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Clinical review: Severe asthma
Spyros Papiris, Anastasia Kotanidou, Katerina Malagari, Charis Roussos
Critical Care , 2002, DOI: 10.1186/cc1451
Abstract: Treatment for acute, severe asthma includes the administration of oxygen, β2-agonists (by continuous or repetitive nebulisation), and systemic corticosteroids. Subcutaneous administration of epinephrine or terbutaline should be considered in patients not responding adequately to continuous nebulisation, in those unable to cooperate, and in intubated patients not responding to inhaled therapy. The exact time to intubate a patient in status asthmaticus is based mainly on clinical judgment, but intubation should not be delayed once it is deemed necessary. Mechanical ventilation in status asthmaticus supports gas-exchange and unloads ventilatory muscles until aggressive medical treatment improves the functional status of the patient. Patients intubated and mechanically ventilated should be appropriately sedated, but paralytic agents should be avoided. Permissive hypercapnia, increase in expiratory time, and promotion of patient-ventilator synchronism are the mainstay in mechanical ventilation of status asthmaticus. Close monitoring of the patient's condition is necessary to obviate complications and to identify the appropriate time for weaning. Finally, after successful treatment and prior to discharge, a careful strategy for prevention of subsequent asthma attacks is imperative.Bronchial asthma has a wide clinical spectrum ranging from a mild, intermittent disease to one that is severe, persistent, and difficult to treat, which in some instances can also be fatal [1,2,3,4]. Asthma deaths, although uncommon (one in 2000 asthmatics), have increased over the last decades [2], with more than 5000 deaths reported annually in the USA and 100,000 deaths estimated yearly throughout the world [1,2]. Patients at greater risk for fatal asthma attacks are mainly those with severe, unstable disease, although death can occur to anyone if the asthma attack is intense enough [2,3,4]. Most deaths from asthma are preventable, however, particularly those among young persons. Morbidity in
Soluble TNF Mediates the Transition from Pulmonary Inflammation to Fibrosis
Nikos Oikonomou, Vaggelis Harokopos, Jonathan Zalevsky, Christos Valavanis, Anastasia Kotanidou, David E. Szymkowski, George Kollias, Vassilis Aidinis
PLOS ONE , 2006, DOI: 10.1371/journal.pone.0000108
Abstract: Background Fibrosis, the replacement of functional tissue with excessive fibrous tissue, can occur in all the main tissues and organ systems, resulting in various pathological disorders. Idiopathic Pulmonary Fibrosis is a prototype fibrotic disease involving abnormal wound healing in response to multiple sites of ongoing alveolar epithelial injury. Methodology/Principal Findings To decipher the role of TNF and TNF-mediated inflammation in the development of fibrosis, we have utilized the bleomycin-induced animal model of Pulmonary Fibrosis and a series of genetically modified mice lacking components of TNF signaling. Transmembrane TNF expression is shown to be sufficient to elicit an inflammatory response, but inadequate for the transition to the fibrotic phase of the disease. Soluble TNF expression is shown to be crucial for lymphocyte recruitment, a prerequisite for TGF-b1 expression and the development of fibrotic lesions. Moreover, through a series of bone marrow transfers, the necessary TNF expression is shown to originate from the non-hematopoietic compartment further localized in apoptosing epithelial cells. Conclusions These results suggest a primary detrimental role of soluble TNF in the pathologic cascade, separating it from the beneficial role of transmembrane TNF, and indicate the importance of assessing the efficacy of soluble TNF antagonists in the treatment of Idiopathic Pulmonary Fibrosis.
