Реферат
BackgroundSARS-CoV-2(Severe acute respiratory syndrome coronavirus 2) has been circulating worldwide for three years. It mainly causes upper respiratory tract infection, which can manifest as pulmonary infection and even respiratory distress syndrome in severe cases. Different autoantibodies can be detected in patients infected with COVID-19.ObjectivesTo explore autoantibodies related to rheumatic diseases after COVID-19 infection.MethodsNinety-eight inpatients were tested for antinuclear antibodies (ANA), antibodies to extractable nuclear antigens(ENA), anti-neutrophil cytoplasmic antibodies（ANCA), anticardiolipin antibodies,a-β2GPI (IgG/IgM). They were from a tertiary hospital in Guangzhou during the COVID-19 epidemic. Data were described statistically.ResultsNinety-eight hospitalized patients were tested for relevant antibodies. The average age was 50.64±19.54;67 (68.4%) were male, 64 (65.3%) were COVID-19 positive, 90 (90.9%) had rheumatic diseases, and 56 of them were COVID-19 positive patients with rheumatic diseases.There were 76 patients tested for antinuclear antibodies;29 （38.16%）were negative, 18 （23.68%）had a 1/80 titre, and 29（28.16%） had a titre greater than 1:80. The 31 covid patients were positive for ANA. In the high-titer group, 19 patients with rheumatic diseases were positive for COVID-19, and 12 patients had an exacerbation of the rheumatic diseases (6 of whom had previously had pulmonary fibrosis). Of 31 covid patients, only two were non-rheumatic patients, and both were elderly, aged 85 and 100, respectively.Fifty-six patients had ENA results, and 29 for positive antibodies, 8 for ds-DNA antibodies, 2 for anti-Sm antibodies, 6 for anti-nucleosome antibodies, 12 for anti-U1RNP antibodies, 2 for anti-Scl-70 antibodies, 12 for anti-SS-A antibodies, 3 for anti-mitochondrial M2 antibodies, 2 for anti-centromere antibodies, 1 for anti-Po antibodies, and one for anti-Jo-1 antibody. All 56 patients had rheumatic diseases, and no new patients were found.There were 62 patients with ANCA data. P-ANCA was positive in 12 cases(19.35%), and MPO-ANCA was positive in 2 cases. An 85-year-old non-rheumatic COVID-19 patient was P-ANCA positive. She had a history of hypertension, colon cancer, CKD3, coronary heart disease, and atrial flutter.In the anticardiolipin antibodies group, there were 62 patients;only 6 were positive, and 2 were rheumatic patients infected with COVID-19. Antiphospholipid antibodies were detected in 33 patients, and a-β2GPI was tested in one patient, an 82-year-old COVID-19 patient with gout, diabetes, and cerebral infarction in the past. We did not find a statistical difference in the above results.ConclusionWe have not found a correlation between SARS-CoV-2 and serum autoantibodies of rheumatic immune diseases. It needs large samples and an extended follow-up to research.AcknowledgementsThis work was supported by Scientific and Technological Planning Project of Guangzhou City [202102020150], Guangdong Provincial Basic and Applied Basic Research Fund Project [2021A1515111172], National Natural Science Foundation of China Youth Fund [82201998] and Third Affiliated Hospital of Sun Yat-Sen University Cultivating Special Fund Project for National Natural Science Foundation of China [2022GZRPYQN01].Disclosure of Interestsone declared.
