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 improvethe 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.

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.

Background: The use of HFNC (High Flow Nasal Cannula) in the management of acute respiratory failure has been fully established in clinical practice. Conversely, less data is available supporting its use in chronic hypoxemic–hypercapnic respiratory failure. The aim of the present study is to evaluate the efficacy of HFNC in chronic hypercapnic respiratory failure associated with stable COPD. Methods: In this retrospective single-center longitudinal observational study, 40 patients treated with HFNC at home followed at the COPD Clinic of Respiratory Diseases (University of Campania L. Vanvitelli Monaldi Hospital, Naples) were included. All patients are re-assessed at our clinic at T0, T3, T6 and T12 months through functional respiratory tests and blood gas analysis. Results: After 12 months, significant reductions in pCO₂ (arterial partial pressure of carbon dioxide) (from 58.5 to 48.0 mmHg) and lactates (from 1.60 to 0.90 mmol/L) were observed, and MIP and MEP improved significantly. Patients receiving HFNC flows ≥50 L/min experienced greater reductions in pCO₂ and fewer exacerbations. Multivariate analysis identified HFNC flow rate (p = 0.0046), hours of use/day (p = 0.0157), lactate levels (p = 0.0301), and FEV₁ (forced expiratory volume in 1 s) (p = 0.0491) as independent predictors of reduction in PaCO₂. Higher BMI and greater airway obstruction were associated with a reduced response. Conclusions: Treatment with HFNC represents a reasonable therapeutic choice to reduce AEs-COPD and reduce PaCO₂ and lactates in stable COPD patients.

Background/Objectives: Skeletal muscle wasting is a frequent and clinically consequential comorbidity in COPD, affecting 15–50% of patients and predicting reduced exercise tolerance, impaired quality of life, hospitalization, and mortality. However, no consensus exists on the optimal diagnostic approach, and the role of nutritional assessment remains underemphasized despite its contribution to muscle depletion. Methods: This narrative review synthesizes evidence from original research, systematic reviews, and consensus statements on diagnostic methods for evaluating muscle mass, strength, physical performance, and nutritional status in COPD. Results: Computed tomography and magnetic resonance imaging offer accurate assessment of muscle mass but are limited by cost and accessibility. Dual-energy X-ray absorptiometry provides a low-radiation alternative but cannot assess muscle quality. Bioelectrical impedance analysis and ultrasound are portable and inexpensive, yet lack standardized COPD-specific cut-offs. Functional tests provide clinically meaningful performance data but do not directly measure muscle mass. In parallel, nutritional screening tools and dietary assessment can identify modifiable risk factors and are associated with sarcopenia prevalence and prognosis in COPD. The choice of diagnostic approach significantly influences prevalence estimates. Conclusions: Optimal assessment of muscle wasting in COPD requires a multimodal approach combining muscle mass quantification, strength measurement, physical performance evaluation, and nutritional assessment. Standardized COPD-specific diagnostic criteria are needed. A practical algorithm integrating simple screening tools with targeted confirmatory assessments, including nutritional evaluation, may help guide clinical practice.

Identification of risk factors for severe outcome of Sars-Cov-2 infection is an important issue in COVID-19 management. Much attention has been focused on comorbidities as well as drugs taken by patients. Usage of proton pump inhibitors (PPIs) appears to potentially influence disease course. These drugs are known to reduce stomach acid and also modulate the immune system. Their use, prior to and during COVID-19 infection, seems to predispose to the development of more severe pneumonia and therefore to a greater risk of mortality. Instead, the use of Histamine receptor 2 antagonists (H2RAs) seems to be associated with a better outcome in patients with COVID-19, in terms of symptoms, risk of intubation and death. As PPIs are essential for treatment of many disorders, usage of these drugs should be balanced considering the benefits and risk ratio, in order to guarantee their correct use for the necessary time. It remains to be clarified whether the detrimental effects, in terms of COVID19 severe outcome, are due to PPIs or to the underlying disease for which they are administered. New controlled-randomized trials are required to better understand their impact in SARS-COV-2 infections. *Vanvitelli/Monaldi COVID Group: Adriano Cristinziano, Carolina Delle Donne, Cecilia Calabrese, Fabio Perrotta, Filippo Scialò, Francesco Lassandro, Gennaro Mazzarella, Giorgio Paoli, Leonardo De Luca, Maria Galdo, Miriam Buonincontro, Roberta Cianci, Rosalba Donizzetti, Stefano Sanduzzi Zamparelli, Tullio Valente, Vito D’Agnano, Vittorio Bisogni