Diagnostic value of triggering receptor expressed on myeloid cells-1 and C-reactive protein for patients with lung infiltrates: an observational study
Ilias Porfyridis, Diamantis Plachouras, Vasiliki Karagianni, Anastasia Kotanidou, Spyridon A Papiris, Helen Giamarellou, Evangelos J Giamarellos-Bourboulis
BMC Infectious Diseases , 2010, DOI: 10.1186/1471-2334-10-286
Abstract: 68 patients admitted to a medical ward with acute respiratory illness were enrolled in the study. Neutrophil and monocyte TREM-1 expression were measured by flow cytometry, sTREM-1 by an enzyme immunoassay and C-reactive protein by nephelometry. Clinical pulmonary infection score was recorded.34 patients were diagnosed with bacterial community acquired pneumonia (group A) and 34 with non-bacterial pulmonary disease (group B). Median serum TREM-1 concentration was 102.09 pg/ml in group A and lower than 15.10 pg/ml (p < 0.0001) in group B. Mean±SE neutrophil TREM-1 expression was 4.67 ± 0.53 MFI in group A and 2.64 ± 0.25 MFI (p = 0.001) in group B. Monocyte TREM-1 expression was 4.2 ± 0.42 MFI in group A and 2.64 ± 0.35 MFI (p = 0.007) in group B and mean±SE CRP was 18.03 ± 2 mg/ml in group A and 7.1 ± 1.54 mg/ml (p < 0.001) in group B. A cut-off of 19.53 pg/ml of sTREM-1 with sensitivity 82.6% and specificity 63% to discriminate between infectious and non-infectious pulmonary infiltrates was found. sTREM-1 at admission greater than 180 pg/ml was accompanied with unfavourable outcome.TREM-1 myeloid expression and sTREM-1 are reliable markers of bacterial infection among patients with pulmonary infiltrates; sTREM-1 is a predictor of final outcome.Early diagnosis of lung infections remains a challenge. There is no gold standard for diagnosing microbial infection as clinical and laboratory signs are neither sensitive nor specific enough, and microbiological studies often remain negative. The presence of a new infiltrate on plain chest radiograph is considered indicative for diagnosing pneumonia, especially when is supported by clinical and laboratory findings. However it is difficult to differentiate a chest infiltrate of bacterial origin from a chest infiltrate of non-bacterial origin solely based on radiological criteria [1]. The diagnosis of infection is not always clear in the acute setting in patients with respiratory tract disease and a surrogate marker of infecti
Compartmentalization of lipid peroxidation in sepsis by multidrug-resistant gram-negative bacteria: experimental and clinical evidence
Chryssoula Toufekoula, Vassileios Papadakis, Thomas Tsaganos, Christina Routsi, Stylianos E Orfanos, Anastasia Kotanidou, Dionyssia-Pinelopi Carrer, Maria Raftogiannis, Fotini Baziaka, Evangelos J Giamarellos-Bourboulis
Critical Care , 2013, DOI: 10.1186/cc11930
Abstract: Lethal sepsis was induced in rats by the intraperitoneal injection of one MDR isolate of Pseudomonas aeruginosa. Produced malondialdehyde (MDA) was measured in tissues 5 hours after bacterial challenge with the thiobarbiturate assay followed by high-performance liquid chromatography (HPLC) analysis. Results were compared with those from a cohort of patients with ventilator-associated pneumonia (VAP) and sepsis by MDR Gram-negative bacteria. More precisely, serum MDA was measured on 7 consecutive days, and it was correlated with clinical characteristics.MDA of septic rats was greater in the liver, spleen, and aortic wall, and it was lower in the right kidney compared with sham operated-on animals. Findings were confirmed by the studied cohort. Circulating MDA was greater in patients with hepatic dysfunction and acute respiratory distress syndrome (ARDS) compared with patients without any organ failures. The opposite was found for patients with acute renal dysfunction. No differences were found between patients with ARDS without or with cardiovascular (CV) failure and patients without any organ failure. Serial measurements of MDA in serum of patients indicated that levels of MDA were greater in survivors of hepatic dysfunction and ARDS and lower in survivors of acute renal dysfunction.Animal findings and results of human sepsis are complementary, and they suggest a compartmentalization of lipid peroxidation in systemic infections by MDR gram-negative bacteria.Oxidative stress results from an imbalance between production of reactive oxygen and nitrogen species (ROS and RNS) and endogenous antioxidant defense mechanisms [1]. A growing body of evidence suggests that many of the effects of cellular dysfunction under oxidative stress are mediated by products of nonenzymatic reactions, such as the peroxidative degradation of polyunsaturated fatty acids. Aldehyde molecules generated during lipid peroxidation are considered ultimate mediators of toxic effects elicited by oxid