Реферат
Smoking is a significant social problem threatening the population's health, especially during the coronavirus pandemic. Due to the problem's urgency, we present a clinical case of SARS-CoV-2 infection in a patient with 10 years of smoking and concomitant chronic obstructive pulmonary disease (chronic bronchitis and peribronchial pneumosclerosis). Patient L.K., 42 years old, on 13.10.2022, was hospitalized for several hours at the Emergency Hospital of the Ministry of Health of Chuvashia (Cheboksary) with a severe new coronavirus infection. Secondary diagnosis: Chronic obstructive pulmonary disease Case history: for about two to three weeks, the patient noted an increase in body temperature to 37.2-37.4 degreeC and a cough. He has smoked for about 10 years, 1 pack per day. Computed tomography showed signs of bilateral COVID-associated pneumonitis, alveolitis with 85% involvement and consolidation sites, signs of chronic bronchitis, and peribronchial pneumosclerosis. The diagnosis of COVID-19 was confirmed by a polymerase chain reaction in a nasopharyngeal smear. The NEWS2 score was 9. After the treatment started, the patient died. Histological examination showed perivascular sclerosis, peribronchial pneumosclerosis, atrophic changes in the ciliated epithelium, and structural and functional alteration of the bronchial mucosa. In addition, areas of hemorrhage and inflammatory infiltrate in the bronchial wall were found. Coronavirus is known not to cause bronchitis but bronchiolitis. In the presented case, the patient showed signs of transition of bronchitis to the acute stage. Therefore, it can be assumed that the coronavirus acts as a complicating factor. In addition to the described changes, signs of viral interstitial pneumonia, pulmonary edema, and early development of acute respiratory distress syndrome were identified.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
Реферат
The coronavirus SARS-CoV-2 was detected in isolates of pneumonia patients in January 2020. The virus cannot multiply extracellularly but requires access to the cells of a host organism. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as a receptor, to which it docks with its spikes. ACE2 belongs to the renin angiotensin system (RAS), whose inhibitors have been used for years against high blood pressure. Renin is an endopeptidase that is predominantly formed in the juxtaglomerular apparatus of the kidney and cleaves the decapeptide angiotensin I (Ang I) from angiotensinogen. Through the angiotensin-converting enzyme (ACE), another 2 C-terminal amino acids are removed from Ang I, so that finally the active octapeptide angiotensin II (Ang II) is formed. The biological effect of Ang II via the angiotensin II receptor subtype 1 (AT1-R) consists of vasoconstriction, fibrosis, proliferation, inflammation, and thrombosis formation. ACE2 is a peptidase that is a homolog of ACE. ACE2 is predominantly expressed by pulmonary alveolar epithelial cells in humans and has been detected in arterial and venous endothelial cells. In contrast to the dicarboxy-peptidase ACE, ACE2 is a monocarboxypeptidase that cleaves only one amino acid from the C-terminal end of the peptides. ACE2 can hydrolyze the nonapeptide Ang-(1-9) from the decapeptide Ang I and the heptapeptide Ang-(1-7) from the octapeptide Ang II. Ang-(1-7) acts predominantly antagonistically (vasodilatory, anti-fibrotic, anti-proliferative, anti-inflammatory, anti-thrombogenetically) via the G protein-coupled Mas receptor to the AT1-R-mediated effects of Ang II. In the pathogenesis of COVID-19 infection, it is therefore assumed that there is an imbalance due to overstimulation of the AT1 receptor in conjunction with a weakening of the biological effects of the Mas receptor.Copyright © 2022 Dustri-Verlag Dr. K. Feistle.
Реферат
BackgroundThe main systemic sclerosis (SSc) manifestations are skin thickening, microangiopathy and ischemic changes in tissues, fibrotic damage to the lungs, heart, kidneys, and digestive system, arthritis, and myopathy. Acute phase reactants (APR) like erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) reflect inflammation activity in various inflammatory conditions. Ferritin is a protein bound to iron;low serum ferritin indicates iron deficiency and/or anemia. Instead, high ferritin levels are associated with inflammatory and non-inflammatory conditions such as dermatomyositis, pulmonary fibrosis, lupus, systemic COVID-19, vasculitis, tissue damage, thromboembolic complications, and metastatic cancer. The possible role of ferritin in SSc as APR is unclear.ObjectivesWe aimed to assess whether ferritin levels can reflect the severity of SSc and predict the outcome.Methods241 files of SSc patients with information on serum ferritin level (ferritin over 300 mg/dL is considered elevated) who visited the Rambam Rheumatology Institute in the years 2004-2021were used for retrospective analysis. Patients' demographic, clinical, laboratory, imaging, and respiratory function data were collected from electronic hospital files. Statistics included Student's T-test, Pearson's chi-squared test, and Kaplan-Meier curve;statistical significance was determined as p<0.05.Results36 patients (FerEl-SSc) had elevated ferritin values;the rest (n=205) represented the second group (FerNor-SSc). Significant differences were seen in gender (male 44.4% - 15.6%), disease duration (4.56 - 7.7 years), modified Rodnan skin score (12.3 - 6.9), as well as in incidence of lung (65.7% - 38.7%), heart (51.4% - 21.1%), and renal (28.6% - 5.9%) involvement. Increased ferritin correlated with elevated ESR, CRP, creatinine, creatine kinase, troponin, and reduced hemoglobin, impaired pulmonary function tests and reduced left ventricular ejection fraction on echocardiography. Patients with elevated ferritin had a significant increase in mortality rates (52.8% and 35.1%) and non-significant reduction in survival.ConclusionOur study demonstrated that ferritin has a potential as a sensitive marker for SSc severity in term of skin thickening, vital organ complications, and mortality. The ferritin test is simple and inexpensive, it can add to the complex SSc assessment and contribute to treatment decision-making in complicated SSc.