Search

Abstract This study examines the radiological and clinical evolution of a case involving mixed idiopathic pulmonary fibrosis and chronic hypersensitivity pneumonitis, utilizing conventional CT imaging and artificial intelligence tool. Through a series of exams and clinical assessments, the patient was followed for over 3 years, highlighting the challenge in differentiating these interstitial pathologies and the importance of a multidisciplinary approach. The radiological progression towards pulmonary fibrosis was correlated with clinical symptoms, emphasizing the significance of early diagnosis and regular follow‐up. The combined use of advanced technologies offers a more comprehensive framework in managing complex lung diseases, enhancing the quality of care and understanding of interstitial pathologies.

Abstract Background Idiopathic pulmonary fibrosis (IPF) is a debilitating and progressive lung disease of unknown aetiology, characterized by the relentless deposition of fibrotic tissue. Biomarkers may play a pivotal role as indicators of disease presence, progression, and treatment response. Sirtuins, a family of enzymes with ADP ribosyltransferase or deacetylase activity, have been implicated in several diseases, including pulmonary fibrosis. Methods A cross-sectional, prospective, observational single-center study was conducted to investigate the potential role of serum SIRTs levels as biomarkers in patients with IPF. Demographic, clinical, and functional data and serological samples were collected from 34 patients with IPF followed at the Interstital Lung and Rare Diseases Outpatient Clinic of the Vanvitelli Pneumology Clinic, Monaldi Hospital, Naples, Italy and from 19 age-matched controls. Results Serum SIRT-1 levels were significantly reduced in IPF patients compared to controls (median IPF 667 [435–858] pg/mL versus controls 925 [794–1173] pg/mL; p

Interstitial lung diseases (ILDs) encompass a heterogeneous group of over 200 disorders that require individualized treatment. Antifibrotic agents, such as nintedanib and pirfenidone, have remarkably revolutionized the treatment landscape of patients with idiopathic pulmonary fibrosis (IPF). Moreover, the approval of nintedanib has also expanded the therapeutic options for patients with progressive pulmonary fibrosis other than IPF. However, despite recent advances, current therapeutic strategies based on antifibrotic agents and/or immunomodulation are associated with non-negligible side effects. Therefore, several studies have explored the inhalation route aiming to spread higher local concentrations while limiting systemic toxicity. In this review, we examined the currently available literature about preclinical and clinical studies testing the efficacy and safety of inhalation-based antifibrotics, immunomodulatory agents, antioxidants, mucolytics, bronchodilators, and vasodilator agents in ILDs.

Benign endobronchial tumors are rare clinical entities characterized by considerable variability in etiology and clinical presentation. The authors report four cases of endobronchial hamartomas treated and followed up from 2018 to 2023. Three of these cases, with identical endobronchial localization in the right lower lobe, were radically treated in flexible bronchoscopy with the only use of biopsy forceps. Another case with a different localization in the left main bronchus was treated with a laser through rigid bronchoscopy. In addition, the authors outline the main interventional pulmonological strategies for the treatment of benign tumors with endobronchial growth based on the existing literature.

Idiopathic pulmonary fibrosis (IPF) has traditionally been considered the archetype of progressive fibrotic interstitial lung diseases (f-ILDs), but several other f-ILDs can also manifest a progressive phenotype. Integrating genomic signatures into clinical practice for f-ILD patients may help to identify patients predisposed to a progressive phenotype. In addition to the risk of progressive pulmonary fibrosis, there is a growing body of literature examining how pharmacogenomics influences treatment response, particularly regarding the efficacy and safety profiles of antifibrotic and immunomodulatory agents. In this narrative review, we discuss current studies in IPF and other forms of pulmonary fibrosis, including systemic autoimmune disorders associated ILDs, sarcoidosis and hypersensitivity pneumonitis. We also provide insights into the future direction of research in this complex field.

