4 results on '"Meduri, Gianfranco Umberto"'
Search Results
2. Diagnostic workup for ARDS patients
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Papazian, Laurent, Calfee, Carolyn S, Chiumello, Davide, Luyt, Charles-Edouard, Meyer, Nuala J, Sekiguchi, Hiroshi, Matthay, Michael A, and Meduri, Gianfranco Umberto
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Biomedical and Clinical Sciences ,Clinical Sciences ,Rare Diseases ,Pneumonia & Influenza ,Pneumonia ,Sepsis ,Hematology ,Infectious Diseases ,Lung ,Clinical Research ,Acute Respiratory Distress Syndrome ,Detection ,screening and diagnosis ,4.1 Discovery and preclinical testing of markers and technologies ,Infection ,Respiratory ,Good Health and Well Being ,Biomarkers ,Biopsy ,Diagnosis ,Differential ,Diagnostic Imaging ,Humans ,Phenotype ,Precision Medicine ,Respiratory Distress Syndrome ,ARDS ,CT scan ,Ultrasonography ,BAL ,Diffuse alveolar damage ,Personalized medicine ,Phenotype-endotype ,Phenotype–endotype ,Public Health and Health Services ,Emergency & Critical Care Medicine ,Clinical sciences - Abstract
Acute respiratory distress syndrome (ARDS) is defined by the association of bilateral infiltrates and hypoxaemia following an initial insult. Although a new definition has been recently proposed (Berlin definition), there are various forms of ARDS with potential differences regarding their management (ventilator settings, prone positioning use, corticosteroids). ARDS can be caused by various aetiologies, and the adequate treatment of the responsible cause is crucial to improve the outcome. It is of paramount importance to characterize the mechanisms causing lung injury to optimize both the aetiological treatment and the symptomatic treatment. If there is no obvious cause of ARDS or if a direct lung injury is suspected, bronchoalveolar lavage (BAL) should be strongly considered to identify microorganisms responsible for pneumonia. Blood samples can also help to identify microorganisms and to evaluate biomarkers of infection. If there is no infectious cause of ARDS or no other apparent aetiology is found, second-line examinations should include markers of immunologic diseases. In selected cases, open lung biopsy remains useful to identify the cause of ARDS when all other examinations remain inconclusive. CT scan is fundamental when there is a suspicion of intra-abdominal sepsis and in some cases of pneumonia. Ultrasonography is important not only in evaluating biventricular function but also in identifying pleural effusions and pneumothorax. The definition of ARDS remains clinical and the main objective of the diagnostic workup should be to be focused on identification of its aetiology, especially a treatable infection.
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- 2016
3. Plasma Biomarker Analysis in Pediatric ARDS: Generating Future Framework from a Pilot Randomized Control Trial of Methylprednisolone: A Framework for Identifying Plasma Biomarkers Related to Clinical Outcomes in Pediatric ARDS
- Author
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Kimura, Dai, Saravia, Jordy, Rovnaghi, Cynthia R, Meduri, Gianfranco Umberto, Schwingshackl, Andreas, Cormier, Stephania A, and Anand, Kanwaljeet J
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Biomedical and Clinical Sciences ,Clinical Sciences ,Pediatric ,Clinical Research ,Clinical Trials and Supportive Activities ,Acute Respiratory Distress Syndrome ,Lung ,Rare Diseases ,Evaluation of treatments and therapeutic interventions ,6.1 Pharmaceuticals ,Respiratory ,Good Health and Well Being ,ARDS ,biomarker ,pediatric ,methylprednisolone ,MMP-8 ,Ang-2 ,ICAM-1 ,sRAGE ,Paediatrics and Reproductive Medicine ,Other Medical and Health Sciences ,Paediatrics - Abstract