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
Реферат
Background: Implantation of the double J stent is a common procedure in urology. The function of this device is to maintain the flow of urine from the ureteropelvic junction to the urinary bladder when the ureter is blocked or partially blocked for some reason. Once in place, the stent may cause low back pain, hematuria, symptoms of urinary irritation, a reduction in labor capacity, infection and calcification which are side effects that are easy to manage. However, severe complications can occur, such as the insertion of the stent into the circulatory system, such as the vena cava, which, although uncommon, is one of the most severe and difficult to manage. This work reports the case of a patient with the accidental insertion of a double J stent into the inferior vena cava.Case Description: An 80-year-old female patient with repeated urinary tract infections using a double J stent due to stenosis of the right distal ureter distal presenting retroperitoneal fibrosis secondary to previous radiotherapy. The patient had Lynch syndrome, ovarian and uterine cancer, colorectal cancer, and nephrolithiasis. She had been submitted to multiple previous surgeries. Due to the possibility of viral infection by COVID 19, chest computed tomography was performed, which suggested the insertion of the double J stent in the inferior vena cava, confirmed by abdominal computed tomography. As the distal end of the stent was within the bladder, the decision was made to remove the stent by cystoscopy, with the implantation of a new stent using fluoroscopic control for the confirmation of its trajectory. No intraoperative or postoperative complications occurred and the patient is currently in outpatient follow-up.Conclusions: Situations such as this require caution during the implantation of the drainage device, with the occurrence of resistance indicating the need to discontinue the procedure and perform a new assessment with imaging exams. No intraoperative or postoperative complications occurred and the patient is currently in outpatient follow-up.
Реферат
Introduction/Objective Post-COVID-19 cholangiopathy is a novel entity first noted in patients recovering from critical COVID-19 infection. Since its initial description in May 2021, all cases reported to date have been in patients with a history of critical COVID-19, defined as requiring ICU admission, the development of respiratory or circulatory failure requiring intubation or ECMO, or vasopressor support. Here we report three cases of post-COVID-19 cholangiopathy arising in patients who recovered from non-severe COVID-19. Methods/Case Report Six cases of COVID-19-related cholangiopathy were identified by retrospective review, three of which involved patients who verifiably did not develop critical COVID-19. Histology slides for each case were reviewed and all showed features of secondary sclerosing cholangitis. Patient 1 is a 41yo female who developed COVID-19 after liver transplant (LT). Despite administration of monoclonal antibodies, she required re-transplantation 6 weeks later. Explant histology showed bile infarcts, severe hepatocytic and canalicular cholestasis, ductular reaction, organizing portal vein thrombi, and necrotic bile ducts accompanied by bile lakes. Patient 2 is a 47yo male with alcoholic cirrhosis who was diagnosed with COVID-19 at the time of LT workup, and underwent LT 90 days later. In addition to alcohol-related cirrhosis, explant histology showed dilated bile ducts with periductal fibrosis, as well as severe ductular reaction with proliferating ductules containing thick, inspissated bile. Patient 3 is a 54yo male with history of LT for PSC who developed mild COVID-19 five years after LT. Allograft function subsequently worsened and biopsy 6 months later showed bile duct damage and loss of ~35% of bile ducts;repeat biopsy 14 months after his COVID diagnosis showed periportal fibrosis with edema, ductular reaction, marked hepatocellular and canalicular cholestasis, and ductopenia with loss of 60% bile ducts. Average time between COVID-19 diagnosis and onset of COVID-related cholangiopathy was 3 months (range: 6 weeks-6 months). These patients were also all immunocompromised with two due to prior LT and one being cirrhotic. Results (if a Case Study enter NA) NA. Conclusion Although previously reported only in patients with severe COVID-19, the cases described represent the first evidence that cholangiopathy, manifested by sclerosing cholangitis, can arise even in patients who were not critically ill, although this may require an immunocompromised state to develop.