Interstitial lung diseases comprise a heterogenous range of diffuse lung disorders, potentially resulting in pulmonary fibrosis. While idiopathic pulmonary fibrosis has been recognized as the paradigm of a progressive fibrosing interstitial lung disease, other conditions with a progressive fibrosing phenotype characterized by a significant deterioration of the lung function may lead to a burden of significant symptoms, a reduced quality of life, and increased mortality, despite treatment. There is now evidence indicating that some common underlying biological mechanisms can be shared among different chronic fibrosing disorders; therefore, different biomarkers for disease-activity monitoring and prognostic assessment are under evaluation. Thus, understanding the common pathways that induce the progression of pulmonary fibrosis, comprehending the diversity of these diseases, and identifying new molecular markers and potential therapeutic targets remain highly crucial assignments. The purpose of this review is to examine the main pathological mechanisms regulating the progression of fibrosis in interstitial lung diseases and to provide an overview of potential biomarker and therapeutic options for patients with progressive pulmonary fibrosis.

Non‐small cell lung cancer (NSCLC) accounts for 75-80% of all lung cancer cases. Stage III NSCLC represents a highly heterogenous stage characterized by different disease presentations and a wide range of treatment options. For patients with good performance status and unresectable-stage III NSCLC with programmed death-ligands 1 (PD-L1) tumor proportion score (TPS) ≥1%, durvalumab consolidation immunotherapy after a platinum-based chemo-radiotherapy is strongly recommended. However, age, poor performance status, underlying comorbidities may represent contraindications for chemotherapy to be used in a subgroup of patients. Herein, we report a case of an 80-year-old male affected by a stage IIIB lung adenocarcinoma with overexpression of PD-L1 (TPS 90%) treated with pembrolizumab, an immune checkpoint inhibitor targeting PD-1/PD-L1 pathways, which shows a complete resolution of lung lesion after four cycles of treatment. Although randomized controlled trials are required, this case report may suggest the potential role of pembrolizumab for chemotherapy unsuitable patients with overexpressing PD-L1 unresectable-stage III NSCLC.

Alectinib is a highly selective tyrosine kinase inhibitor of anaplastic lymphoma kinase (ALK) that is approved as first-line treatment in adult patients with ALK-positive non-small cell lung cancer (NSCLC) and as second-line in patients previously treated with crizotinib, and has been shown in the literature to significantly prolong progression-free survival compared to chemotherapy in patients with advanced non-small cell lung cancer. The authors describe a clinical case of a 24-year-old woman with malignant massive pleural effusion caused by ALK rearranged pulmonary adenocarcinoma with pleural and pericardial metastasis, in which, despite a dramatic clinical debut, the correct and timely management of the diagnostic and therapeutic path allowed for extraordinary therapeutic success.

Background and rationale. The therapeutic interventions against lung cancer are currently based on a fully personalized approach to the disease with considerable improvement of patients’ outcome. Alongside continuous scientific progresses and research investments, massive technologic efforts, innovative challenges, and consolidated achievements together with research investments are at the bases of the engineering and manufacturing revolution that allows a significant gain in clinical setting. Aim and methods. The scope of this review is thus to focus, rather than on the biologic traits, on the analysis of the precision sensors and novel generation materials, as semiconductors, which are below the clinical development of personalized diagnosis and treatment. In this perspective, a careful revision and analysis of the state of the art of the literature and experimental knowledge is presented. Results. Novel materials are being used in the development of personalized diagnosis and treatment for lung cancer. Among them, semiconductors are used to analyze volatile cancer compounds and allow early disease diagnosis. Moreover, they can be used to generate MEMS which have found an application in advanced imaging techniques as well as in drug delivery devices. Conclusions. Overall, these issues represent critical issues only partially known and generally underestimated by the clinical community. These novel micro-technology-based biosensing devices, based on the use of molecules at atomic concentrations, are crucial for clinical innovation since they have allowed the recent significant advances in cancer biology deciphering as well as in disease detection and therapy. There is an urgent need to create a stronger dialogue between technologists, basic researchers, and clinicians to address all scientific and manufacturing efforts towards a real improvement in patients’ outcome. Here, great attention is focused on their application against lung cancer, from their exploitations in translational research to their application in diagnosis and treatment development, to ensure early diagnosis and better clinical outcomes.