Metformin attenuates ventilator-induced lung injury
George Tsaknis, Ilias I Siempos, Petros Kopterides, Nikolaos A Maniatis, Christina Magkou, Matina Kardara, Stefania Panoutsou, Anastasia Kotanidou, Charis Roussos, Apostolos Armaganidis
Critical Care , 2012, DOI: 10.1186/cc11439
Abstract: Twenty-four rabbits were randomly assigned to pretreatment with metformin (250 mg/Kg body weight/day per os) or no medication for two days. Explanted lungs were perfused at constant flow rate (300 mL/min) and ventilated with injurious (peak airway pressure 23 cmH2O, tidal volume ≈17 mL/Kg) or protective (peak airway pressure 11 cmH2O, tidal volume ≈7 mL/Kg) settings for 1 hour. Alveolar capillary permeability was assessed by ultrafiltration coefficient, total protein concentration in bronchoalveolar lavage fluid (BALF) and angiotensin-converting enzyme (ACE) activity in BALF.High-pressure ventilation of the ex-vivo lung preparation resulted in increased microvascular permeability, edema formation and microhemorrhage compared to protective ventilation. Compared to no medication, pretreatment with metformin was associated with a 2.9-fold reduction in ultrafiltration coefficient, a 2.5-fold reduction in pulmonary edema formation, lower protein concentration in BALF, lower ACE activity in BALF, and fewer histological lesions upon challenge of the lung preparation with injurious ventilation. In contrast, no differences regarding pulmonary artery pressure and BALF total cell number were noted. Administration of metformin did not impact on outcomes of lungs subjected to protective ventilation.Pretreatment with metformin preserves alveolar capillary permeability and, thus, decreases the severity of ventilator-induced lung injury in this model.Despite its firmly established role as a fundamental life-support modality for critically ill patients, mechanical ventilation (MV) may elicit ventilator-induced lung injury (VILI), which is characterized by alveolar edema and hemorrhage. Recognized mechanisms of VILI include alveolar over-distention by high tidal volumes (volutrauma) and cyclic opening and closing of alveoli (atelectrauma), which operate in concert to trigger inflammatory processes (biotrauma), oxidant/antioxidant imbalance, intra-alveolar coagulation and disturbances
Early apoptosis of blood monocytes in the septic host: is it a mechanism of protection in the event of septic shock?
Evangelos J Giamarellos-Bourboulis, Christina Routsi, Diamantis Plachouras, Vassiliki Markaki, Maria Raftogiannis, Dimitrios Zervakis, Vassilios Koussoulas, Stylianos Orfanos, Anastasia Kotanidou, Apostolos Armaganidis, Charis Roussos, Helen Giamarellou
Critical Care , 2006, DOI: 10.1186/cc4921
Abstract: Blood monocytes were isolated from 90 patients with septic syndrome due to ventilator-associated pneumonia on days 1, 3, 5 and 7 from the initiation of symptoms. Apoptosis was defined after incubation with annexin-V-fluorescein isothiocyanate and propidium iodine and reading by a flow cytometer. The function of first-day monocytes was evaluated from the concentrations of tumour necrosis factor alpha (TNFα) and IL-6 in supernatants of cell cultures after triggering with endotoxins. TNFα, IL-6 and IL-8 were estimated in serum by an enzyme immunoassay.Mortality rates of patients with apoptosis ≤50% compared with patients with apoptosis >50% were 49.12% and 15.15%, respectively (P < 0.0001). Kaplan-Meier analysis showed a 28-day survival benefit in patients with septic shock and monocyte apoptosis >50% compared with those patients with apoptosis ≤50% (P = 0.0032). Production of IL-6 by monocytes on the first day by patients with apoptosis ≤50% was similar compared with monocytes isolated from healthy controls. Serum concentrations of TNFα were higher in patients with monocyte apoptosis ≤50% and septic shock compared with patients with apoptosis >50% on day 