domains: direct oncological involvement, vascular dissemination, treatment-related injury, and cirrhosis-associated mimics. Within each domain, computed tomography (CT) provides most of the chest assessment, while magnetic resonance imaging, echocardiography, and angiography address more specific anatomical or diagnostic questions. We next discuss common patterns of pulmonary metastasis alongside benign nodules common in transplant candidates, and the biological and small-lesion limitations of functional imaging. Thoracic findings gain meaning in the context of hepatic disease, vascular anatomy, and treatment history. Enhancement and alpha-fetoprotein have never been validated as noninvasive rule-out tests for pulmonary metastasis, so the choice between sampling and surveillance rests on multidisciplinary judgement of the costs of uncertainty, procedural feasibility, and evidence strength.

Obstructive sleep apnea (OSA) is a common yet underdiagnosed condition strongly linked to the cardiovascular-kidney-metabolic (CKM) syndrome continuum, a systemic disorder characterized by interconnected metabolic, renal, and cardiovascular abnormalities. Despite overlapping risk factors, particularly obesity, current CKM staging does not formally include OSA as a potential modifier of CKM progression from early stages. Here, we conducted a narrative review revealing that OSA shares demographic and biological substrates with CKM syndrome, independently associates with cardiovascular, metabolic, and renal dysfunction through multiple shared mechanisms, and responds to intervention, including lifestyle changes, positive airway pressure, and pharmacotherapy. Integrating systematic OSA screening and management into CKM assessment, especially at early stages, may enhance risk stratification and enable personalized preventive care. This approach shows potential in mitigating disease progression and improving quality of life across the CKM spectrum. These findings support recognizing OSA as an important factor in CKM progression and highlight the potential benefits of its early identification to mitigate disease burden and improve patient outcomes.