In individuals with chronic obstructive pulmonary disease (COPD), skeletal muscle wasting and changes in muscle fiber composition limit the muscle strength with consequences on daily physical activities. In the present study we aimed to investigate about the interconnection among upper limb strength, body composition and health related quality of life (HRQoL) in patients with COPD to verify the impact of muscle mass loss on HRQoL. Twenty-six consecutive patients (69.2% male; age: 69.7±7.29 years) with COPD were included. Patients underwent pulmonary function tests. Body composition was evaluated through Bioelectrical Impedance Analysis (BIA); handgrip test was used for measure upper limb strength. St George’s Respiratory Questionnaire (SGRQ) was used to evaluate patients’ HRQoL. Upper limb muscle strength was negatively correlated with SGRQ (Pearson= -0.571; p=0.002) in particular with activity and impact domains (Pearson= -0.668; p

Abstract Introduction The performance of seven cardiovascular (CV) risk algorithms is evaluated in a multicentric cohort of ankylosing spondylitis (AS) patients. Performance and calibration of traditional CV predictors have been compared with the novel paradigm of machine learning (ML). Methods A retrospective analysis of prospectively collected data from an AS cohort has been performed. The primary outcome was the first CV event. The discriminatory ability of the algorithms was evaluated using the area under the receiver operating characteristic (ROC) curve (AUC), which is like the concordance-statistic (c-statistic). Three ML techniques were considered to calculate the CV risk: support vector machine (SVM), random forest (RF), and k-nearest neighbor (KNN). Results Of 133 AS patients enrolled, 18 had a CV event. c-statistic scores of 0.71, 0.61, 0.66, 0.68, 0.66, 0.72, and 0.67 were found, respectively, for SCORE, CUORE, FRS, QRISK2, QRISK3, RRS, and ASSIGN. AUC values for the ML algorithms were: 0.70 for SVM, 0.73 for RF, and 0.64 for KNN. Feature analysis showed that C-reactive protein (CRP) has the highest importance, while SBP and hypertension treatment have lower importance. Conclusions All of the evaluated CV risk algorithms exhibit a poor discriminative ability, except for RRS and SCORE, which showed a fair performance. For the first time, we demonstrated that AS patients do not show the traditional ones used by CV scores and that the most important variable is CRP. The present study contributes to a deeper understanding of CV risk in AS, allowing the development of innovative CV risk patient-specific models.

Chronic obstructive pulmonary disease (COPD) is characterized by respiratory symptoms and non-reversible airflow limitation with recurrent episodes of acute exacerbations. The concurrent presence of bronchiectasis in patients with COPD is associated with reduced respiratory function as well as increased exacerbation risk. Adiponectin is a promising biomarker in COPD, as greater high molecular weight (HMW) oligomer levels have been observed among COPD patients. Here, we investigate adiponectin levels in two groups of COPD patients characterized by the presence or absence of bronchiectasis (BCO), comparing both groups to healthy controls. We evaluated serum adiponectin levels in COPD patients, those with BCO, and healthy subjects and characterized the pattern of circulating adiponectin oligomers. We found that forced volume capacity % (FVC%) and forced expiratory volume % (FEV1%) were lower for BCO patients than for COPD patients. COPD patients had higher levels of adiponectin and its HMW oligomers than healthy controls. Interestingly, BCO patients had higher levels of adiponectin than COPD patients. We showed that expression levels of IL-2, -4, and -8, IFN-γ, and GM-CSF were significantly higher in BCO patients than in healthy controls. Conversely, IL-10 expression levels were lower in BCO patients. Our data suggest that the increased levels of adiponectin detected in the cohort of BCO patients compared to those in COPD patients without bronchiectasis might be determined by their worse airway inflammatory state. This hypothesis suggests that adiponectin could be considered as a biomarker to recognize advanced COPD patients with bronchiectasis.

COVID-19 is an infective disease resulting in widespread respiratory and non-respiratory symptoms prompted by SARS-CoV-2 infection. Interaction between SARS-CoV-2 and host cell receptors prompts activation of pro-inflammatory pathways which are involved in epithelial and endothelial damage mechanisms even after viral clearance. Since inflammation has been recognized as a critical step in COVID-19, anti-inflammatory therapies, including both steroids and non-steroids as well as cytokine inhibitors, have been proposed. Early treatment of COVID-19 has the potential to affect the clinical course of the disease regardless of underlying comorbid conditions. Non-steroidal anti-inflammatory drugs (NSAIDs), which are widely used for symptomatic relief of upper airway infections, became the mainstay of early phase treatment of COVID-19. In this review, we discuss the current evidence for using NSAIDs in early phases of SARS-CoV-2 infection with focus on ketoprofen lysine salt based on its pharmacodynamic and pharmacokinetic features.

