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Author

Didier Dequanter

Other affiliations: Institut Jules Bordet
Bio: Didier Dequanter is an academic researcher from Université libre de Bruxelles. The author has contributed to research in topics: Laryngopharyngeal reflux & Head and neck cancer. The author has an hindex of 19, co-authored 102 publications receiving 2813 citations. Previous affiliations of Didier Dequanter include Institut Jules Bordet.


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TL;DR: Olfactory and gustatory disorders are prevalent symptoms in European CO VID-19 patients, who may not have nasal symptoms, and the sudden anosmia or ageusia need to be recognized by the international scientific community as important symptoms of the COVID-19 infection.
Abstract: To investigate the occurrence of olfactory and gustatory dysfunctions in patients with laboratory-confirmed COVID-19 infection. Patients with laboratory-confirmed COVID-19 infection were recruited from 12 European hospitals. The following epidemiological and clinical outcomes have been studied: age, sex, ethnicity, comorbidities, and general and otolaryngological symptoms. Patients completed olfactory and gustatory questionnaires based on the smell and taste component of the National Health and Nutrition Examination Survey, and the short version of the Questionnaire of Olfactory Disorders-Negative Statements (sQOD-NS). A total of 417 mild-to-moderate COVID-19 patients completed the study (263 females). The most prevalent general symptoms consisted of cough, myalgia, and loss of appetite. Face pain and nasal obstruction were the most disease-related otolaryngological symptoms. 85.6% and 88.0% of patients reported olfactory and gustatory dysfunctions, respectively. There was a significant association between both disorders (p < 0.001). Olfactory dysfunction (OD) appeared before the other symptoms in 11.8% of cases. The sQO-NS scores were significantly lower in patients with anosmia compared with normosmic or hyposmic individuals (p = 0.001). Among the 18.2% of patients without nasal obstruction or rhinorrhea, 79.7% were hyposmic or anosmic. The early olfactory recovery rate was 44.0%. Females were significantly more affected by olfactory and gustatory dysfunctions than males (p = 0.001). Olfactory and gustatory disorders are prevalent symptoms in European COVID-19 patients, who may not have nasal symptoms. The sudden anosmia or ageusia need to be recognized by the international scientific community as important symptoms of the COVID-19 infection.

2,030 citations

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TL;DR: Data show that SNB is a reliable and safe oncological technique for staging the clinically N0 neck in patients with T1 and T2 oral cancer.

255 citations

Journal ArticleDOI
TL;DR: The aim of this article is to review recent developments in the biological understanding of head and neck squamous cell carcinomas.
Abstract: Background. The aim of this article is to review recent developments in the biological understanding of head and neck squamous cell carcinomas. Methods and Results. We describe the markers according to their function and their prognostic or predictive roles. Some associations can be found between molecular markers and invasiveness, aggressiveness, degree of differentiation, and tumor stage, but only a few clinical studies have shown an impact on prognosis. In addition, despite an increasing number of articles relating to this topic, the small number of patients included in the studies reported reduces the clinical implications of these results. Few studies applied a more comprehensive molecular analysis approach, such as DNA microarrays or differential expression profiling by polymerase chain reaction, to identify a combination of markers that could be more informative than a single molecular marker. Conclusion. Some progress has been made with respect to molecular markers and head and neck cancers. Translational and prospective, hypothesis-driven research must proceed with sufficient rigor to facilitate the clinical applicability of such results. © 2005 Wiley Periodicals, Inc. Head Neck27: XXX–XXX, 2005