Реферат
Introduction: Variants in PPP1R13L are associated with severe childhood-onset cardiomyopathy resulting in rapid progression to death or cardiac transplantation. PPP1R13L is proposed to encode a protein that limits the transcriptional activity of the NFkappaB pathway leading to elevated IL-1, IL-6, and TNF-alpha production in murine models. Optimal medical management for PPP1R13L-related cardiomyopathy is unknown. Here we report usage of a targeted anti-IL-1 immuno-modulatory therapy resulting in cardiac stabilization in a pediatric patient with congenital cardiomyopathy secondary to PPP1R13L variants. Case Report: A 4-year-old boy presented acutely with fever in the setting of persistent abdominal pain, vomiting, fatigue, and decreased appetite for two months following a mild COVID-19 related illness. Echocardiogram revealed severely depressed biventricular systolic function with an ejection fraction of 30%. Due to acute decompensated heart failure symptoms with hemodynamic instability, he was intubated and placed on continuous inotropic infusions with aggressive diuresis. Cardiac MRI demonstrated extensive subepicardial to near transmural fibrosis by late gadolinium enhancement in right and left ventricles. An implantable cardioverter-defibrillator (ICD) was placed due to frequent runs of polymorphic non-sustained ventricular tachycardia. Testing for viral pathogens was positive for rhino/enterovirus. Initial genetic testing was non-diagnostic (82-gene cardiomyopathy panel) but given the patient's significant presentation whole genome sequencing was pursued that showed two separate PPP1R13L variants in trans (c.2167A>C,p.T723P and c.2179_2183del,p. G727Hfs*25, NM_006663.4). Patient serum cytokine testing revealed elevations in IL-10 (4.7 pg/mL) and IL-1beta (20.9 pg/mL). Given the patient's tenuous circumstances and concern for continued progression of his cardiac disease, a trial of IL-1 inhibition via anakinra dosed at 3 mg/kg or 45 mg daily was initiated following hospital discharge. With approximately 6 months of therapy, the patient's cardiac function is stable with normalization of IL-10 and IL-1beta serum levels. Notably, the ventricular arrhythmia decreased after initiation of anakinra with no ICD shocks given. Therapy overall has been well tolerated without infectious concerns. Conclusion(s): In patients with PPP1R13L-related cardiomyopathy, immuno-modulatory therapies should be considered in an attempt to slow cardiac disease progression.Copyright © 2023 Elsevier Inc.
Реферат
Reaching a proper diagnosis for critically ill patients is like collecting pieces of puzzle and bed side lung ultrasound (LUS) becomes a crucial piece complementary to clinical and laboratory pieces. It is a bed side, real time tool for diagnosis of patients in ICU who are critical to be transferred to radiology unit especially in Covid-19 pandemic with risk of infection transmission. The aim was to evaluate the accuracy of lung ultrasound in assessment of critically ill patients admitted to Respiratory Intensive Care Unit (RICU), moreover to assess its diagnostic performance in different pulmonary diseases as compared to the gold standard approach accordingly. This observational prospective (cross sectional) study with a total 183 patients who met the inclusion criteria,were selected from patients admitted at the RICU;Chest Department, Zagazig University Hospitals, during the period from September 2019 to September 2021. LUS examination was performed to diagnose the different pulmonary diseases causing RF. All cases were examined by LUS on admission. From a total 183 patients, 111 patients 60.7% were males and 72 patients 39.3% were females, with a mean age of 56+/-12.77 years, 130 patients were breathing spontaneously received conservative management with O2 therapy, 32 patients needed NIV while 21 patients needed IMV with ETT. Exacerbated COPD was the most common disease finally diagnosed followed by bacterial pneumonia, exacerbated ILD, post Covid-19 fibrosis and pulmonary embolism in32, 29,27, 19 and 11 patients respectively with corresponding diagnostic accuracy of LUS 97.3%, AUC=0.943, 93.9% (AUC=0.922), 96.7%(AUC=0.920), 97.8%, AUC=0.895, and 97.8% respectively, while Covid-19 pneumonia was the final diagnosis in 8 patients with LUS diagnostic accuracy of 97.8% (AUC=0.869) with no statistical significant difference p-value=0.818 with bacterial pneumonia in distribution of US profiles. A profile was the commonest detected US profile among the studied patients followed by B profile, C profile, A/B profile and A' profile in 37.2%, 24.6%, 15.8% 4.9%, and 3.8% of cases respectively. Bed side LUS has a reliable, valuable diagnostic performance when integrated with clinical and laboratory data for the diagnosis of most pulmonary diseases in RICU.Copyright © 2023, Colegio de Farmaceuticos de la Provincia de Buenos Aires. All rights reserved.
