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The elderly may represent a specific cluster of high-risk patients for developing COVID-19 with rapidly progressive clinical deterioration. Indeed, in older individuals, immunosenescence and comorbid disorders are more likely to promote viral-induced cytokine storm resulting in life-threatening respiratory failure and multisystemic involvement. Early diagnosis and individualized therapeutic management should be developed for elderly subjects based on personal medical history and polypharmacotherapy. Our review examines the pathogenesis and clinical implications of ageing in COVID-19 patients; finally, we discuss the evidence and controversies in the management in the long-stay residential care homes and aspects of end-of-life care for elderly patients with COVID-19.

Obesity, through adipose tissue (AT) inflammation and dysregulation, represents a critical factor for COVID-19; here, we investigated whether serum levels of adiponectin, HMW oligomers, leptin, and resistin are modulated and/or correlated with clinical and biochemical parameters of severe COVID-19 patients. This study included 62 severe COVID-19 patients; 62 age and sex-matched healthy subjects were recruited as a control group. Anthropometric and biochemical parameters were obtained and compared. Adiponectin, HMW oligomers, leptin, and resistin were analyzed by ELISA. The adiponectin oligomerization state was visualized by Western blotting. When compared to healthy subjects, total adiponectin levels were statistically lower in severe COVID-19 while, in contrast, the levels of leptin and resistin were statistically higher. Interestingly, HMW adiponectin oligomers negatively correlated with leptin and were positively associated with LUS scores. Resistin showed a positive association with IL-6, IL-2R, and KL-6. Our data strongly support that adipose tissue might play a functional role in COVID-19. Although it needs to be confirmed in larger cohorts, adiponectin HMW oligomers might represent a laboratory resource to predict patient seriousness. Whether adipokines can be integrated as a potential additional tool in the evolving landscape of biomarkers for the COVID-19 disease is still a matter of debate. Other studies are needed to understand the molecular mechanisms behind adipokine’s involvement in COVID-19.

Over the last decade, immunotherapy has revolutionized lung cancer treatments, particularly in non-small cell lung cancer, where immune checkpoint inhibitors have achieved significant clinical success. However, high percentages of patients do not respond initially or eventually develop a resistance to these therapies. This review explores the evolution and challenges of immunotherapy in lung cancer, highlighting its clinical milestones and intrinsic and extrinsic resistance mechanisms. We investigate tumor-intrinsic resistance factors, including alterations in antigen presentation, the loss of Beta-2 microglobulin function, impaired interferon signaling, immune editing, epigenetic modifications, and tumor-extrinsic resistance, such as an immunosuppressive lung tumor microenvironment, dysregulated cytokine profiles, and the upregulation of immune checkpoints. Then, we focus on the emerging role of resistance biomarkers and the development of personalized treatment strategies to overcome these challenges. The complex interplay between tumor biology and immune modulation in lung cancer paves the way for novel approaches for improving the effectiveness of immunotherapeutic treatments.

Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, leading to defective ion transport and impaired function of various organs. Chronic inflammation, oxidative stress, and microbial dysbiosis are key pathological features of CF patients, contributing to disease progression, lung damage, and an increased susceptibility to infections. Emerging evidence suggests that in CF patients these factors can promote cancer development, especially lung cancer. Chronic inflammation in CF, driven by immune cell dysfunction, results in the release of pro-inflammatory cytokines and reactive oxygen species (ROSs), fostering an environment conducive to cancer initiation. Oxidative stress can amplify cellular damage and hinder airway remodeling. ROSs not only damage cellular components such as lipids, proteins, and DNA but also disrupt lung homeostasis, creating a favorable environment for cancer development. Furthermore, the lung microbiome in CF patients is often dysbiotic, with a reduced diversity and the predominance of pathogenic bacteria such as Pseudomonas aeruginosa, which exacerbate inflammation and may contribute to carcinogenesis. This review explores the mechanisms linking CF to lung cancer, examining the potential clinical implications of these mechanisms for early detection, monitoring, and targeted therapies for lung cancer prevention in CF patients.

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.