ObjectiveLung injury activates multiple pro-inflammatory pathways, including neutrophils, epithelial, and endothelial injury, and coagulation factors leading to acute respiratory distress syndrome (ARDS). Low-dose methylprednisolone therapy (MPT) improved oxygenation and ventilation in early pediatric ARDS without altering duration of mechanical ventilation or mortality. We evaluated the effects of MPT on biomarkers of endothelial [Ang-2 and soluble intercellular adhesion molecule-1 (sICAM-1)] or epithelial [soluble receptor for activated glycation end products (sRAGE)] injury, neutrophil activation [matrix metalloproteinase-8 (MMP-8)], and coagulation (plasminogen activator inhibitor-1).DesignDouble-blind, placebo-controlled randomized trial.SettingTertiary-care pediatric intensive care unit (ICU).PatientsMechanically ventilated children (0-18 years) with early ARDS.InterventionsBlood samples were collected on days 0 (before MPT), 7, and 14 during low-dose MPT (n = 17) vs. placebo (n = 18) therapy. The MPT group received a 2-mg/kg loading dose followed by 1 mg/kg/day continuous infusions from days 1 to 7, tapered off over 7 days; placebo group received equivalent amounts of 0.9% saline. We analyzed plasma samples using a multiplex assay for five biomarkers of ARDS. Multiple regression models were constructed to predict associations between changes in biomarkers and the clinical outcomes reported earlier, including P/F ratio on days 8 and 9, plateau pressure on days 1 and 2, PaCO2 on days 2 and 3, racemic epinephrine following extubation, and supplemental oxygen at ICU discharge.ResultsNo differences occurred in biomarker concentrations between the groups on day 0. On day 7, reduction in MMP-8 levels (p = 0.0016) occurred in the MPT group, whereas increases in sICAM-1 levels (p = 0.0005) occurred in the placebo group (no increases in sICAM-1 in the MPT group). sRAGE levels decreased in both MPT and placebo groups (p
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- 2016
4. Prolonged higher dose methylprednisolone vs. conventional dexamethasone in COVID-19 pneumonia: a randomised controlled trial (MEDEAS)
- Author
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Salton F., Confalonieri P., Centanni S., Mondoni M., Petrosillo N., Bonfanti P., Lapadula G., Lacedonia D., Voza A., Carpene N., Montico M., Reccardini N., Meduri G. U., Ruaro B., Confalonieri M., Citton G. M., Bozzi C., Tavano S., Pozzan R., Andrisano A. G., Jaber M., Mari M., Trotta L., Mondini L., Barbieri M., Ruggero L., Antonaglia C., Soave S., Torregiani C., Bogatec T., Baccelli A., Nalesso G., Re B., Pavesi S., Barbaro M. P. F., Giuliani A., Ravaglia C., Poletti V., Scala R., Guidelli L., Golfi N., Vianello A., Achille A., Lucernoni P., Gaccione A. T., Romagnoli M., Fraccaro A., Malacchini N., Malerba M., Ragnoli B., Zamparelli A. S., Bocchino M., Blasi F., Spotti M., Miele C., Piedepalumbo F., Barone I., Baglioni S., Dodaj M., Franco C., Andrani F., Mangia A., Mancini A., Carrozzi L., Rafanelli A., Casto E., Rogliani P., Ora J., Carpagnano G. E., Di Lecce V., Tamburrini M., Papi A., Contoli M., Luzzati R., Zatta M., Di Bella S., Caraffa E., Francisci D., Tosti A., Pallotto C., De Rosa F. G., Pecori A., Franceschini M., Carlin M., Orsini V., Pollastri E., Rugova A., Sabbatini F., Soria A., Rossi M., Santantonio T., Meli R., Sauro S., Fedeli C., Mangini E., Biolo G., Nunnari A., Pietrangelo A., Corradini E., Bocchi D., Boarini C., Zucchetto A., Lanini