SARS-CoV-2 infection can induce a broad range of clinical symptoms, and the most severe cases are characterized by an uncontrolled inflammatory response with the overproduction of proinflammatory cytokines. Elevated levels of C-reactive protein, interleukin-1B, and interleukin-6 have become key signatures of severe COVID-19. For this reason, the use of 6 mg of dexamethasone has become a standard of care, although this regime may not be optimal. Even though various glucocorticoid doses have been proposed, it is still unclear which dose should be used to prevent adverse effects while at the same time reducing the inflammatory response. Here, we compared two different doses of corticosteroids in 52 elderly hospitalized patients with severe to critical COVID-19 to assess efficacy and safety. We showed that in patients receiving a higher dose of prednisone, the time to negative swab was significantly longer. Furthermore, although neither dose was correlated with the risk of death, patients receiving the high dose were more likely to have adverse events such as hyperglycemia, leukocytosis, an increase in systemic blood pressure, and others. Finally, the BMI, WBC number, and NLR value were directly related to death. In conclusion, although the optimal glucocorticoid dose is still undefined, our retrospective study supports the absence of beneficial effects in the utilization of higher doses of corticosteroids in elderly patients with severe to critical COVID-19.

SARS-CoV-2 infection leads to a heterogenous spectrum of clinical conditions ranging from self-limiting upper airway infection to severe respiratory failure. Carbocysteine is a thioether mucolytic with antioxidant and anti-inflammatory activities. Carbocysteine has been shown to have anti-viral effects on human rhinovirus, RSV and the influenza virus as well as interfering with upper airway ciliary motility, the first site of SARS-CoV-2 infection, leading to more effective mucus clearance and potential containment of viral spread towards the lower airway. Positive effects, in terms of limiting superimposed bacterial infection and reducing oxidative stress, have also been documented in COPD patients. Accordingly, Carbocysteine should also be considered in both post-exposure prophylaxis and early-phase treatment of COVID-19 in combination with other agents (monoclonal antibodies, antivirals, non-steroidal anti-inflammatory agents, and inhaled corticosteroids). In this review, we explored the pharmacokinetic and pharmacodynamic aspects of Carbocysteine to delineate its potential therapeutic impact in patients with COVID-19.

Abstract Background Tracheobronchial malignant stenosis is a life-threatening condition which may cause recurrent infections due to lung atelectasis. Despite immunotherapy is less toxic than standard chemotherapy, recurrent lung infections may represent a challenge for this treatment. We report a clinical case of a patient with metastatic squamous cell carcinoma suffering from pulmonary infections due to central airway obstruction who underwent endoscopic recanalization followed by immunotherapy. Case presentation A 64 year-old man was referred to our attention for the management of metastatic squamous cell carcinoma obstructing the right main bronchus with recurrent pulmonary infections. Patient exhibited strong positive PD-L1 expression (> 50%). Advanced disease stage contraindicated surgical treatment. Although therapy with immune check point inhibitors was indicated as first-line treatment, recurrent pulmonary infections made it unfeasible. Therefore, we planned a combined approach including endoscopic recanalization of central airway in order to resolve lung atelectasis, and lung infection followed by immunotherapy treatment with pembrolizumab in order to avoid local and systemic disease progression. Conclusions At 16-week follow-up, the patient was alive in stable disease with improvement of clinical condition and no signs of lung infection.

COVID-19 encompasses a broad spectrum of clinical conditions caused by SARS-CoV-2 infection. More severe cases experience acute respiratory and/or multiorgan failure. KL-6 is a glycoprotein expressed mainly from type II alveolar cells with pro-fibrotic properties. Serum KL-6 concentrations have been found in patients with COVID-19. However, the relevance of KL-6 in patients with severe and critical COVID-19 has not been fully elucidated. Methods: Retrospective data from consecutive severe to critical COVID-19 patients were collected at UOC Clinica Pnuemologica “Vanvitelli”, A.O. dei Colli, Naples, Italy. The study included patients with a positive rhinopharyngeal swab for SARS-CoV-2 RNA with severe or critical COVID-19. Results: Among 87 patients, 24 had poor outcomes. The median KL-6 value in survivors was significantly lower when compared with dead or intubated patients (530 U/mL versus 1069 U/mL p < 0.001). KL-6 was correlated with body mass index (BMI) (r: 0.279, p: 0.009), lung ultrasound score (LUS) (r: 0.429, p < 0.001), Chung Score (r: 0.390, p < 0.001). KL-6 was associated with the risk of death or oro-tracheal intubation (IOT) after adjusting for gender, BMI, Charlson Index, Chung Score, and PaO2/FIO2 (OR 1.003 95% CI 1.001–1.004, p < 0.001). Serum KL-6 value of 968 has a sensitivity of 79.2%, specificity of 87.1%, PPV 70.4%, NPV 91.5%, AUC: O.85 for risk of death or IOT. Conclusions: The presented research highlights the relevance of serum KL-6 in severe to critical COVID-19 patients in predicting the risk of death or IOT.