Реферат
Aim. To determine the prevalence and show the features of the development of newly diagnosed heart failure (HF) in patients with dyspnea after a coronavirus disease 2019 (COVID-19). Material and methods. This clinical prospective observational study was conducted during 2020-2022. The study consecutively included 368 outpatients with shortness of breath, who applied to the clinic. Depending on the presence of prior COVID-19, the patients were divided into 2 groups: the first group consisted of 205 patients with shortness of breath after COVID-19, the second group - 163 patients without prior COVID-19. All patients underwent a clinical examination within 3 days after presentation with an assessment of outpatient records and other medical documents for the differential diagnosis of dyspnea. The severity of dyspnea was determined using the Modified Medical Research Council Dyspnoea Scale (mMRC). The diagnosis of HF was verified in accordance with the 2020 Russian Society of Cardiology guidelines and in some cases reclassified in accordance with the 2021European Society of Cardiology guidelines. For further analysis, 2 subgroups of patients with HF were identified depending on the presence and absence of prior COVID-19. The subgroup analysis excluded patients with acute heart failure, acute illness, and conditions requiring hospitalization and/or intensive care. Results. Among 368 patients who presented to the clinic with dyspnea during 2020-2022, 205 patients (55,7%) had COVID-19. The average period of treatment after COVID-19 was 3,5 [1,5;22,4] months. Patients after COVID-19 applied earlier after the onset of dyspnea, which is associated with higher mMRC score. The prevalence of HF among patients with shortness of breath after COVID-19 was significantly higher than in patients without this pathology in history, and amounted to 19,0% vs 9,8% (p=0,021). Prior COVID-19 increased the relative risk (RR) of HF in patients with shortness of breath by 1,7 times. RR for HF in systolic blood pressure >140 mm Hg increased by 1,9 times, while in diastolic blood pressure >90 mm Hg - by 1,9 times, with the development of a hypertensive crisis - by 28%, with a heart rate >80 bpm at rest - by 1,4 times, with the development of type 2 diabetes - by 31%, in the presence of pulmonary fibrosis - by 2,3 times. Patients with shortness of breath after COVID-19 had more severe HF, both according to clinical tests and according to the blood concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP), mainly with the preserved ejection fraction (EF) with a higher prevalence of left atrial (LA) enlargement in combination with a decrease in right ventricular (RV) systolic function and its dilatation. In patients after COVID-19 in the presence of chronic kidney disease, the RR for HF increased by 4,5 times;in the presence of C-reactive protein >4 mg/l - by 1,6 times. Conclusion. Every fifth patient with shortness of breath 3,5 months after COVID-19 had more severe HF, both according to clinical tests and according to blood NT-proBNP concentration, mainly with preserved EF with a higher prevalence of LA increase in combination with a decrease in RV systolic function and its dilatation. The risk of HF is interrelated with the female sex and multiple comorbidities.Copyright © 2023, Silicea-Poligraf. All rights reserved.
Реферат
The study is devoted to a comparative analysis and retrospective evaluation of laboratory and instrumental data with the severity of lung tissue damage in COVID-19 of patients with COVID-19. An improvement was made in the methodology for interpreting and analyzing dynamic changes associated with COVID-19 on CT images of the lungs. The technique includes the following steps: pre-processing, segmentation with color coding, calculation and evaluation of signs to highlight areas with probable pathology (including combined evaluation of signs). Analysis and interpretation is carried out on the emerging database of patients. At the same time the following indicators are distinguished: the results of the analysis of CT images of the lungs in dynamics;the results of the analysis of clinical and laboratory data (severity course of the disease, temperature, saturation, etc.). The results of laboratory studies are analyzed with an emphasis on the values of the main indicator - interleukin-6. This indicator is a marker of significant and serious changes characterizing the severity of the patient's condition. © 2023 IEEE.
Реферат
Introduction/Objective Since the emergence of a novel SARS-CoV-2 virus caused coronavirus disease 2019 (COVID-19), a great number of autopsy studies have been published. However, histopathologic studies focused on pulmonary barotrauma are very rare. Here we report an autopsy confined to the lungs on a young COVID-19 patient. Methods/Case Report The patient was a 37-year-old male, non-smoker, with no significant past medical history, and a body mass index of 24.1, who presented with shortness of breath and cough. A computerized tomography (CT) showed features of atypical pneumonia. The main abnormal laboratory data included elevated partial thromboplastin time, fibrinogen, and D-Dimer. The patient had been on mechanical ventilation for 35 days, and was complicated by recurrent pneumothoraces, hypotension, and worsening hypoxia. An autopsy limited to the lungs was performed after the patient expired. Grossly, the lungs showed increased weight, adhesions on visceral pleural surface, patchy consolidation and dilated subpleural cysts. Histological examination revealed cystically dilated/remodeled airspaces with extensive coagulative necrosis, focal alveolar hemorrhage and edema, focal confluent fibrosis, and subpleural blebs. Fresh fibrinous thrombi were seen in small- and medium-sized vessels. Viral cytopathic changes or significant inflammation were not observed. The findings in the lungs were consistent with barotrauma in COVID-19. Results (if a Case Study enter NA) NA. Conclusion This case demonstrates various histopathologic changes of the lungs in a previously healthy and young COVID-19 patient with prolonged hospital course of mechanical ventilation. The features of diffuse alveolar damage with inflammation usually seen in the early stage of barotrauma are not identified. Our findings in the lungs may represent the histopathologic characteristics of the later stage of barotrauma in COVID-19.
