Publications by authors named "Paolo Parrella"

10 Publications

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Clinical application of nasal nitric oxide measurement in allergic rhinitis: A systematic review and meta-analysis.

Ann Allergy Asthma Immunol 2020 10 11;125(4):447-459.e5. Epub 2020 Jul 11.

Istituti Clinici Scientifici Maugeri IRCCS, Pavia, Italy. Electronic address:

Background: Nasal nitric oxide (nNO) is considered a biomarker of nasal inflammation.

Objective: To perform a systematic review with meta-analysis and meta-regressions on the association between nNO levels and allergic rhinitis (AR).

Methods: PubMed, Web of Science, Scopus, and EMBASE databases were systematically searched. Differences between cases and controls were expressed as standardized mean differences (SMD) with 95% confidence intervals (CI).

Results: Overall, 39 articles were included: 30 containing data on nNO measured by nasal aspiration (1881 patients with AR and 1337 controls) and 12 assessing nNO by nasal exhalation (525 patients with AR and 350 controls). Compared with controls, AR presented significantly higher nNO values both during nasal aspiration (SMD, 1.309; 95% CI, 0.841-1.777; P < .001) and nasal exhalation (SMD, 0.708; 95% CI, 0.303-1.114; P = .001). Sensitivity and subgroup analyses confirmed that the results for the evaluated outcomes were not affected by the presence of clinical confounding factors (asthma, nasal polyps, inhaled corticosteroids, smoking history), this being valid for both perennial and seasonal diseases during exposure to allergens. For the aspiration method, meta-regressions indicated that older age and a better pulmonary function were associated with a lower difference in nNO levels between patients with AR and controls, whereas an increasing aspiration flow was associated with a high effect size.

Conclusion: nNO levels are higher in AR, particularly when using high aspiration flows and in younger patients, who often perceive this condition as a source of disability. Further studies are needed to evaluate the usefulness of this biomarker for monitoring airway disorders and optimizing strategies in different settings (community, hospital, rehabilitation).
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http://dx.doi.org/10.1016/j.anai.2020.07.003DOI Listing
October 2020

Adapted recreational football small-sided games improve cardiac capacity, body composition and muscular fitness in patients with type 2 diabetes.

J Sports Med Phys Fitness 2020 Sep 12;60(9):1261-1268. Epub 2020 Jun 12.

Department of Human Movement Sciences and Wellbeing, Parthenope University, Naples, Italy -

Background: The usefulness of adapted small-sided games (SSGs) in improving cardiac function in subjects with T2DM is still debated. Here we evaluated the effects of 18 weeks indoor muscular activation training (6 weeks; IMA) followed by adapted SSGs football training (12 weeks) on cardiac function, muscular fitness, body composition and adiponectin expression in sedentary T2DM volunteers.

Methods: Six T2DM patients underwent IMA protocol of 6 weeks, twice a week followed by 12 weeks SSGs (5-a-side, once a week) training. Glucose, lipid profile and serum homocysteine concentration, body composition (BC), bone mineral density (DEXA), were determined at baseline and after 18 weeks (IMA+SSGs). VO2max and muscular fitness were recorded at baseline and after IMA (6 weeks) and SSGs (12 weeks), respectively.

Results: No significant differences were found for VO2max and muscular fitness after 6weeks of IMA. After 18 weeks (6 weeks IMA + 12 weeks SSGs) of training, significant improvements were found in the following parameters: work capacity, VO2peak, Ventilation (VEpeak), breathing reserve consumption and oxygen uptake efficiency slope (P<0.05); leg fitness (P<0.05), BC (P<0.05), vertebral column T-score (P<0.01) and adiponectin (total and high-molecular-weight; P<0.05). Compared to baseline, a reduction in serum homocysteine occurred after 18 weeks of training (P<0.05).

Conclusions: We evidenced that weekly adapted SSGs friendly football matches for 12 weeks improve cardiorespiratory capacity and the expression of independent markers associated with cardiovascular risk in T2DM patients, suggesting an overall reduced CVD-risk in these patients. These preliminary data encourage us to test the efficacy of this type of exercise in a larger population.
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http://dx.doi.org/10.23736/S0022-4707.20.10498-5DOI Listing
September 2020

Nasal Nitric Oxide in Chronic Rhinosinusitis with or without Nasal Polyps: A Systematic Review with Meta-Analysis.

J Clin Med 2020 Jan 11;9(1). Epub 2020 Jan 11.

Cardio-Pulmonary Rehabilitation Dept, Istituti Clinici Scientifici Maugeri IRCCS, 82037 Telese Terme (BN), Italy.

Background And Aims: There has been a recent growing interest in the role of nasal nitric oxide (nNO) as a biomarker for osteomeatal complex obstruction in paranasal sinus diseases. By using meta-analysis, we systematically reviewed the literature to establish the possible link between nNO concentration and chronic rhinosinusitis with nasal polyps (CRSwNP) or without (CRSsNP).