Purpose: To investigate the early CT findings in COVID-19 pneumonia as compared to influenza A virus H1N1 (AH1N1), with focus on vascular enlargement within consolidation or ground glass opacity (GGO) areas. Methods: 50 patients with COVID-19 pneumonia were retrospectively compared to 50 patients with AH1N1 pneumonia diagnosed during the 2009 pandemic. Two radiologists reviewed chest CT scans independently and blindly, with discordance resolved by consensus. Dilated or tortuous vessels within hyperdense lesions were recorded. Results: COVID-19 pneumonia presented with bilateral (96%), peripheral areas of GGO (22%), consolidation (4%) or combined GGO-consolidation (74%). The vascular enlargement sign in COVID-19 pneumonia was much more commonly present in COVID-19 (45/50, 90%) versus AH1N1 pneumonia (12/50, 24%) (p < 0.001). Vascular enlargement was more often present in lower lobes with a peripheral distribution. Conclusions: Vascular enlargement in consolidative/GGO areas may represent a reasonably common early CT marker in COVID-19 patients and is of uncertain etiology. Although speculative, theoretical mechanisms could potentially reflect acute inflammatory changes, pulmonary endothelial activation, or acute stasis. Further studies are necessary to verify specificity and to study if prognostic for clinical outcomes.

BackgroundSarcopenia is a progressive loss of skeletal muscle mass whose pathophysiology has been proposed to possibly involve mechanisms of altered inflammatory status and endocrine function. Adiponectin has been shown to modulate inflammatory status and muscle metabolism. However, the possible association between adiponectin levels and sarcopenia is poorly understood. In order to fill this gap, in the present manuscript we aimed to summarize the current evidence with a systematic review and a meta-analysis of studies reporting serum adiponectin levels in patients with sarcopenia compared to non-sarcopenic controls.MethodsAn electronic search through Medline/PubMed, Cochrane Library, and Science Direct was performed till March 1, 2020. From the included papers, meta-analysis of cross-sectional studies comparing serum levels of adiponectin between patients with sarcopenia and controls was performed.ResultsOut of 1,370 initial studies, seven studies were meta-analyzed. Sarcopenic participants had significantly higher levels of adiponectin Hedges’ g with 95% confidence interval (CI): 1.20 (0.19–2.22), p = 0.02 than controls. Subgroup analysis, performed in Asian population and focused on identification of the condition based on AWGS criteria, reported higher adiponectin levels in sarcopenic population (2.1 (0.17–4.03), p = 0.03 and I2 = 98.98%. Meta-regression analysis revealed female gender to significantly influence the results as demonstrated by beta = 0.14 (95% CI (0.010–0.280), p = 0.040).ConclusionsOur meta-analysis found evidence that sarcopenia is associated with higher adiponectin levels. However, caution is warranted on the interpretation of these findings, and future longitudinal research is required to disentangle and better understand the topic.

The endothelium is composed of a monolayer of endothelial cells, lining the interior surface of blood and lymphatic vessels. Endothelial cells display important homeostatic functions, since they are able to respond to humoral and hemodynamic stimuli. Thus, endothelial dysfunction has been proposed as a key and early pathogenic mechanism in many clinical conditions. Given the relevant repercussions on cardiovascular risk, the complex interplay between endothelial dysfunction and systemic arterial hypertension has been a matter of study in recent years. Numerous articles have been published on this issue, all of which contribute to providing an interesting insight into the molecular mechanisms of endothelial dysfunction in arterial hypertension and its role as a biomarker of inflammation, oxidative stress, and vascular disease. The prognostic and therapeutic implications of endothelial dysfunction have also been analyzed in this clinical setting, with interesting new findings and potential applications in clinical practice and future research. The aim of this review is to summarize the pathophysiology of the relationship between endothelial dysfunction and systemic arterial hypertension, with a focus on the personalized pharmacological and rehabilitation strategies targeting endothelial dysfunction while treating hypertension and cardiovascular comorbidities.