Реферат
Background: Neutrophil extracellular traps (NETs) are composed of processed chromatin bound to granular and selected cytoplasmic proteins and released by neutrophils. NETs consist of smooth filaments composed of stacked nucleosomes. Fully hydrated NETs have a cloud-like appearance and occupy a space 10-15-fold larger than the volume of the cells they originate from. DNases are the enzymes that cleave extracellular DNA including NETs. Together with their protective role in microbial infections, NETs are involved in multiple pathological processes and represent key events in a variety of pathologies including cancer, autoimmunity, and cardiovascular disease. Sites of NETs concentration are dangerous for the host if the process of NETs formation becomes chronic or the mechanism of NETs removal does not work. NETosis has been linked to the development of periodontitis, cystic fibrosis, type 2 diabetes, COVID-19 or rheumatoid arthritis as well as cancer progression. Purpose(s): Thus, the destruction of NETs is of primary significance in many pathologies. In our approach, we are focusing on mimicking one of the natural mechanisms of destroying excessive NETs by delivering deoxyribonuclease I to the specific site of pathological NETs accumulation by modifying the nanoparticles using an anti-nucleosome monoclonal antibody (2C5). The antibody is specific to nucleosomes and can recognize histones in NETs. DNase I is U.S. Food and Drug Administration (FDA)-approved active component and is commonly used in therapeutic methods of modern medicine for cystic fibrosis to clear extracellular DNA fibers in the lungs and systemic lupus erythematosus. Recent findings have also shown the effectiveness of DNase I in the digestion of NETs. However, the low serum stability and fast deactivation by environmental stimuli have been considered as the limiting factors for clinical applications of DNase I, which can be overcome by its targeted specific delivery in pharmaceutical nanocarriers. Method(s): In this study, we generate NETs in vitro using human neutrophils and HL-60 cells differentiated into granulocyte-like cells. We used interleukin-8, lipopolysaccharide from E.Coli (LPS), phorbol myristate acetate (PMA), and calcium ionophore A23187 (CI) to generate the NETs. We confirmed the specificity of 2C5 toward NETs by ELISA, which showed that it binds to NETs with the specificity like that for purified nucleohistone substrate. We further utilized that feature to create two delivery systems (liposomes and micelles) for DNAse I enzyme to destroy NETs, which was confirmed by staining NETs with SYTOX Green dye and followed by flow cytometric measurements and microscopic images. Conclusion(s): Our results suggest that 2C5 could be used to identify and visualize NETs and serve as a ligand for NET-targeted diagnostics and therapies. Also, we proved that our carrier can successfully deliver DNase to NETs to provide their degradation.
Реферат
Objectives: Death from SARS-CoV-2 pneumonia resulted from progressive respiratory failure in most patients. Whenever accessible, venovenous extracorporeal membrane oxygenation (VVECMO) was implemented to rescue patients with refractory hypoxemia. Reported mortality in this population reached values from 20 to 50 percent, but the direct causes of death were not so widely acknowledged. The aim of our study was to characterize mortality in patients treated with VVECMO support. Method(s): Retrospective review of a prospectively collected database in an ECMO referral centre. All patients with diagnosis of SARS-CoV-2 infection treated with VVECMO support were included. Survivors and nonsurvivors were compared using t-student and chi2 methods. A Cox regression analysis was performed to identify predictors of mortality at admission. Result(s): Ninety-three patients were included (29% female). Median age was 54+/-12 years, mean SOFA was 5.7+/-2.9 and SAPS II was 35.6+/-13.6. Hospital mortality was 24.7%. Main causes of death were septic shock in 39.1% (9 patients), irreversible lung fibrosis 30.4% (7 patients) and catastrophic hemorrhage in 4.3% (4 patients). End-of-life care measures (withdrawal or withholding) were adopted in 65.2% of non-survivals. Patients who died were older (55 vs 48 years, p<0.05), had longer disease course (19 vs 15.3 days, p<0.05), longer invasive mechanical ventilation course before cannulation (8.5 vs 5 days, p<0.05), lower static lung compliance (25.5 vs 31.8 mL/cmH2O, p<0.05) and were ventilated with lower PEEP (8 vs 10 cmH2O, p<0.05) on cannulation. On a Cox-regression model, only prone ventilation before cannulation (HR 9,7;CI 95% 1,4- 68,6;p<0.05) and SAPS II (HR 1.04;CI 95% 1,001- 1,083;p<0.05) predicted mortality. Conclusion(s): Mortality in patients with severe SARSCoV-2 pneumonia treated with VVECMO was exceedingly low in our study, when compared with other series. Only one-third died from progressive lung disease, which suggests that protocol improvement can further reduce mortality.
