14 research outputs found
Prevalence of HBV/HCV Co-Infection and Associated Risk Factors in People Living with HIV
No full textImmune Thrombocytopenia in a Very Elderly Patient With Covid-19
No full textImmune thrombocytopenia (ITP) is an autoimmune disorder characterized by a decreased number of platelets and mucocutaneous bleeding. Many viruses have been identified as triggers of the autoimmune process, including human immunodeficiency virus (HIV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), parvovirus, rubella, and measles. Association with the new severe acute respiratory syndrome coronavirus, SARS-CoV-2 infection (Covid-19 infection) has been rarely reported. Here, we report the oldest case of ITP patient triggered by the novel coronavirus infection. He showed inadequate response to IVIG but responded to corticosteroids with no severe adverse events. Further studies are warranted to determine the optimal therapeutic strategies for ITP with the Covid-19 infection
Prevalence of Syphilitic Hepatitis Among HIV-Infected Patients in Istanbul, Turkey, a Region with an Increasing Incidence of Syphilis and HIV Infection
No full textRetrospective Evaluation of Twenty Seven Patients with Diabetic Foot Infection
No full textAim: This study analyzed diabetic foot infections (DFI) in patients who were followed up in our clinic
Evaluation of clinical outcomes of vaccinated and unvaccinated patients with hospitalization for COVID-19
No full textWe aimed to compare vaccinated and unvaccinated patients hospitalized with COVID-19 in terms of disease severity, need for intensive care unit (ICU) admission, and death. In addition, we determined the factors affecting the COVID-19 severity in vaccinated patients. Patients aged 18-65 years who were hospitalized for COVID-19 between September and December 2021 were retrospectively analyzed in three groups: unvaccinated, partially vaccinated, and fully vaccinated. A total of 854 patients were included. Mean age was 47.9 +/- 10.6 years, 474 patients (55.5%) were male. Of these, 230 patients (26.9%) were fully vaccinated, 97 (11.3%) were partially vaccinated, and 527 (61.7%) were unvaccinated. Of the fully vaccinated patients, 67% (n 5 153) were vaccinated with CoronaVac and 33% (n 5 77) were vaccinated with Pfizer-BioNTech. All patients (n 5 97) with a single dose were vaccinated with Pfizer-BioNTech. One hundred thirteen (13.2%) patients were transferred to ICU. A hundred (11.7%) patients were intubated and 77 (9.0%) patients died. Advanced age (P 5 0.028, 95% CI 5 1.00-1.07, OR 5 1.038) and higher Charlson Comorbidity Index (CCI) (P 3 (19.1 vs 5.8%, P < 0.01, OR 5 3.7). Therefore, the booster vaccine especially in individuals with comorbidities should not be delayed, since the survival expectation is low in patients with a high comorbidity index
Clinical and laboratory predictors of mortality in Staphylococcus aureus bacteremia
No full textAbstract This study aimed to describe the epidemiological and clinical features of patients admitted to non-intensive care hospital wards due to Staphylococcus aureus bacteremia (SAB) and to identify predictors of mortality to improve patient outcomes. This single-center retrospective study included hospitalized patients with SAB between 2016 and 2024. We retrieved clinical and microbiological data retrospectively from the electronic medical record system. The research comprised 356 patients with SAB. The 30-day and in-hospital mortality rates were 7.3% (n = 26) and 9.8% (n = 35), respectively. The multivariate analysis revealed neutrophil-to-lymphocyte ratio (NLR) (HR = 1.08; 95% CI = 1.02–1.13; p = 0.002), CRP (HR = 1.01; 95% CI = 1-1.02 ; p = 0.04), and albumin (HR = 0.83; 95% CI = 0.73-0.95; p = 0.008) as predictors for 30-day mortality. Pneumonia (HR = 15.03; 95% CI = 2.05–109.71; p = 0.008), leukemia (HR = 28.72; 95% CI = 1.56-525.92; p = 0.002), and sepsis (HR = 7.06; 95% CI = 1.02–48.53; p = 0.002) were identified as significant risk factors for mortality. Using the Cox regression analysis, age (HR: 1.05, CI:1.01–1.10, p = 0.01), leukemia (HR: 0.80, CI:0.71–0.90, p < 0.001), and low albumin level (HR: 11.76; CI:1.76–78.42, p = 0.01) were identified as independent risk factors affecting in-hospital mortality. We used the receiver operating characteristic (ROC) curve to predict the30-day mortality. The area under the ROC curve values were 0.619 (p = 0.044) for NLR, 0.692 (p = 0.001) for CRP, and 0.791 (p < 0.001) for albumin. The highest sensitivity and specificity at 30-day mortality were obtained from CRP and albumin, with a sensitivity of 65.4% and a specificity of 78.5% for albumin. Elevated NLR and CRP levels, along with decreased albumin levels, may predict poor clinical outcomes and could assist clinicians in optimizing the management of this bacterial infection. As a result, early diagnosis and appropriate antibiotic treatments are crucial in reducing mortality in SAB