Viral infections are frequent among patients with thoracic malignancies prompted by dysregulation of innate and adaptative immune response. Clinical symptoms and radiological findings of both viral pneumonia and lung adenocarcinoma may overlap resulting in diagnostic and clinical challenges.We present the case of a women admitted to our department presenting with an acute manifestation of coronavirus OC43 pneumonia with underlying undiagnosed lung adenocarcinoma.

Latest evidences from literature suggest that SARS-CoV-2 disease 2019 (COVID-19) is commonly complicated with coagulopathy and that disseminated intravascular coagulation is present in the majority of deceased patients. Particularly, conventional coagulation parameters appear to be significantly altered in patients with poor prognosis. A wide-ranging cross- talk between coagulative haemostasis and inflammation, as well as the activation of coagulation cascade during viral infections, are well established. Another important evidence which may explain coagulation disorders in COVID-19 is the increase of thrombus formation under conditions of hypoxia. Despite the exact pathophysiological mechanism of coronavirus-induced thromboembolism needs to be further investigated, this finding suggests that it is good practice to assess the risk of thrombosis in COVID-19 patients to improve the clinical management in terms of anticoagulation therapy. Anticoagulants, mainly low-molecular-weight heparin (LMWH), should be tailored in patients meeting sepsis induced coagulopathy (SIC) criteria or with markedly elevated D-dimer. In this context, further studies are needed to optimise the decision making in therapeutic approach.

Testicular carcinoma recurrences represent a rare finding (1-6% in non-seminomatous germ cell tumours). However, cases of recurrence have been described many years later. We report a case of late recurrence of embryonic testicular carcinoma, after 26 years, with pulmonary metastases. Following evidence of increase of alpha-fetoprotein (AFP), the patient underwent a total body computed tomography scan that exhibited two pulmonary nodules, one in upper left lobe and other in left hilar region with multiple mediastinal and retrocrural lymph node enlargements All consolidations showed increased sugar uptake value at PET CT. Biopsies of lung consolidations confirmed diagnosis of recurrence of testicular carcinoma.

Coronavirus disease (COVID-19) is caused by SARS-CoV-2 virus, which can result in serious respiratory illnesses such as pneumonia leading to respiratory failure. It was first reported in Wuhan, Hubei, China, in December 2019 and rapidly spread globally, becoming a pandemic in March 2020. Among comorbidities observed in SARS-CoV-2 positive patients, hypertension (68.3%) and type 2-diabetes (30.1%) are the most frequent conditions. Although symptoms are highly heterogeneous (ranging from absence of symptoms to severe acute respiratory failure), patients with metabolic-associated diseases often experience worse COVID-19 outcomes. This review investigates the association between metabolic disorders and COVID-19 severity, exploring the molecular mechanisms potentially underlying this relationship and those that are responsible for more severe COVID-19 outcomes. In addition, the role of the main biological processes that may connect metabolic alterations to SARS-CoV-2 infection such as hyperglycemia, immune system deregulation, ACE-2 receptor modulation, and inflammatory response is described. The impact of metabolic disorders on the prognosis of COVID-19 has major implications in public health especially for countries affected by a high incidence of metabolic diseases.

Abstract Background Cystic fibrosis is an autosomal recessive disorder characterized by chronic progressive multisystem involvement. AH1N1 virus infections caused classic influenza symptoms in the majority of cystic fibrosis patients while others experienced severe outcomes. Case presentation We report a case of late incidental cystic fibrosis diagnosis in a young Caucasian man suffering from respiratory failure following infection due to AH1N1 influenza virus. The patient was admitted to our department with fever, cough, and dyspnea at rest unresponsive to antibiotics Conclusions Late diagnosis of cystic fibrosis in uncommon. This report highlights the importance of early cystic fibrosis diagnosis to minimize risk of occurrence of potential life-threatening complications.

