Background: Diagnostic work-up of pulmonary embolism (PE) remains a challenge. Methods: We retrospectively studied all patients referred for computed tomography pulmonary angiography (CTPA) with suspicion of PE during a 12-month period (2018). The diagnostic accuracy of different D-dimer (Dd) cutoff thresholds for ruling out PE was evaluated. Furthermore, the association of Dd and red cell distribution width (RDW) with embolus location, CTPA findings, and patient outcome was recorded. Results: One thousand seventeen (n = 1017) patients were finally analyzed (mean age: 64.6 years (SD = 11.8), males: 549 (54%)). PE incidence was 18.7%. Central and bilateral embolism was present in 44.7% and 59.5%, respectively. Sensitivity and specificity for conventional and age-adjusted Dd cutoff was 98.2%, 7.9%, and 98.2%, 13.1%, respectively. A cutoff threshold (2.1 mg/L) with the best (64.4%) specificity was identified based on Receiver Operating Characteristics analysis. Moreover, a novel proposed Dd cutoff (0.74 mg/L) emerged with increased specificity (20.5%) and equal sensitivity (97%) compared to 0.5 mg/L, characterized by concurrent reduction (17.2%) in the number of performed CTPAs. Consolidation/atelectasis and unilateral pleural effusion were significantly associated with PE (p < 0.05, respectively). Patients with consolidation/atelectasis or intrapulmonary nodule(s)/mass on CTPA exhibited significantly greater median Dd values compared to patients without the aforementioned findings (2.34, (IQR 1.29–4.22) vs. 1.59, (IQR 0.81–2.96), and 2.39, (IQR 1.45–4.45) vs. 1.66, (IQR 0.84–3.12), p < 0.001, respectively). RDW was significantly greater in patients who died during hospitalization (p = 0.012). Conclusions: Age-adjusted Dd increased diagnostic accuracy of Dd testing without significantly decreasing the need for imaging. The proposed Dd value (0.74 mg/L) showed promise towards reducing considerably the need of CTPA. Multiple radiographic findings have been associated with increased Dd values in our study.

Background: In recent years, blood eosinophils have been evaluated as a surrogate biomarker for eosinophilic airway inflammation and as a prognostic indicator of the outcomes of hospitalized COPD subjects. During an exacerbation of COPD, eosinopenia has been proposed as a prognostic marker of adverse outcomes. Objectives: The aim of the present post hoc analysis was to elucidate the effectiveness of blood eosinophils for predicting the need of NIV in subjects with COPD exacerbation. Methods: Consecutive subjects admitted to a hospital for COPD exacerbation were included in the analysis. The eosinophil count from the first complete blood count was used to designate the eosinophil groups. The relationship between the clinical characteristics and blood eosinophil counts, as dichotomized using 150 cells/μL, was evaluated. Results Subjects with blood eosinophil number < 150 k/μL had a more severe disease on admission compared to subjects with ≥150 k/μL, regarding pH 7.400 (7.36, 7.44) vs. 7.42 (7.38, 7.45), p = 0.008, PO₂/FiO₂ levels 238.1 (189.8, 278.6) vs. 276.2 (238.2, 305.6), p < 0.001, CRP (mg/L) levels 7.3 (3.1, 19.9) vs. 3.5 (0.7, 7.8), p < 0.001 and required a longer hospital stay (days) 10.0 (8.0, 14.0) vs. 5.0 (3.0, 7.0) p < 0.001 respectively. The number of blood eosinophils correlated with the levels of CRP upon admission (p < 0.001, r = −0.334), with arterial pH upon admission (p < 0.030, r = 0.121), with PO₂/FiO₂ (p < 0.001, r = −0.248), and with duration of hospital stay (p < 0.001, r = −0.589). In the multinomial logistic regression analysis, blood eosinophil count < 150 k/μL was an independent predictor of the use of NIV during hospital stay. Conclusion: During COPD exacerbation, low blood eosinophil levels upon admission are related to more severe disease and can be used as a predictor of the need of NIV. Further prospective studies are needed to identify the use of blood eosinophil levels as a predictor of unfavorable outcomes.

Background: Lung cancer (LC) is a complex-to-treat disease and remains the leading cause of cancer-related mortality. Methods: Our aim was to investigate the prognostic role of neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and monocyte to lymphocyte ratio (MLR) in patients with LC. In this retrospective study, examining the period between 1 June 2020 and 31 May 2024, we recorded consecutive patients who presented to the Department of Respiratory Medicine, University Hospital of Patras, Patras, Greece, and received a first diagnosis of LC. The primary outcome was mortality risk analysis based on NLR, PLR, and MLR at diagnosis. Secondary outcomes included associations of tumor, node, metastasis (TNM) staging, and smoking with NLR, PLR, and MLR at diagnosis. Results: We identified 353 patients with a first diagnosis of LC. The mean age ± SD at the time of diagnosis was 68.1 ± 9.1 years. Most patients were male (77.9%, n = 275) and current or ex-smokers (58.1%, n = 205, and 39.1%, n = 138, respectively). Histological diagnosis was non-small-cell lung cancer (NSCLC), small-cell lung cancer (SCLC), and not otherwise specified (NOS) in 67.1% (n = 237), 29.8% (n = 105), and 3.1% (n = 11) of patients, respectively. Adenocarcinoma NSCLC was more common (40.2%, n = 142) compared to squamous NSCLC (25.5%, n = 90). In 12.9% of patients, we identified EGFR, KRAS, ALK, or BRAF molecular driver mutations, while PD-L1 expression was positive in 20.7% of patients. The majority of enrolled patients presented with advanced stage IV LC at diagnosis (63.2%, n = 223). Kaplan–Meier curves showed that patients with higher than the median NLR and PLR at diagnosis were associated with significantly higher mortality risk compared to those with lower than the median [HR: 0.58, (95% CI: 0.42 to 0.81) p = 0.0009 and HR: 0.71, (95% CI: 0.53 to 0.95) p = 0.02, respectively], while no differences in mortality risk were observed between patients with higher versus lower than the median MLR [HR: 0.84, (95% CI: 0.63 to 1.12) p = 0.22]. With regard to secondary outcomes, no associations between higher versus lower than the median NLR, PLR, or MLR values and TNM staging [4.0 (95% CI: 4.0–4.0) vs. 4.0 (95% CI: 4.0–4.0), p = 0.95, 4.0 (95% CI: 4.0–4.0) vs. 4.0 (95% CI: 4.0–4.0), p = 0.09, 4.0 (95% CI: 4.0–4.0) vs. 4.0 (95% CI: 4.0–4.0), p = 0.4, respectively], as well as smoking status [70 (95% CI: 60–80) vs. 80 (95% CI: 60–80), p = 0.10, 70 (95% CI: 60–80) vs. 80 (95% CI: 60–80), p = 0.46, 80 (95% CI: 60–80) vs. 70 (95% CI: 60–80), p = 0.96, respectively] were reported. Conclusions: NLR and PLR could serve as reliable and clinician-friendly prognosticators of clinical outcomes in patients with LC. Further validation cohorts are sorely needed to prove this notion.