Реферат
Objectives The study compared the impact of the COVID pandemic on the Belgian people with Cystic Fibrosis (pwCF) with the international pwCF and the general Belgian population. Methods pwCF followed in a Belgian CF center were eligible. Their demographic and clinical outcome data was compared with the international pwCF (Carr et al, JCF 2022) and with the general Belgian population (epistat.sciensano.be/covid). CF registry annual data collections for 2020 and 2021 included if a test was performed for SARS-CoV-2 (by any specific method), and the respective result. Details on COVID symptoms and treatment were collected separately in a form from Global CF. Results Among the 1392 pwCF seen in 2020 and/or 2021, over half of the pwCF were tested for SARS CoV-2 (51% in 2020, 59% in 2021), similar for pwCF with or without a transplant (57% vs 54%). With similar positivity rate with or without transplant (13%), 179 pwCF had a positive result either in 2020 (50) or 2021 (141). This positivity rate was higher than in the general Belgian population (8.6%). Compared to the international pwCF, Belgian pwCF presented with more risk factors (transplant, age). Details and outcome are showed in tables below. Conclusion Belgian pwCF infected by SARS-CoV-2 tended to be less hospitalized but have more deaths than the international pwCF, in line with a higher transplant rate. While pwCF were on average younger, hospitalization was more frequent than for the general Belgian population, but death only if transplanted. [Formula presented]Copyright © 2023 European Cystic Fibrosis Society
Реферат
Lung cancer is the most common cancer in males and the second most common among females both in Europe and worldwide. Moreover, lung cancer is the leading cause of death due to cancer in males. The European region accounts for 23% of total cancer cases and 20% of cancer-related deaths. Relationships have been described between a number of infectious agents and cancers, but our knowledge of the role of viruses, both respiratory and systemic, in the pathogenesis of lung cancer is still rudimentary and has been poorly disseminated. In this chapter, we review the available evidence on the involvement of HPV, Epstein-Barr virus, HIV, cytomegalovirus and measles virus in the epidemiology and pathogenesis of lung cancer.Copyright © ERS 2021.
Реферат
Introduction: SARS-CoV-2 is responsible for the current global pandemic. SARS-CoV-2 infection underlies the novel viral condition coronavirus disease 2019 (COVID-19). COVID-19 causes significant pulmonary sequelae contributing to serious morbidities. The pathogenesis of COVID-19 is complex with a multitude of factors leading to varying levels of injury numerous extrapulmonary organs. This review of 124 published articles documenting COVID- 19 autopsies included 1,142 patients. Method(s): A PubMed search was conducted for COVID-19 autopsy reports published before March 2021 utilizing the query COVID-19 Autopsy. There was no restriction regarding age, sex, or ethnicity of the patients. Duplicate cases were excluded. Findings were listed by organ system from articles that met selection criteria. Result(s): Pulmonary pathology (72% of articles;866/1142 patients): diffuse alveolar damage (563/866), alveolar edema (251/866), hyaline membrane formation (234/866), type II pneumocyte hyperplasia (165/866), alveolar hemorrhage (164/866), and lymphocytic infiltrate (87/866). Vascular pathology (41% of articles;771/1142 patients): vascular thrombi (439/771)-microvascular predominance (294/439)-and inflammatory cell infiltrates (116/771). Cardiac pathology (41% of articles;502/1142 patients): cardiac inflammation (186/502), fibrosis (131/502), cardiomegaly (100/502), hypertrophy (100/502), and dilation (35/502). Hepatic pathology (33% of articles;407/1142 patients): steatosis (106/402) and congestion (102/402). Renal pathology (30% of articles;427/1142 patients): renal arteries arteriosclerosis (111/427), sepsis-associated acute kidney injury (81/427) and acute tubular necrosis (77/427). Conclusion(s): This review revealed anticipated pulmonary pathology, along with significant extrapulmonary involvement secondary to COVID-19, indicating widespread viral tropism throughout the human body. These diverse effects require additional comprehensive longitudinal studies to characterize short-term and long-term COVID-19 sequelae and inform COVID-19 treatment.