162 citations

Journal ArticleDOI
TL;DR: To develop and validate the Reflux Symptom Score (RSS), a self‐administered patient‐reported outcome questionnaire for patients with laryngopharyngeal reflux (LPR).
Abstract: Objectives/hypothesis To develop and validate the Reflux Symptom Score (RSS), a self-administered patient-reported outcome questionnaire for patients with laryngopharyngeal reflux (LPR). Study design Prospective controlled study. Methods A total of 113 patients with LPR were enrolled and treated with diet and 3 months of pantoprazole, alginate, and/or magaldrate depending on the LPR characteristics (acid, nonacid, or mixed). Eighty asymptomatic individuals completed the study. Patients and controls completed the RSS twice within a 7-day period to assess test-retest reliability. Internal consistency was measured using Cronbach's α for the RSS items in patients and controls. Validity was assessed by comparing the baseline RSS with the Reflux Symptom Index (RSI) and Voice Handicap Index (VHI). Seventy-seven patients completed the RSS at baseline and after 6 and 12 weeks of treatment to assess responsiveness to change. The RSS cutoff for determining the presence and absence of LPR was examined by receiver operating characteristic analysis. Results Test-retest reliability (rs = 0.921) and internal consistency reliability (α = 0.969) were high. RSS exhibited high external validity indicated by a significant correlation with the RSI (rs = 0.831). Internal validity was excellent based on the higher RSS in patients compared with controls (P = .001). RSS, RSI, and VHI scores significantly improved from pre- to posttreatment, indicating a high responsiveness to change. RSS >13 can be considered suggestive of LPR-related symptoms. RSS was not influenced by the occurrence of gastroesophageal reflux disease, LPR subtypes, or patient characteristics. Conclusions RSS is a self-administered patient-reported outcome questionnaire that demonstrates high reliability and excellent criterion-based validity. RSS can be used in diagnosing and monitoring LPR disease. Level of evidence 3b Laryngoscope, 130:E98-E107, 2020.

95 citations


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25 Aug 2020-JAMA
TL;DR: This review discusses current evidence regarding the pathophysiology, transmission, diagnosis, and management of COVID-19, the novel severe acute respiratory syndrome coronavirus 2 pandemic that has caused a worldwide sudden and substantial increase in hospitalizations for pneumonia with multiorgan disease.
Abstract: Importance The coronavirus disease 2019 (COVID-19) pandemic, due to the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a worldwide sudden and substantial increase in hospitalizations for pneumonia with multiorgan disease. This review discusses current evidence regarding the pathophysiology, transmission, diagnosis, and management of COVID-19. Observations SARS-CoV-2 is spread primarily via respiratory droplets during close face-to-face contact. Infection can be spread by asymptomatic, presymptomatic, and symptomatic carriers. The average time from exposure to symptom onset is 5 days, and 97.5% of people who develop symptoms do so within 11.5 days. The most common symptoms are fever, dry cough, and shortness of breath. Radiographic and laboratory abnormalities, such as lymphopenia and elevated lactate dehydrogenase, are common, but nonspecific. Diagnosis is made by detection of SARS-CoV-2 via reverse transcription polymerase chain reaction testing, although false-negative test results may occur in up to 20% to 67% of patients; however, this is dependent on the quality and timing of testing. Manifestations of COVID-19 include asymptomatic carriers and fulminant disease characterized by sepsis and acute respiratory failure. Approximately 5% of patients with COVID-19, and 20% of those hospitalized, experience severe symptoms necessitating intensive care. More than 75% of patients hospitalized with COVID-19 require supplemental oxygen. Treatment for individuals with COVID-19 includes best practices for supportive management of acute hypoxic respiratory failure. Emerging data indicate that dexamethasone therapy reduces 28-day mortality in patients requiring supplemental oxygen compared with usual care (21.6% vs 24.6%; age-adjusted rate ratio, 0.83 [95% CI, 0.74-0.92]) and that remdesivir improves time to recovery (hospital discharge or no supplemental oxygen requirement) from 15 to 11 days. In a randomized trial of 103 patients with COVID-19, convalescent plasma did not shorten time to recovery. Ongoing trials are testing antiviral therapies, immune modulators, and anticoagulants. The case-fatality rate for COVID-19 varies markedly by age, ranging from 0.3 deaths per 1000 cases among patients aged 5 to 17 years to 304.9 deaths per 1000 cases among patients aged 85 years or older in the US. Among patients hospitalized in the intensive care unit, the case fatality is up to 40%. At least 120 SARS-CoV-2 vaccines are under development. Until an effective vaccine is available, the primary methods to reduce spread are face masks, social distancing, and contact tracing. Monoclonal antibodies and hyperimmune globulin may provide additional preventive strategies. Conclusions and Relevance As of July 1, 2020, more than 10 million people worldwide had been infected with SARS-CoV-2. Many aspects of transmission, infection, and treatment remain unclear. Advances in prevention and effective management of COVID-19 will require basic and clinical investigation and public health and clinical interventions.

