clinical characteristics and predictors of the duration of sarscov2 viral shedding CORD-Papers-2021-10-25 (Version 1)

Title: Clinical characteristics and predictors of the duration of SARSCoV2 viral shedding in 140 healthcare workers
Abstract: BACKGROUND: Epidemiological and clinical features of patients with COVID19 have been reported, but none of them focused on medical staff, and few predictors of the duration of viral shedding have been reported. It is urgent to help healthcare workers prevent and recover quickly from the coronavirus disease 2019 (COVID19). METHODS: We enrolled 140 medical workers with COVID19 in Wuhan. Epidemiological, demographic, clinical, laboratory, radiological, treatment and clinical outcome data were collected, and predictors of the duration of viral shedding were explored through multivariable linear regression analysis. RESULTS: The medical staff with COVID19 presented mild clinical symptoms and showed a low frequency of abnormal laboratory indicators. All the medical staff were cured and discharged, of whom 96 (68.6%) were female, 39 (27.9%) had underlying diseases, the median age was 36.0 years, and 104 (74.3%) were infected whilst working in hospital. The median duration of viral shedding was 25.0 days (IQR:20.030.0). Multivariable linear regression analysis showed reducing viral shedding duration was associated with receiving recombinant human interferon alpha (rIFN) treatment, whilst the prolonged duration of viral shedding correlated with the use of glucocorticoid treatment, the durations from the first symptom to hospital admission and the improvement in chest computed tomography (CT) evidence. Moreover, infected healthcare workers with lymphocytes less than 1.1 10(9)/L on admission had prolonged viral shedding. CONCLUSION: Medical staff with timely medical interventions shows milder clinical features. Glucocorticoid treatment and lymphocytes less than 1.1 109/L are associated with prolonged viral shedding. Early admission and rIFN treatment help shorten the duration of viral shedding.
Published: 9/21/2020
Journal: J Intern Med
DOI: 10.1111/joim.13160
DOI_URL: http://doi.org/10.1111/joim.13160
Author Name: Liu, W
Author link: https://covid19-data.nist.gov/pid/rest/local/author/liu_w
Author Name: Liu, Y
Author link: https://covid19-data.nist.gov/pid/rest/local/author/liu_y
Author Name: Xu, Z
Author link: https://covid19-data.nist.gov/pid/rest/local/author/xu_z
Author Name: Jiang, T
Author link: https://covid19-data.nist.gov/pid/rest/local/author/jiang_t
Author Name: Kang, Y
Author link: https://covid19-data.nist.gov/pid/rest/local/author/kang_y
Author Name: Zhu, G
Author link: https://covid19-data.nist.gov/pid/rest/local/author/zhu_g
Author Name: Chen, Z
Author link: https://covid19-data.nist.gov/pid/rest/local/author/chen_z
sha: 395e92dc4e6fac8b99413779b93cfd9fe79eb75e
license: no-cc
license_url: [no creative commons license associated]
source_x: Medline; PMC
source_x_url: https://www.medline.com/https://www.ncbi.nlm.nih.gov/pubmed/
pubmed_id: 32959400
pubmed_id_url: https://www.ncbi.nlm.nih.gov/pubmed/32959400
pmcid: PMC7537050
pmcid_url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7537050
url: https://www.ncbi.nlm.nih.gov/pubmed/32959400/ https://doi.org/10.1111/joim.13160
has_full_text: TRUE
Keywords Extracted from Text Content: [2, 4, 11, 13] , Table 3 eosinophil rIFN-alpha 6.75-12.5 Oxygen neutrophil SARS-CoV-2 blood interleukin-10 high-dose glucocorticoids [11, 15] Wuhan cellular W. Liu WDRY2020-K137 fibrinogen humans coronavirus inhaled lymphocyte IL-10 C-reactive coxsackievirus human interferon alpha SARS-CoV-2 [6 Throat swab specimens Glucocorticoid 45/114 T-cell aminotransferase patients lower respiratory samples Wuhan University Human-to-human serum ferritin ALT chest SAA lactate dehydrogenase 55/113 glucocorticoid Glucocorticoids Patients Vero cells throat COVID-19 serum amyloid A alpha-hydroxybutyrate dehydrogenase intravenous Fig. 2f † oral alanine aminotransferase ribavirin Lymphocyte lymphocytes SARS-CoV coronavirus disease 2019 Wuhan, China [1] [2] [3] [4 inpatients a-HBDH cephalosporins cardiac IL-6 hepatic enteral lung ritonavir lopinavir influenza A virus immune cells erythrocyte blood oxygen oxygen SARS-CoV-2 infections pulmonary glucocorticoids eye patient immunoglobulin human immunodeficiency virus LDH interleukin-6 Fisher's CRP AST levofloxacin rIFN-a leucocyte IFN-a D-dimer serum ganciclovir FDP chest CT kidney aspartate aminotransferase birds cellular immune response assessment Wuhan, intravenous glucocorticoids methylprednisolone adenovirus moxifloxacin Oral Wuhan