7; similar findings occurred for serum IL-6 on days 1 and 7 and for serum IL-8 on days 1 and 5.Early apoptosis of monocytes upon presentation of clinical signs of sepsis is connected to a favourable outcome. These findings are of particular importance for the patient with septic shock, where they might constitute a mechanism of pathogenesis.Apoptotic cascade is a process already described to supervene during the evolution of sepsis in lymphocytes, in tissue macrophages and in intestinal epithelia, and it is connected to organ dysfunction [1]. Although data for the apoptosis of cells of the adaptive immune system are available, little evidence exists for the implication of the innate immune system [2]. The need for knowledge in that field is further aggravated by the central role of monocytes in the pathogenesis of sep
Static and dynamic mechanics of the murine lung after intratracheal bleomycin
Effrosyni D Manali, Charalampos Moschos, Christina Triantafillidou, Anastasia Kotanidou, Ioannis Psallidas, Sophia P Karabela, Charis Roussos, Spyridon Papiris, Apostolos Armaganidis, Georgios T Stathopoulos, Nikolaos A Maniatis
BMC Pulmonary Medicine , 2011, DOI: 10.1186/1471-2466-11-33
Abstract: Single intratracheal injections of saline (50 μL) or bleomycin (2 mg/Kg in 50 μL saline) were administered to C57BL/6 (n = 40) and Balb/c (n = 32) mice. Injury/fibrosis score, tissue volume density (TVD), collagen content, airway resistance (RN), tissue damping (G) and elastance coefficient (H), hysteresivity (η), and area of pressure-volume curve (PV-A) were determined after 7 and 21 days (inflammation and fibrosis stage, respectively). Statistical hypothesis testing was performed using one-way ANOVA with LSD post hoc tests.Both C57BL/6 and Balb/c mice developed weight loss and lung inflammation after bleomycin. However, only C57BL/6 mice displayed cachexia and fibrosis, evidenced by increased fibrosis score, TVD, and collagen. At day 7, PV-A increased significantly and G and H non-significantly in bleomycin-exposed C57BL/6 mice compared to saline controls and further increase in all parameters was documented at day 21. G and H, but not PV-A, correlated well with the presence of fibrosis based on histology, TVD and collagen. In Balb/c mice, no change in collagen content, histology score, TVD, H and G was noted following bleomycin exposure, yet PV-A increased significantly compared to saline controls.Lung dysfunction in the bleomycin model is more pronounced during the fibrosis stage rather than the inflammation stage. Forced oscillation mechanics are accurate indicators of experimental bleomycin-induced lung fibrosis. Quasi-static PV-curves may be more sensitive than forced oscillations at detecting inflammation and fibrosis.Pulmonary fibrosis (PF), the progressive destruction of functional lung parenchyma and its conversion to scar tissue, can lead to severe decline in lung function, dyspnoea and death [1-3]. Among the various methods available to model PF in laboratory animals, the bleomycin model is the most widely used. Systemic or local pulmonary administration of bleomycin elicits an initial inflammatory reaction, followed by fibrosis at later time-points [4-
Inhaled activated protein C protects mice from ventilator-induced lung injury
Nikolaos A Maniatis, Eleftheria Letsiou, Stylianos E Orfanos, Matina Kardara, Ioanna Dimopoulou, Georgios Nakos, Marilena E Lekka, Charalambos Roussos, Apostolos Armaganidis, Anastasia Kotanidou
Critical Care , 2010, DOI: 10.1186/cc8976
Abstract: Inhaled APC (12.5 μg drotrecogin-α × 4 doses) or saline was given to tracheotomized C57/Bl6 mice starting 20 min prior to initiation of injurious mechanical ventilation with tidal volume 25 mL/Kg for 4 hours and then hourly thereafter; control groups receiving inhaled saline were ventilated with 8 mL/Kg for 30 min or 4 hr. We measured lung function (respiratory system elastance H), arterial blood gases, surrogates of vascular leak (broncho-alveolar lavage (BAL) total protein and angiotensin-converting enzyme (ACE)-activity), and parameters of inflammation (BAL neutrophils and lung tissue myeloperoxidase (MPO) activity). Morphological alterations induced by mechanical ventilation were examined in hematoxylin-eosin lung tissue sections. The activation status of ERK was probed in lung tissue