3,371 citations

Journal ArticleDOI
TL;DR: The extrapulmonary organ-specific pathophysiology, presentations and management considerations for patients with COVID-19 are reviewed to aid clinicians and scientists in recognizing and monitoring the spectrum of manifestations, and in developing research priorities and therapeutic strategies for all organ systems involved.
Abstract: Although COVID-19 is most well known for causing substantial respiratory pathology, it can also result in several extrapulmonary manifestations. These conditions include thrombotic complications, myocardial dysfunction and arrhythmia, acute coronary syndromes, acute kidney injury, gastrointestinal symptoms, hepatocellular injury, hyperglycemia and ketosis, neurologic illnesses, ocular symptoms, and dermatologic complications. Given that ACE2, the entry receptor for the causative coronavirus SARS-CoV-2, is expressed in multiple extrapulmonary tissues, direct viral tissue damage is a plausible mechanism of injury. In addition, endothelial damage and thromboinflammation, dysregulation of immune responses, and maladaptation of ACE2-related pathways might all contribute to these extrapulmonary manifestations of COVID-19. Here we review the extrapulmonary organ-specific pathophysiology, presentations and management considerations for patients with COVID-19 to aid clinicians and scientists in recognizing and monitoring the spectrum of manifestations, and in developing research priorities and therapeutic strategies for all organ systems involved.