Methods: We systematically searched the EMBASE, PubMed, Scopus, and Web of Science databases for related studies. Differences between controls and cases were reported as standardized mean difference (SMD), with 95% confidence intervals (95% CI), using the random-effects method.

Results: We selected 23 articles for the final analysis: 15 with data on 461 CRSwNP patients and 384 healthy controls, 10 with data on 183 CRSsNP patients and 260 controls, and 14 studies on 372 CRSwNP and 297 CRSsNP patients. CRSwNP patients showed significantly lower nNO values when compared to both healthy controls (SMD: -1.495; 95% CI: -2.135, -0.854; < 0.0001) and CRSsNP patients (SMD: -1.448; 95% CI: -2.046, -0.850; < 0.0001). Sensitivity and subgroup analyses confirmed the results, which were further refined by regression models. They showed that an increasing aspiration flow is related to a greater difference in nNO levels between cases and control subjects. We also documented lower nNO levels in CRSsNP patients with respect to controls (SMD: -0.696; 95% CI: -1.189, -0.202; = 0.006), being this result no longer significant when excluding patients in therapy with intranasal corticosteroids. As shown by regression models, the increased Lund-Mackay score indicates a high effect size.

Conclusions: nNO levels are significantly lower in CRSwNP, especially when using higher aspiration flows. Additional studies are needed to define one single standardized method and normal reference values for nNO.
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http://dx.doi.org/10.3390/jcm9010200DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020063PMC
January 2020

What Is the Cardiac Impact of Chemotherapy and Subsequent Radiotherapy in Lymphoma Patients?

Antioxid Redox Signal 2019 11 23;31(15):1166-1174. Epub 2019 Sep 23.

Department of Translational Medical Sciences, Federico II University, Naples, Italy.

Anthracyclines are widely used in anticancer protocols, but can induce cardiotoxicity by mechanisms that mainly involve oxidative damage and mitochondrial dysfunction. Radiotherapy (RT) can also impair cardiac function by promoting myocardial fibrosis, microvascular damage, and decreased density of myocardial capillaries. Hence, we aim at investigating prospectively whether RT impacts heart function in lymphoma patients who had been already treated with anthracyclines. Twenty-nine consecutive patients with Hodgkin or non-Hodgkin lymphomas underwent echocardiography at baseline (before antineoplastic treatments), and then every 2 months, until 6 months after treatment completion. Echo evaluation included standard two-dimensional and speckle tracking. Twenty-two patients treated with anthracycline-based regimens were eligible. Out of the 22 patients, 8 received chemotherapy (CT) only (subgroup 1), while 14 underwent RT after CT [subgroup 2 (S2)]. At the end of CT, ejection fraction was significantly reduced in the whole population. At 6 months after completion of therapies, E/E' increased and global longitudinal strain was compromised in S2, suggesting additional damage induced by RT after CT. On the basis of the data from our small prospective study, we can hypothesize that in lymphoma patients, anthracyclines can worsen cardiac function, and RT may have an additional unfavorable myocardial impact.
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http://dx.doi.org/10.1089/ars.2019.7842DOI Listing
November 2019

Inflammatory, Serological and Vascular Determinants of Cardiovascular Disease in Systemic Lupus Erythematosus Patients.

Int J Mol Sci 2019 Apr 30;20(9). Epub 2019 Apr 30.

Department of Translational Medical Sciences, Federico II University, 80131 Naples, Italy.

Background And Aim: Systemic lupus erythematosus (SLE) is associated with increased risk of cardiovascular disease (CVD). Among many mechanisms, accelerated atherosclerosis, endothelial dysfunction, and hypercoagulability play a main role. Here, we investigate whether inflammatory, serological and clinical markers of SLE determine and correlate with arterial stiffness in SLE patients.

Materials And Methods: Routine blood samples, inflammatory mediators, specific antibodies, and 24 h proteinuria were measured in 43 SLE patients and 43 age and sex-matched controls using routine laboratory assays. We also assessed arterial stiffness by measuring radial artery applanation tonometry-derived augmentation index (AI), normalized AI (AIx@75), aortic pulse pressure, central systolic, diastolic and peripheral blood pressure.

Results: SLE patients showed a significantly greater arterial stiffness vs. controls, as demonstrated by the significantly higher AIx@75 and aortic pulse pressure. Interestingly, regression analysis showed that age, systolic pulse pressure, inflammatory markers (erythrocyte sedimentation rate and C-reactive protein), daily dose of glucocorticoids, and cumulative organ damage positively correlated with arterial stiffness.