Human genetic and immunological determinants of critical COVID-19 pneumonia
No full textCOVID Human Genetic Effort: Adem Karbuz, Adrian Gervais, Ahmad Abou Tayoun, Alessandro Aiuti, Alexandre Belot, Alexandre Bolze, Alexandre Gaudet, Anastasiia Bondarenko, Zhiyong Liu, András N. Spaan, Andrea Guennoun, Andres Augusto Arias, Anna M. Planas, Anna Sediva, Anna Shcherbina, Anna-Lena Neehus, Anne Puel, Antoine Froidure, Antonio Novelli, Aslınur Özkaya Parlakay, Aurora Pujol, Aysun Yahşi, Belgin Gülhan, Benedetta Bigio, Bertrand Boisson, Beth A. Drolet, Carlos Andres Arango Franco, Carlos Flores, Carlos Rodríguez-Gallego, Carolina Prando, Catherine M. Biggs, Charles-Edouard Luyt, Clifton L. Dalgard, Cliona O’Farrelly, Daniela Matuozzo, David Dalmau, David S. Perlin, Davood Mansouri, Diederik van de Beek, Donald C. Vinh, Elena Dominguez-Garrido, Elena W. Y. Hsieh, Emine Hafize Erdeniz, Emmanuelle Jouanguy, Esra Şevketoglu, Estelle Talouarn, Eugenia Quiros-Roldan, Evangelos Andreakos, Eystein Husebye, Fahad Alsohime, Filomeen Haerynck, Giorgio Casari, Giuseppe Novelli, Gökhan Aytekin, Guillaume Morelle, Gulsum Alkan, Gulsum Iclal Bayhan, Hagit Baris Feldman, Helen C. Su, Horst von Bernuth, Igor Resnick, Ingrid Bustos, Isabelle Meyts, Isabelle Migeotte, Ivan Tancevski, Jacinta Bustamante, Jacques Fellay, Jamila El Baghdadi, Javier Martinez-Picado, Jean-Laurent Casanova, Jeremie Rosain, Jeremy Manry, Jie Chen, John Christodoulou, Jonathan Bohlen, José Luis Franco, Juan Li, Juan Manuel Anaya, Julian Rojas, Junqiang Ye, K. M. Furkan Uddin, Kadriye Kart Yasar, Kai Kisand, Keisuke Okamoto, Khalil Chaïbi, Kristina Mironska, László Maródi, Laurent Abel, Laurent Renia, Lazaro Lorenzo, Lennart Hammarström, Lisa F. P. Ng, Lluis Quintana-Murci, Lucia Victoria Erazo, Luigi D. Notarangelo, Luis Felipe Reyes, Luis M. Allende, Luisa Imberti, Majistor Raj Luxman Maglorius Renkilaraj, Marcela Moncada-Velez, Marie Materna, Mark S. Anderson, Marta Gut, Marwa Chbihi, Masato Ogishi, Melike Emiroglu, Mikko R. J. Seppänen, Mohammed J. Uddin, Mohammed Shahrooei, Natalie Alexander, Nevin Hatipoglu, Nico Marr, Nihal Akçay, Oksana Boyarchuk, Ondrej Slaby, Ozge Metin Akcan, Peng Zhang, Pere Soler-Palacín, Peter K. Gregersen, Petter Brodin, Pierre Garçon, Pierre-Emmanuel Morange, Qiang Pan-Hammarström, Qinhua Zhou, Quentin Philippot, Rabih Halwani, Rebeca Perez de Diego, Romain Levy, Rui Yang, Şadiye Kübra Tüter Öz, Saleh Al Muhsen, Saliha Kanık-Yüksek, Sara Espinosa-Padilla, Sathishkumar Ramaswamy, Satoshi Okada, Sefika Elmas Bozdemir, Selma Erol Aytekin, Şemsi Nur Karabela, Sevgi Keles, Sevtap Senoglu, Shen-Ying Zhang, Sotirija Duvlis, Stefan N. Constantinescu, Stephanie Boisson-Dupuis, Stuart E. Turvey, Stuart G. Tangye, Takaki Asano, Tayfun Ozcelik, Tom Le Voyer, Tom Maniatis, Tomohiro Morio, Trine H. Mogensen, Vanessa Sancho-Shimizu, Vivien Beziat, Xavier Solanich, Yenan Bryceson, Yu-Lung Lau & Yuval ItanSARS-CoV-2 infection is benign in most individuals but, in around 10% of cases, it triggers hypoxaemic COVID-19 pneumonia, which leads to critical illness in around 3% of cases. The ensuing risk of death (approximately 1% across age and gender) doubles every five years from childhood onwards and is around 1.5 times greater in men than in women. Here we review the molecular and cellular determinants of critical COVID-19 pneumonia. Inborn errors of type I interferons (IFNs), including autosomal TLR3 and X-chromosome-linked TLR7 deficiencies, are found in around 1–5% of patients with critical pneumonia under 60 years old, and a lower proportion in older patients. Pre-existing auto-antibodies neutralizing IFNα, IFNβ and/or IFNω, which are more common in men than in women, are found in approximately 15–20% of patients with critical pneumonia over 70 years old, and a lower proportion in younger patients. Thus, at least 15% of cases of critical COVID-19 pneumonia can be explained. The TLR3- and TLR7-dependent production of type I IFNs by respiratory epithelial cells and plasmacytoid dendritic cells, respectively, is essential for host defence against SARS-CoV-2. In ways that can depend on age and sex, insufficient type I IFN immunity in the respiratory tract during the first few days of infection may account for the spread of the virus, leading to pulmonary and systemic inflammation.The Laboratory of Human