The assessment of patients likely to undergo lung resection surgery is a multidisciplinary approach involving pulmonologists, surgeons and anaesthesiologists. In thoracic surgery, medical operability is also a calculation of postoperative lung function. A mobile application – PreParAPP MSD – to calculate postoperative lung function has been developed with the endorsement of the Italian Society of Anaesthesia, Analgesia and Intensive Care and with the unconditional support of MSD Italia. Thanks to a simple graphic interface, the calculation becomes fast and intuitive, while the possibility of storing and sharing data in an analytical and computerised way with other clinicians might help with the full assessment of patients without forcing them to undergo several medical examinations. These simple calculated parameters are performed by a minority of clinicians, generally anaesthesiologists. In our facility, there is a team involved in the perioperative evaluation of lung resection surgery (13 pulmonologists, 9 surgeons and 5 anaesthesiologists). In order to evaluate the possible Awareness towards postoperative lung function calculation better, we organised an internal survey with 27 clinicians who are members of such a team before and after the introduction of the PreParAPP MSD. It was found that after the introduction of PreParAPP MSD, the percentage of clinicians involved in postoperative lung function calculation rose from 18% to 70%. The implementation of a digital tool may help to improve guideline adherence, in accordance with other experiences in which such tools represented the start for various quality improvement purposes throughout the medical field.

Intercostal artery pseudoaneurysms (IAP) are extremely rare but its sudden rupture represents a life-threatening complication. We report an unusual case of a late intercostal artery pseudoaneurysm, after a video-assisted thoracoscopic surgery, presenting as a large intra-parenchymal lung mass. Diagnosis was made by biphasic computed tomography angiography and contrast-enhanced pulsed-wave doppler ultrasound. To minimize the risk of aneurysm bleeding immediate angiographic embolization was planned and successfully performed.IAP should be considered in presence of lung mass in patients who have previously undergone an intervention with intercostal approach to prevent life-threatening complications.

Lung cancer is the leading cause of cancer-related death worldwide and majority of patients are diagnosed in advanced/metastatic disease stage. Sites of distant metastases mainly include contralateral lung, lymph nodes, brain, bones, adrenal glands and liver; skeletal muscles metastases (SMMs) are less common. Psoas muscle and diaphragm metastases are mainly found during autopsy, as their involvement commonly is asymptomatic. We report a case of a 60-year-old female, suffering from non-small cell lung cancer (NSCLC), with refractory lower back pain, as expression of malignant psoas syndrome (MPS). MPS is a rare and difficult-to-treat cancer-pain syndrome, unresponsive to majority of analgesic therapy, related to psoas muscle metastasis; it is usually caused by different tumors such as uterus, ovary, bladder, prostate, colon-rectum, lymphoma, melanoma and sarcoma and represents an uncommon finding in NSCLC patients.

Since the beginning of 2020, the new pandemic caused by SARS-CoV-2 and named coronavirus disease 19 (COVID 19) has changed our socio-economic life. In just a few months, SARS-CoV-2 was able to spread worldwide at an unprecedented speed, causing hundreds of thousands of deaths, especially among the weakest part of the population. Indeed, especially at the beginning of this pandemic, many reports highlighted how people, suffering from other pathologies, such as hypertension, cardiovascular diseases, and diabetes, are more at risk of severe outcomes if infected. Although this pandemic has put the entire academic world to the test, it has also been a year of intense research and many important contributions have advanced our understanding of SARS-CoV-2 origin, its molecular structure and its mechanism of infection. Unfortunately, despite this great effort, we are still a long way from fully understanding how SARS-CoV-2 dysregulates organismal physiology and whether the current vaccines will be able to protect us from possible future pandemics. Here, we discuss the knowledge we have gained during this year and which questions future research should address.

Ischemic heart disease is currently a major cause of mortality and morbidity worldwide. Nevertheless, the actual therapeutic scenario does not target myocardial cell regeneration and consequently, the progression toward the late stage of chronic heart failure is common. Endothelial progenitor cells (EPCs) are bone marrow-derived stem cells that contribute to the homeostasis of the endothelial wall in acute and chronic ischemic disease. Calcium modulation and other molecular pathways (NOTCH, VEGFR, and CXCR4) contribute to EPC proliferation and differentiation. The present review provides a summary of EPC biology with a particular focus on the regulatory pathways of EPCs and describes promising applications for cardiovascular cell therapy.