homogenates by immunoblotting and in paraffin sections by immunohistochemistry. The effect of APC on ERK signaling downstream of the thrombin receptor was tested on A549 human lung epithelial cells by immunoblotting. Statistical analyses were performed using ANOVA with appropriate post-hoc testing.In mice subjected to VILI without APC, we observed hypoxemia, increased respiratory system elastance and inflammation, assessed by BAL neutrophil counts and tissue MPO activity. BAL total protein levels and ACE activity were also elevated by VILI, indicating compromise of the alveolo-capillary barrier. In addition to preserving lung function, inhaled APC prevented endothelial barrier disruption and attenuated hypoxemia and the inflammatory response. Mechanistically, we found a strong activation of ERK in lung tissues by VILI, which was prevented by APC, suggestive of pathogenetic involvement of the Mitogen-Activated Kinase pathway. In cultured human lung epithelial cells challenged by thrombin, APC abrogated the activation of ERK and its downstream effector, cytosolic Phospholipase A2.Topical application of APC by inhalation may effectively reduce lung injury induced by mechanical ventila
The Role of Cardiopulmonary Exercise Test in IPF Prognosis
Christina Triantafillidou,Effrosyni Manali,Panagiotis Lyberopoulos,Likourgos Kolilekas,Konstantinos Kagouridis,Sotirios Gyftopoulos,Konstantinos Vougas,Anastasia Kotanidou,Manos Alchanatis,Anna Karakatsani,Spyros A. Papiris
Pulmonary Medicine , 2013, DOI: 10.1155/2013/514817
Abstract: Background. In IPF, defects in lung mechanics and gas exchange manifest with exercise limitation due to dyspnea, the most prominent and disabling symptom. Aim. To evaluate the role of exercise testing through the 6MWT (6-minute walk test) and CPET (cardiopulmonary exercise testing) in the survival of patients with IPF. Methods. This is a prospective, observational study evaluating in 25 patients the relationship between exercise variables through both the 6MWT and CPET and survival. Results. By the end of the observational period 17 patients were alive (33% mortality). Observation ranged from 9 to 64 months. VE/VCO2 slope (slope of relation between minute ventilation and CO2 production), VO2 peak/kg (peak oxygen consumption/kg), VE/VCO2 ratio at anaerobic threshold, 6MWT distance, desaturation, and DLCO% were significant predictors of survival while VE/VCO2 slope and VO2 peak/kg had the strongest correlation with outcome. The optimal model for mortality risk estimation was VO2 peak/kg + DLCO% combined. Furthermore, VE/VCO2 slope and VO2 peak/kg were correlated with distance and desaturation during the 6MWT. Conclusion. The integration of oxygen consumption and diffusing capacity proved to be a reliable predictor of survival because both variables reflect major underlying physiologic determinants of exercise limitation. 1. Introduction Idiopathic pulmonary fibrosis (IPF) is an irreversibly progressive lung disease with substantial morbidity and mortality. No effective pharmacological treatment has been established so far [1]. Nonetheless, as research concerning IPF develops, we realize the heterogeneity of this disease which defines final prognosis [1]. Several retrospective longitudinal studies suggest a median survival time of 2 to 3 years from the time of diagnosis; nevertheless, more recent data suggest that this could be an underestimate [2]. Thus, defining prognosis remains difficult but it is of critical clinical importance. Many prognostic factors of disease severity and outcome have been studied in IPF, either at baseline or at serial measurements over time [3]. Clinical predictors include age, gender, smoking status, dyspnea, pulmonary hypertension, and comorbidities such as emphysema [2, 4–7]. Imaging studies have shown that the overall extent of fibrosis on high-resolution computerized tomography also correlates with survival [2, 8]. Regarding pathologic predictors, the fibroblastic foci profusion has been shown in some studies to predict survival while not in others [9, 10]. Physiologic indices as predictors of survival are more extensively
Letter to Editor  [PDF]
Anastasia Maggina
Open Journal of Accounting (OJAcct) , 2013, DOI: 10.4236/ojacct.2013.24013
Abstract: Letter to Editor
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