S., Salton, F, Confalonieri, P, Centanni, S, Mondoni, M, Petrosillo, N, Bonfanti, P, Lapadula, G, Lacedonia, D, Voza, A, Carpene, N, Montico, M, Reccardini, N, Meduri, G, Ruaro, B, Confalonieri, M, Citton, G, Bozzi, C, Tavano, S, Pozzan, R, Andrisano, A, Jaber, M, Mari, M, Trotta, L, Mondini, L, Barbieri, M, Ruggero, L, Antonaglia, C, Soave, S, Torregiani, C, Bogatec, T, Baccelli, A, Nalesso, G, Re, B, Pavesi, S, Barbaro, M, Giuliani, A, Ravaglia, C, Poletti, V, Scala, R, Guidelli, L, Golfi, N, Vianello, A, Achille, A, Lucernoni, P, Gaccione, A, Romagnoli, M, Fraccaro, A, Malacchini, N, Malerba, M, Ragnoli, B, Zamparelli, A, Bocchino, M, Blasi, F, Spotti, M, Miele, C, Piedepalumbo, F, Barone, I, Baglioni, S, Dodaj, M, Franco, C, Andrani, F, Mangia, A, Mancini, A, Carrozzi, L, Rafanelli, A, Casto, E, Rogliani, P, Ora, J, Carpagnano, G, Di Lecce, V, Tamburrini, M, Papi, A, Contoli, M, Luzzati, R, Zatta, M, Di Bella, S, Caraffa, E, Francisci, D, Tosti, A, Pallotto, C, De Rosa, F, Pecori, A, Franceschini, M, Carlin, M, Orsini, V, Pollastri, E, Rugova, A, Sabbatini, F, Soria, A, Rossi, M, Santantonio, T, Meli, R, Sauro, S, Fedeli, C, Mangini, E, Biolo, G, Nunnari, A, Pietrangelo, A, Corradini, E, Bocchi, D, Boarini, C, Zucchetto, A, Lanini, S, Salton, Francesco, Confalonieri, Paola, Centanni, Stefano, Mondoni, Michele, Petrosillo, Nicola, Bonfanti, Paolo, Lapadula, Giuseppe, Lacedonia, Donato, Voza, Antonio, Carpenè, Nicoletta, Montico, Marcella, Reccardini, Nicolò, Meduri, Gianfranco Umberto, Ruaro, Barbara, MEDEAS Collaborative, Group, and Confalonieri, Marco
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Pulmonary and Respiratory Medicine ,glucocorticoids ,Settore MED/10 - Malattie dell'Apparato Respiratorio ,pneumonia ,COVID-19 ,glucocorticoid ,dexamethasone ,ARDS ,acute respiratory distress syndrome ,methylprednisolone - Abstract
BackgroundDysregulated systemic inflammation is the primary driver of mortality in severe coronavirus disease 2019 (COVID-19) pneumonia. Current guidelines favour a 7–10-day course of any glucocorticoid equivalent to dexamethasone 6 mg daily. A comparative randomised controlled trial (RCT) with a higher dose and a longer duration of intervention was lacking.MethodsWe conducted a multicentre, open-label RCT to investigate methylprednisolone 80 mg as a continuous daily infusion for 8 days followed by slow taperingversusdexamethasone 6 mg once daily for up to 10 days in adult patients with COVID-19 pneumonia requiring oxygen or noninvasive respiratory support. The primary outcome was reduction in 28-day mortality. Secondary outcomes were mechanical ventilation-free days at 28 days, need for intensive care unit (ICU) referral, length of hospitalisation, need for tracheostomy, and changes in C-reactive protein (CRP) levels, arterial oxygen tension/inspiratory oxygen fraction (PaO2/FIO2) ratio and World Health Organization Clinical Progression Scale at days 3, 7 and 14.Results677 randomised patients were included. Findings are reported as methylprednisolone (n=337)versusdexamethasone (n=340). By day 28, there were no significant differences in mortality (35 (10.4%)versus41 (12.1%); p=0.49) nor in median mechanical ventilation-free days (median (interquartile range (IQR)) 23 (14)versus24 (16) days; p=0.49). ICU referral was necessary in 41 (12.2%)versus45 (13.2%) (p=0.68) and tracheostomy in 8 (2.4%)versus9 (2.6%) (p=0.82). Survivors in the methylprednisolone group required a longer median (IQR) hospitalisation (15 (11)versus14 (11) days; p=0.005) and experienced an improvement in CRP levels, but not inPaO2/FIO2ratio, at days 7 and 14. There were no differences in disease progression at the prespecified time-points.ConclusionProlonged, higher dose methylprednisolone did not reduce mortality at 28 days compared with conventional dexamethasone in COVID-19 pneumonia.
- Published
- 2022
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