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  < 0.001 ). In contrast, serum SIRT-3 levels were significantly increased in IPF patients compared to controls (median IPF 338 [230–500] pg/mL versus controls 154 [99.8–246] pg/mL; p  < 0.001). There were no statistically significant differences in serum SIRT-6 and SIRT-7 levels between IPF and controls. In addition, we found a significant positive correlation between SIRT-1 and lung function parameters such as FEV 1 % (ϱ=0.417; p  = 0.016), FVC% (ϱ=0.449; p  = 0.009) and DL CO % (ϱ=0.393; p  = 0.024), while a significant negative correlation was demonstrated between SIR-1 and GAP score, demonstrating a significant reduction in SIRT-1 in advanced Gender-Age-Physiology (GAP) stages 2–3 compared to GAP stage 1 ( p  = 0.008). Conclusions This prospective, cross-sectional study showed that SIRT-1 was associated with lung function and IPF severity and that both SIRT-1 and SIRT-3 could be considered as potential biomarkers of IPF, whereas SIRT-6 and SIRT-7 were not associated with IPF.

The treatment of ankylosing spondylitis (AS) and psoriatic arthritis (PsA) positively changed since the introduction of anti-TNFα drugs. These treatments were shown to reduce the symptoms and signs of the diseases and improve the quality of life. However, a variable percentage of patients do not respond to anti-TNFα or can exhibit a loss of response and, furthermore, despite anti-TNFα drugs' proven efficacy in reducing peripheral radiographic progression in PsA, the impact in reducing radiographic damage in AS is still debated. Recently, the discovery of new pathogenic mechanisms paved the way to the development of new drugs that target other pro-inflammatory cytokines. In particular, the inhibition of interleukin (IL)-17, which is the principal cytokine produced by Th17 lymphocytes, a pro-inflammatory subset involved in both inflammation and new bone formation in AS and PsA, demonstrated promising results. The new molecule secukinumab, an IL-17A inhibitor, showed its efficacy and safety in phase III randomized clinical trials in AS and PsA and is the first non-anti-TNFα biologic approved for the treatment of AS, providing a useful alternative treatment strategy in both diseases. The aim of this article was to review the pathophysiological basis, the efficacy and the safety of secukinumab treatment in AS and PsA patients.

Psoriatic arthritis (PsA) is a chronic inflammatory disease characterized by psoriasis, synovitis, enthesitis, spondylitis and association with other extra-articular manifestations. Chronic inflammation of involved tissues possibly leads to structural damage and to a reduction in function and quality of life. The treatment of PsA dramatically changed with the introduction of anti-tumor necrosis factor (TNF)-α drugs, which have been shown to reduce the symptoms and signs of the disease, and slow radiographic progression. However, some patients do not respond to anti-TNFα or have a loss of response. Recently, the discovery of new pathogenic mechanisms have made possible the development of new drugs that target pro-inflammatory cytokines, such as interleukin (IL)-12, IL-23 and IL-17, or interfere with cellular pathways involved in skin, joint and entheseal inflammation. New molecules, namely ustekinumab, secukinumab, and apremilast have shown efficacy and safety over the various components of the disease in randomized clinical trials. These drugs have been recently approved for the treatment of PsA and included in new treatment recommendations. Other molecules are currently being tested in phase III clinical trials and are potential new treatment options for PsA. The aim of this review is to update the new pathways involved in the development of the disease and the emerging treatments for PsA beyond TNFα inhibition.

Background: Accelerating recovery and preventing the progression to more severe outcomes for patients with coronavirus disease 2019 (COVID-19) is of paramount importance. Non-steroidal anti-inflammatory agents (NSAIDs) have been widely adopted in the international recommendations for non-severe COVID-19 management. Among NSAIDs, evidence about the efficacy of ketoprofen lysin salt (KLS) in the treatment of non-severe COVID-19 has not been reported. Methods: This retrospective study compared the outcomes of 120 patients with mild to moderate COVID-19 treated at home with KLS between March 2021 and May 2023 compared with the outcomes of 165 patients who received corticosteroids. The outcomes included hospitalization, the need for oxygen supplementation, clinical recovery from acute COVID-19, and time to negative swabs. Results: Symptoms persisted in a lower percentage of patients in the KLS group compared to the corticosteroids group (p < 0.0001) and for a shorter period (p = 0.046). We found 6 patients (5%) in the KLS group were hospitalized compared to 45 (27%) in the corticosteroids group (p < 0.001). A higher percentage of patients in the corticosteroids group require oxygen administration (p < 0.001). In addition, patients taking corticosteroids showed a longer viral shedding period compared to those taking KLS (p = 0.004). A final multivariate analysis suggests that KLS might reduce hospitalization risk, the need for oxygen supplementation, and the persistence of post-COVID-19 symptoms when compared to an oral corticosteroid after adjusting for significant co-variables. Conclusions: KLS might have a positive effect on clinical recovery in non-severe COVID-19 patients. A comparison with other NSAIDs in terms of difference in efficacy and safety should be investigated in further trials.

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.