2,113 citations

Journal ArticleDOI
Carly G. K. Ziegler, Samuel J. Allon, Sarah K. Nyquist, Ian M. Mbano1, Vincent N. Miao, Constantine N. Tzouanas, Yuming Cao2, Ashraf S. Yousif3, Julia Bals3, Blake M. Hauser3, Blake M. Hauser4, Jared Feldman4, Jared Feldman3, Christoph Muus4, Christoph Muus5, Marc H. Wadsworth, Samuel W. Kazer, Travis K. Hughes, Benjamin Doran, G. James Gatter6, G. James Gatter5, G. James Gatter3, Marko Vukovic, Faith Taliaferro7, Faith Taliaferro5, Benjamin E. Mead, Zhiru Guo2, Jennifer P. Wang2, Delphine Gras8, Magali Plaisant9, Meshal Ansari, Ilias Angelidis, Heiko Adler, Jennifer M.S. Sucre10, Chase J. Taylor10, Brian M. Lin4, Avinash Waghray4, Vanessa Mitsialis11, Vanessa Mitsialis7, Daniel F. Dwyer11, Kathleen M. Buchheit11, Joshua A. Boyce11, Nora A. Barrett11, Tanya M. Laidlaw11, Shaina L. Carroll12, Lucrezia Colonna13, Victor Tkachev4, Victor Tkachev7, Christopher W. Peterson14, Christopher W. Peterson13, Alison Yu15, Alison Yu7, Hengqi Betty Zheng15, Hengqi Betty Zheng13, Hannah P. Gideon16, Caylin G. Winchell16, Philana Ling Lin16, Philana Ling Lin7, Colin D. Bingle17, Scott B. Snapper11, Scott B. Snapper7, Jonathan A. Kropski18, Jonathan A. Kropski10, Fabian J. Theis, Herbert B. Schiller, Laure-Emmanuelle Zaragosi9, Pascal Barbry9, Alasdair Leslie19, Alasdair Leslie1, Hans-Peter Kiem13, Hans-Peter Kiem14, JoAnne L. Flynn16, Sarah M. Fortune5, Sarah M. Fortune3, Sarah M. Fortune4, Bonnie Berger6, Robert W. Finberg2, Leslie S. Kean7, Leslie S. Kean4, Manuel Garber2, Aaron G. Schmidt4, Aaron G. Schmidt3, Daniel Lingwood3, Alex K. Shalek, Jose Ordovas-Montanes, Nicholas E. Banovich, Alvis Brazma, Tushar J. Desai, Thu Elizabeth Duong, Oliver Eickelberg, Christine S. Falk, Michael Farzan20, Ian A. Glass, Muzlifah Haniffa, Peter Horvath, Deborah T. Hung, Naftali Kaminski, Mark A. Krasnow, Malte Kühnemund, Robert Lafyatis, Haeock Lee, Sylvie Leroy, Sten Linnarson, Joakim Lundeberg, Kerstin B. Meyer, Alexander V. Misharin, Martijn C. Nawijn, Marko Nikolic, Dana Pe'er, Joseph E. Powell, Stephen R. Quake, Jay Rajagopal, Purushothama Rao Tata, Emma L. Rawlins, Aviv Regev, Paul A. Reyfman, Mauricio Rojas, Orit Rosen, Kourosh Saeb-Parsy, Christos Samakovlis, Herbert B. Schiller, Joachim L. Schultze, Max A. Seibold, Douglas P. Shepherd, Jason R. Spence, Avrum Spira, Xin Sun, Sarah A. Teichmann, Fabian J. Theis, Alexander M. Tsankov, Maarten van den Berge, Michael von Papen, Jeffrey A. Whitsett, Ramnik J. Xavier, Yan Xu, Kun Zhang 
28 May 2020-Cell
TL;DR: The data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.

1,911 citations

Journal ArticleDOI
Aravinthan Varatharaj1, Aravinthan Varatharaj2, Naomi Thomas3, Mark Ellul4, Mark Ellul5, Mark Ellul6, Nicholas W. S. Davies, Thomas A Pollak7, Elizabeth L Tenorio8, Mustafa Sultan3, Ava Easton5, Gerome Breen7, Michael S. Zandi9, Jonathan P. Coles10, Hadi Manji9, Rustam Al-Shahi Salman11, David K. Menon10, Timothy R Nicholson7, Laura A Benjamin5, Laura A Benjamin9, Alan Carson11, Craig J. Smith12, Martin R Turner13, Tom Solomon5, Tom Solomon6, Tom Solomon4, Rachel Kneen6, Rachel Kneen5, Sarah Pett14, Ian Galea2, Ian Galea1, Rhys H. Thomas15, Rhys H. Thomas3, Benedict D Michael6, Benedict D Michael4, Benedict D Michael5, Claire Allen, Neil Archibald, James Arkell, Peter Arthur-Farraj, Mark R. Baker, Harriet A. Ball, Verity Bradley-Barker, Zoe Brown, Stefania Bruno, Lois Carey, Christopher Carswell, Annie Chakrabarti, James Choulerton, Mazen Daher, Ruth Davies, Rafael Di Marco Barros, Sofia Dima, Rachel Dunley, Dipankar Dutta, Richard James Booth Ellis, Alex Everitt, Joseph Fady, Patricia Fearon, Leonora Fisniku, Ivie Gbinigie, Alan Gemski, Emma Gillies, Effrossyni Gkrania-Klotsas, Julie Grigg, Hisham Hamdalla, Jack Hubbett, Neil Hunter, Anne-Catherine Huys, Ihmoda Ihmoda, Sissi Ispoglou, Ashwani Jha, Ramzi Joussi, Dheeraj Kalladka, Hind Khalifeh, Sander Kooij, Guru Kumar, Sandar Kyaw, Lucia Li, Edward Littleton, Malcolm R. Macleod, Mary Joan MacLeod, Barbara Madigan, Vikram Mahadasa, Manonmani Manoharan, Richard Marigold, Isaac Marks, Paul M. Matthews, Michael Mccormick, Caroline Mcinnes, Antonio Metastasio, Philip Milburn-McNulty, Clinton Mitchell, Duncan Mitchell, Clare Morgans, Huw R. Morris, Jasper M. Morrow, Ahmed Mubarak Mohamed, Paula Mulvenna, Louis Murphy, Robert Namushi, Edward J Newman, Wendy Phillips, Ashwin Pinto, David A Price, Harald Proschel, Terry Quinn, Deborah Ramsey, Christine Roffe, Amy L Ross Russell, Neshika Samarasekera, Stephen Sawcer, Walee Sayed, Lakshmanan Sekaran, Jordi Serra-Mestres, Victoria K. Snowdon, Gayle Strike, James Sun, Christina Tang, Mark Vrana, Ryckie G. Wade, Chris Wharton, Lou Wiblin, Iryna Boubriak, Katie Herman, Gordon T. Plant 
TL;DR: This is the first nationwide, cross-specialty surveillance study of acute neurological and psychiatric complications of COVID-19 and provides valuable and timely data that are urgently needed by clinicians, researchers, and funders.