Alterations of adipose tissue occurring in obesity have been recognized as a major risk factor for several cancers. The relationship between adipose tissue and lung cancer, which is the main cancer-related cause of death worldwide, still requires investigation. Perturbations in the adipokine system are likely to interfere with inter-organ crosstalk in lung cancer, which may influence the lung tumor microenvironment. Adiponectin (Acrp30) expression is deregulated in several cancer types. Acrp30 circulates as oligomers with a Low (LMW), Medium (MMW), and High Molecular Weight (HMW), with the latter mediating the main biological effects. Acrp30 acts through AdipoR1 and AdipoR2 receptors. T-cadherin has been described as a non-signaling receptor. This study’s aim was to investigate the regulation of serum Acrp30 and its receptors in sample tissue from non-small cell lung cancer (NSCLC) patients. We recruited 72 NSCLC patients and 60 healthy controls, whom we evaluated in terms of their Acpr30 levels and oligomeric profile. In addition, the expression of AdipoRs in tissues from lung cancer specimens was also measured and compared to coupled healthy lung samples. Our findings show a significant reduction of total Acrp30 levels in NSCLC patients compared to normal subjects, with a specific down-regulation of HMW oligomers. Acrp30 expression was lower in lung adenocarcinoma than other subtypes, regardless of other factors. A significantly higher expression of AdipoR1 was observed, while no differences in R2 and a lower expression of T-cadherin were found in lung cancer specimens compared to normal healthy lung tissues. Involvement of the Acrp30 system in lung cancer may provide new insight into the interaction between adipose tissue and lung and sheds light on its potential ability to influence the lung tumor microenvironment.

ABSTRACT Objective: Preoperative functional evaluation is central to optimizing the identification of patients with non-small cell lung cancer (NSCLC) who are candidates for surgery. The minute ventilation/carbon dioxide output (VE/VCO2) slope has proven to be a predictor of surgical complications and mortality. Pulmonary rehabilitation programs (PRPs) could influence short-term outcomes in patients with COPD undergoing lung resection. Our objective was to evaluate the effects of a PRP on the VE/VCO2 slope in a cohort of patients with COPD undergoing lung resection for NSCLC. Methods: We retrospectively evaluated 25 consecutive patients with COPD participating in a three-week high-intensity PRP prior to undergoing lung surgery for NSCLC, between December of 2015 and January of 2017. Patients underwent complete functional assessment, including spirometry, DLCO measurement, and cardiopulmonary exercise testing. Results: There were no significant differences between the mean pre- and post-PRP values (% of predicted) for FEV1 (61.5 ± 22.0% vs. 62.0 ± 21.1%) and DLCO (67.2 ± 18.1% vs. 67.5 ± 13.2%). Conversely, there were significant improvements in the mean peak oxygen uptake (from 14.7 ± 2.5 to 18.2 ± 2.7 mL/kg per min; p < 0.001) and VE/VCO2 slope (from 32.0 ± 2.8 to 30.1 ± 4.0; p < 0.01). Conclusions: Our results indicate that a high-intensity PRP can improve ventilatory efficiency in patients with COPD undergoing lung resection for NSCLC. Further comprehensive prospective studies are required to corroborate these preliminary results.

Non-small cell lung cancer (NSCLC) accounts for 75-80% of all lung cancer cases. Stage III NSCLC represents a highly heterogenous stage characterized by different disease presentations and a wide range of treatment options. For patients with good performance status and unresectable-stage III NSCLC with programmed death-ligands 1 (PD-L1) tumor proportion score (TPS) ≥1%, durvalumab consolidation immunotherapy after a platinumbased chemo-radiotherapy is strongly recommended. However, age, poor performance status, underlying comorbidities may represent contraindications for chemotherapy to be used in a subgroup of patients. Herein, we report a case of an 80-year-old male affected by a stage IIIB lung adenocarcinoma with overexpression of PD-L1 (TPS 90%) treated with pembrolizumab, an immune checkpoint inhibitor targeting PD-1/PD-L1 pathways, which shows a complete resolution of lung lesion after four cycles of treatment. Although randomized controlled trials are required, this case report may suggest the potential role of pembrolizumab for chemotherapy unsuitable patients with overexpressing PD-L1 unresectable-stage III NSCLC. [ABSTRACT FROM AUTHOR]