There is increasing evidence that COVID-19 induces endothelial dysfunction that may precede thrombotic and cardiovascular complications. The aim of this study is to evaluate endothelial function using peripheral arterial tonometry (EndoPAT). The primary endpoint is the hyperemic vascular response index (LnRHI) at two months post-discharge. Secondary endpoints include the LnRHI during hospitalization and at six-month follow-up, the proportion of patients with endothelial dysfunction (LnRHI ≤ 0.51), and the incidence of thrombotic events, cardiovascular complications, and mortality during the follow-up period. The study included 23 COVID-19 patients and 22 COVID-19-negative, matched controls. The patients exhibited a significant reduction in the LnRHI at two months post-discharge compared to the controls (median = 0.55 [IQR: 0.49–0.68] vs. median = 0.70 [IQR: 0.62–0.83]; p = 0.012). The difference in the LnRHI between patients and controls was evident from hospitalization and persisted at two and six months without significant temporal changes. The proportion of COVID-19 patients with endothelial dysfunction (LnRHI ≤ 0.51) was 61% during hospitalization and 55% at six months. There was no significant difference in thrombotic or cardiovascular events, nor in mortality. This study demonstrates that COVID-19 adversely affects endothelial function, as evidenced by a reduction in the hyperemic vascular response index, and endothelial dysfunction may also persist.

Established treatment regimens for the autosomal dominant hyperimmunoglobulin E syndrome, denominated Job syndrome, are lacking. Thus, Job syndrome still exerts a dramatic impact on patients’ quality of life. Our aim was to present safety and effectiveness of a regimen including co-trimoxazole, omalizumab and inhaled tobramycin in Job syndrome. A 26-year-old woman diagnosed with Job syndrome since infancy through sequencing revealing G342D mutation in STAT3 gene was initiated in the above mentioned treatment regimen; she was followed for 6 months, and to date, none recurrent pulmonary or skin infection was noticed. Furthermore, a considerable improvement in skin lesions was observed. A combination of anti-IgE and longitudinal use of inhaled antibiotics seems well-founded in Job syndrome.

Background: Real-world data on currently used biologic agents in patients with severe asthma are lacking. Methods: In this retrospective study, we recorded between 16 May 2020 and 31 December 2024 consecutive patients who presented to our asthma outpatient clinic received a diagnosis of uncontrolled severe asthma and were treated with biologic agents. Outcomes included a comparison of disease phenotypic characteristics, as well as asthma control, lung function, longitudinal use of corticosteroids, and hospitalizations due to exacerbations at baseline and post-biologic treatment at 6-month follow-up. Results: We identified 80 patients with uncontrolled severe asthma treated with biologic agents. The median age (95% CI) at the time of diagnosis was 67.0 (61.0 to 70.0) years. Most patients were female (65.0%, n = 52) and never smokers (51.3%, n = 41). The median value of ACT (95% CI) was 15 (15 to 16) at the time of diagnosis. The mean FEV₁% predicted ±SD at the baseline was 68.9 ± 22.0. The median value of blood eosinophils (95% CI) was 365 (252 to 448) K/μL in the overall population. One-third (36.3%) of patients were hospitalized due to severe asthma exacerbation in the previous year. Longitudinal use of oral corticosteroids was recorded in 11.3% of included patients. Three patients (3.8%) were treated with omalizumab, 23 patients (28.8%) with mepolizumab, 33 patients (41.2%) with benralizumab and 21 patients (26.2%) with tezepelumab. The median value of ACT (95% CI) post-biologic treatment at 6-month follow-up was 20 (20 to 21), p < 0.0001. The mean FEV₁% predicted ±SD at 6-month follow-up was 77.6 ± 25.2, p = 0.12. The median value of blood eosinophils (95% CI) 6 months after initiation of biologic treatment was 100 (40 to 121) K/μL, p < 0.0001. Elimination of hospitalizations due to asthma flares was recorded in 97.5% of patients (p < 0.0001). With regard to the longitudinal use of oral corticosteroids, we noticed that 96.2% of patients achieved discontinuation. No treatment-related adverse events were noticed. Conclusions: The administration of current biologic agents in patients with severe asthma seems to be both effective and safe, sparing the toxicity of oral corticosteroids.