Genetics of Infectious Diseases is supported by the Howard Hughes Medical Institute, the Rockefeller University, the St Giles Foundation, the National Institutes of Health (NIH) (R01AI088364 and R01AI163029), the National Center for Advancing Translational Sciences (NCATS), the NIH Clinical and Translational Science Award (CTSA) program (UL1 TR001866), a Fast Grant from Emergent Ventures, the Mercatus Center at George Mason University, the Yale Center for Mendelian Genomics and the GSP Coordinating Center funded by the National Human Genome Research Institute (NHGRI) (UM1HG006504 and U24HG008956), the Yale High Performance Computing Center (S10OD018521), the Fisher Center for Alzheimer’s Research Foundation, the Meyer Foundation, the JPB Foundation, the French National Research Agency (ANR) under the ‘Investments for the Future’ program (ANR-10-IAHU-01), the Integrative Biology of Emerging Infectious Diseases Laboratory of Excellence (ANR-10-LABX-62-IBEID), the French Foundation for Medical Research (FRM) (EQU201903007798), the FRM and ANR GENCOVID project (ANR-20-COVI-0003), ANRS Nord-Sud (ANRS-COV05), ANR grant GENVIR (ANR-20-CE93-003), ANR AABIFNCOV (ANR-20-CO11-0001) and ANR MIS-C (ANR 21-COVR-0039, GenMIS-C) projects, the European Union’s Horizon 2020 research and innovation program under grant agreement no. 824110 (EASI-Genomics), the Square Foundation, Grandir—Fonds de solidarité pour l’enfance, the SCOR Corporate Foundation for Science, Fondation du Souffle, The French Ministry of Higher Education, Research, and Innovation (MESRI-COVID-19), Institut National de la Santé et de la Recherche Médicale (INSERM), REACTing-INSERM, and the University of Paris. P.B. was supported by the FRM (EA20170638020) and the MD-PhD programme of the Imagine Institute (with the support of the Fondation Bettencourt Schueller). G.N. is supported by Regione Lazio (Research Group Projects 2020) no. A0375-2020-36663, GecoBiomark. H.C.S. and L.D.N. are supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health
Remdesivir treatment for patients with moderate to severe COVID-19
No full textBackground/aim: Remdesivir, which was first developed for the treatment of Ebola disease but failed to meet expectations, has become hope in the fight against the COVID-19 pandemic. This study aimed to evaluate risk factors for mortality and prognosis of adult moderate/severe COVID-19 patients treated with remdesivir, and safety and tolerability of 5 days of remdesivir treatment
Respiratory viral infections in otherwise healthy humans with inherited IRF7 deficiency
No full textAutosomal recessive IRF7 deficiency was previously reported in three patients with single critical influenza or COVID-19 pneumonia episodes. The patients’ fibroblasts and plasmacytoid dendritic cells produced no detectable type I and III IFNs, except IFN-β. Having discovered four new patients, we describe the genetic, immunological, and clinical features of seven IRF7-deficient patients from six families and five ancestries. Five were homozygous and two were compound heterozygous for IRF7 variants. Patients typically had one episode of pulmonary viral disease. Age at onset was surprisingly broad, from 6 mo to 50 yr (mean age 29 yr). The respiratory viruses implicated included SARS-CoV-2, influenza virus, respiratory syncytial virus, and adenovirus. Serological analyses indicated previous infections with many common viruses. Cellular analyses revealed strong antiviral immunity and expanded populations of influenza- and SARS-CoV-2–specific memory CD4(+) and CD8(+) T cells. IRF7-deficient individuals are prone to viral infections of the respiratory tract but are otherwise healthy, potentially due to residual IFN-β and compensatory adaptive immunity
Inborn errors of type I IFN immunity in patients with life-threatening COVID-19
No full textClinical outcome upon infection with SARS-CoV-2 ranges from silent infection to lethal COVID-19. We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern TLR3- and IRF7-dependent type I interferon (IFN) immunity to influenza virus, in 659 patients with life-threatening COVID-19 pneumonia, relative to 534 subjects with asymptomatic or benign infection. By testing these and other rare variants at these 13 loci, we experimentally define LOF variants in 23 patients (3.5%), aged 17 to 77 years, underlying autosomal recessive or dominant deficiencies. We show that human fibroblasts with mutations affecting this pathway are vulnerable to SARS-CoV-2. Inborn errors of TLR3- and IRF7-dependent type I IFN immunity can underlie life-threatening COVID-19 pneumonia in patients with no prior severe infection