Conclusions: SLE patients show increased arterial stiffness which correlates with markers of inflammation, that is involved in early alterations in arterial walls. Applanation tonometry can be used to screen SLE patients for subclinical vascular damage to implement prevention strategies for CVD.
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http://dx.doi.org/10.3390/ijms20092154DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6540240PMC
April 2019

Antineoplastic Drug-Induced Cardiotoxicity: A Redox Perspective.

Front Physiol 2018 7;9:167. Epub 2018 Mar 7.

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.

Antineoplastic drugs can be associated with several side effects, including cardiovascular toxicity (CTX). Biochemical studies have identified multiple mechanisms of CTX. Chemoterapeutic agents can alter redox homeostasis by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species RNS. Cellular sources of ROS/RNS are cardiomyocytes, endothelial cells, stromal and inflammatory cells in the heart. Mitochondria, peroxisomes and other subcellular components are central hubs that control redox homeostasis. Mitochondria are central targets for antineoplastic drug-induced CTX. Understanding the mechanisms of CTX is fundamental for effective cardioprotection, without compromising the efficacy of anticancer treatments. Type 1 CTX is associated with irreversible cardiac cell injury and is typically caused by anthracyclines and conventional chemotherapeutic agents. Type 2 CTX, associated with reversible myocardial dysfunction, is generally caused by biologicals and targeted drugs. Although oxidative/nitrosative reactions play a central role in CTX caused by different antineoplastic drugs, additional mechanisms involving directly and indirectly cardiomyocytes and inflammatory cells play a role in cardiovascular toxicities. Identification of cardiologic risk factors and an integrated approach using molecular, imaging, and clinical data may allow the selection of patients at risk of developing chemotherapy-related CTX. Although the last decade has witnessed intense research related to the molecular and biochemical mechanisms of CTX of antineoplastic drugs, experimental and clinical studies are urgently needed to balance safety and efficacy of novel cancer therapies.
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http://dx.doi.org/10.3389/fphys.2018.00167DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846016PMC
March 2018

New Drugs, Therapeutic Strategies, and Future Direction for the Treatment of Pulmonary Arterial Hypertension.

Curr Med Chem 2019 ;26(16):2844-2864

Federico II University, Department of Translational Medical Sciences, Naples, Italy.

Despite recent advances in Pulmonary Arterial Hypertension (PAH) treatment, this condition is still characterized by an extremely poor prognosis. In this review, we discuss the use of newly-approved drugs for PAH treatment with already known mechanisms of action (macitentan), innovative targets (riociguat and selexipag), and novel therapeutic approaches with initial up-front combination therapy. Secondly, we describe new potential signaling pathways and investigational drugs with promising role in the treatment of PAH.
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http://dx.doi.org/10.2174/0929867325666180201095743DOI Listing
October 2019

Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond.

Int J Cardiol 2017 Jan 9;227:11-17. Epub 2016 Nov 9.

Division of Cardiology, Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy.

Cardiotoxicity induced by chemotherapeutic agents and radiotherapy is a growing problem. In recent years, an increasing number of new drugs with targeted action have been designed. These molecules, such as monoclonal antibodies and tyrosine kinase inhibitors, can cause different type of toxicities compared to traditional chemotherapy. However, they can also cause cardiac complications such as heart failure, arterial hypertension, QT interval prolongation and arrhythmias. Currently, a field of intense research is the vascular toxicity induced by new biologic drugs, particularly those which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) and other tyrosine kinases. In this review, we aim at focusing on the problem of vascular toxicity induced by new targeted therapies, chemotherapy and radiotherapy, and describe the main mechanisms and emphasizing the importance of early diagnosis of vascular damage, in order to prevent clinical complications.
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http://dx.doi.org/10.1016/j.ijcard.2016.11.174DOI Listing
January 2017

Biomarkers in sarcopenia: A multifactorial approach.

Exp Gerontol 2016 12 12;85:1-8. Epub 2016 Sep 12.

Department of Translational Medical Sciences, University of Naples "Federico II", Naples, Italy. Electronic address:

The slow and continuous loss of muscle mass that progresses with aging is defined as "sarcopenia". Sarcopenia represents an important public health problem, being closely linked to a condition of frailty and, therefore, of disability. According to the European Working Group on Sarcopenia in Older People, the diagnosis of sarcopenia requires the presence of low muscle mass, along with either low grip strength or low physical performance. However, age-related changes in skeletal muscle can be largely attributed to the complex interactions among factors including alterations of the neuromuscular junction, endocrine system, growth factors, and muscle proteins turnover, behavior-related and disease-related factors. Accordingly, the identification of a single biomarker of sarcopenia is unreliable, due to its "multifactorial" pathogenesis with the involvement of a multitude of pathways. Thus, in order to characterize pathophysiological mechanisms and to make a correct assessment of elderly patient with sarcopenia, a panel of biomarkers of all pathways involved should be assessed.
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http://dx.doi.org/10.1016/j.exger.2016.09.007DOI Listing
December 2016