Реферат
Background/Objectives: We previously demonstrated that carrying a single pathogenic CFTR allele increases the risk for COVID-19 severity and mortality rate. We now aim to clarify the role of several uncharacterized rare alleles, including complex (cis) alleles, and in trans combinations. Method(s): LASSO logistic regression was used for the association of sets of variants, stratified by MAF, with severity. Immortalized cystic fibrosis bronchial epithelial cell lines and Fischer Rat Thyroid cells were transfected by plasmid carrying specific CFTR mutations. YFP-based assays were used to measure CFTR activity. Result(s): Here we functionally demonstrate that the rare (MAF=0.007) complex G576V/R668C allelemitigates the disease by a gain of function mechanism. Several novel CFTR ultra-rare (MAF <0.001) alleles were proved to have a reduced function;they are associated with disease severity either alone (single or complex alleles) or with another hypomorphic allele in the second chromosome, with a global reduction of CFTR activity between 40 to 72%. Conclusion(s): CFTR is a bidirectional modulator of COVID-19 outcome. At-risk subjects do not have open cystic fibrosis before viral infection and therefore are not easily recognisable in the general population unless a genetic analysis is performed. As the CFTR activity is partially retained, CFTR potentiator drugs could be an option as add-on therapy for at-risk patients.
Реферат
BACKGROUND: Thoracic computed tomography (CT) scan plays a role in detecting and assessing the progression of COVID-19. It can evaluate the response to the therapy given. In diagnosis, the CT scan of the chest may complement the limitations of reverse transcription polymerase chain reaction (RT-PCR). Several recent studies have discussed the importance of CT scans in COVID-19 patients with false-negative RT-PCR results. The sensitivity of chest CT scan in the diagnosis of COVID-19 is reportedly around 98%. AIM: This study aimed to determine the compatibility of CT scan of the thorax with RT-PCR in suspected COVID-19 patients. MATERIALS AND METHODS: This research was conducted in the Radiology Department of the Wahidin Sudirohusodo Hospital Makassar from April to December 2020 with 350 patients. The method used was a 2 x 2 table diagnostic test. RESULT(S): The study included 188 male patients (53.7%) and 162 female patients (46.2%). The most common age group was 46-65 years (35.4%). The most common types of lesions were ground-glass opacity (163 cases), consolidation (128 cases), and fibrosis (124 cases), mostly found in the inferior lobe with a predominantly peripheral or subpleural distribution. The sensitivity of the CT scan to the PCR examination was 86%, and the specificity was 91%. CONCLUSION(S): Thoracic CT scan was a good modality in establishing the diagnosis of COVID-19. CT scan of the chest with abnormalities could confirm the diagnosis in 88% of cases based on RT-PCR examination. It excluded the diagnosis in 91% based on the RT-PCR examination. The accuracy of the thoracic CT scan was 88% with RT-PCR as the reference value.Copyright © 2023 Sri Asriyani, Albert Alexander Alfonso, Mirna Muis, Andi Alfian Zainuddin, Irawaty Djaharuddin, Muhammad Ilyas.
Реферат
Objective. The prognosis value of fibrosis-4 score (FIB-4) in COVID-19 is controversial. Hence, we conducted a systematic review and meta-analysis to investigate the association between the FIB-4 index and COVID-19 disease progression. Methods. We performed meta-analysis using the PubMed, Embase, and Cochrane databases. A fixed- or random-effects model was used for evaluating heterogeneity. Results. Thirteen studies were included. The meta-analysis of unadjusted results showed that compared to lower FIB-4 index, patients with higher FIB-4 index had increased odds of mortality (OR=5.1, 95%CI 3.67-7.09;P<0.001), ICU admission (OR=2.32, 95%CI: 1.65-3.25, P<0.00001) and need for mechanical ventilator support (OR=3.51, 95%CI: 2.1-5.85, P<0.001). In addition, the meta-analysis of adjusted results showed patients with higher FIB-4 index was associated with increased risk of mortality (OR=3.01, 95%CI: 2.21-4.09, P<0.001) and need for mechanical ventilator support (OR=3.76, 95%CI: 2.08-6.82, P<0.001) compared to patients with lower FIB-4 index. Conclusion. This meta-analysis indicated that high FIB-4 index score was associated with the severity and mortality in COVID-19 infected patients.Copyright © 2022 by the Association of Clinical Scientists, Inc.