990 citations

Journal ArticleDOI
TL;DR: The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is of a scale not seen since the 1918 influenza pandemic and the proportion of infections leading to neurological disease will probably remain small.
Abstract: Summary Background The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is of a scale not seen since the 1918 influenza pandemic. Although the predominant clinical presentation is with respiratory disease, neurological manifestations are being recognised increasingly. On the basis of knowledge of other coronaviruses, especially those that caused the severe acute respiratory syndrome and Middle East respiratory syndrome epidemics, cases of CNS and peripheral nervous system disease caused by SARS-CoV-2 might be expected to be rare. Recent developments A growing number of case reports and series describe a wide array of neurological manifestations in 901 patients, but many have insufficient detail, reflecting the challenge of studying such patients. Encephalopathy has been reported for 93 patients in total, including 16 (7%) of 214 hospitalised patients with COVID-19 in Wuhan, China, and 40 (69%) of 58 patients in intensive care with COVID-19 in France. Encephalitis has been described in eight patients to date, and Guillain-Barre syndrome in 19 patients. SARS-CoV-2 has been detected in the CSF of some patients. Anosmia and ageusia are common, and can occur in the absence of other clinical features. Unexpectedly, acute cerebrovascular disease is also emerging as an important complication, with cohort studies reporting stroke in 2–6% of patients hospitalised with COVID-19. So far, 96 patients with stroke have been described, who frequently had vascular events in the context of a pro-inflammatory hypercoagulable state with elevated C-reactive protein, D-dimer, and ferritin. Where next? Careful clinical, diagnostic, and epidemiological studies are needed to help define the manifestations and burden of neurological disease caused by SARS-CoV-2. Precise case definitions must be used to distinguish non-specific complications of severe disease (eg, hypoxic encephalopathy and critical care neuropathy) from those caused directly or indirectly by the virus, including infectious, para-infectious, and post-infectious encephalitis, hypercoagulable states leading to stroke, and acute neuropathies such as Guillain-Barre syndrome. Recognition of neurological disease associated with SARS-CoV-2 in patients whose respiratory infection is mild or asymptomatic might prove challenging, especially if the primary COVID-19 illness occurred weeks earlier. The proportion of infections leading to neurological disease will probably remain small. However, these patients might be left with severe neurological sequelae. With so many people infected, the overall number of neurological patients, and their associated health burden and social and economic costs might be large. Health-care planners and policy makers must prepare for this eventuality, while the many ongoing studies investigating neurological associations increase our knowledge base.

884 citations