Extracted Text Content in Record: First 5000 Characters:Since December 2019, an increasing number of coronavirus disease 2019 cases have occurred in Wuhan, China [1] [2] [3] [4] . Initially, most of the patients diagnosed with pneumonia of unknown aetiology shared a history of exposure to the Huanan Seafood Market [1] . The pathogen was a novel coronavirus named severe acute respiratory coronavirus 2 (SARS-CoV-2) and discovered in samples of the lower respiratory tract from patients with COVID-19 by deep sequencing analysis [5] . Similar to most coronaviruses, SARS-CoV-2 can infect various mammals (including humans) and birds and can cause respiratory, hepatic enteral and neurological diseases [5] . COVID-19 emerged and rapidly spread amongst susceptible populations due to the high pathogenicity of SARS-CoV-2. A family cluster associated with COVID-19 confirmed person-toperson transmission of SARS-CoV-2 [6] . As of 30 March 2020, 82447 SARS-CoV-2 infection cases (including 3310 deaths) in China and 693282 SARS-CoV-2 infection cases (including 33106 deaths) worldwide have been confirmed [7] . As a † These authors contributed equally to this article. high-risk population, healthcare workers perform their clinical activities in the hospital and are more likely to be exposed to respiratory pathogens. Up to 11 February 2020, 1716 confirmed COVID-19 cases (including 5 deaths) have been observed amongst Chinese medical staff [8] . It has been confirmed that 8358 Italian health workers tested positive for SARS-CoV-2 and 61 doctors died in this pandemic until 30 March 2020, which aggravated the shortage of medical workers [9] . However, clinical manifestations of healthcare workers with COVID-19 have not been reported. In this study, we described the epidemiological and clinical characteristics of COVID-19 amongst healthcare workers in Wuhan, China. Multivariable linear regression analysis was applied to explore predictors of reducing the duration of viral shedding and optimizing treatment options. This study focused on healthcare workers hospitalized between 16 January 2020 and 27 February 2020 with COVID-19 in Union Hospital of Tongji Medical College, Huazhong University of Science and Technology and Renmin Hospital of Wuhan University (Wuhan, China). This research was approved by the Ethics Committee of Renmin Hospital of Wuhan University (WDRY2020-K137). All healthcare workers with COVID-19 enrolled were diagnosed according to the interim guidance from the World Health Organization (WHO) [10] . Severe cases are defined as those with resting blood oxygen saturation level below 93%, resting respiratory rate greater than 30 breaths per minute, or lung infiltration of over 50% within 24-48 h on pulmonary imaging [8] , and nonsevere group included mild and moderate cases. Oral informed consent was obtained, and written consent was waived. The information was obtained from the available electronic medical records of patients. Clinical outcomes were followed until 31 March 2020. We collected epidemiological, demographic, clinical, laboratory, radiological, treatment and outcome data. The data were analysed and checked by two clinicians. For unclear records, we directly contacted the involved doctors or other healthcare providers for clarification. The date of illness onset was defined as the date of initial symptom. Histories of exposure to patients with confirmed or suspected SARS-CoV-2 infection were tracked within two weeks before the onset of illness. The duration of viral shedding was defined as the duration from the illness onset to two consecutive negative results of real-time RT-PCR in lower respiratory samples collected at least one day apart. Fitness for discharge was based on abatement of fever for at least three days, significant relief of respiratory symptoms, improvement in chest computed tomography (CT) evidence and viral clearance. The durations from onset of disease to chest CT confirmation of viral pneumonia, aetiological diagnosis, hospital admission, improvement in chest CT evidence, treatment and the end of viral shedding were recorded. Throat swab specimens were obtained from all patients after admission every three days and every 1-2 days after the first negative result of SARS-CoV-2 or the patient's subjective symptoms improved. SARS-CoV-2 was confirmed by real-time RT-PCR using a previously described protocol [11] . Laboratory tests included a complete blood count, evaluation of infection-related biomarkers, evaluation of serum biochemistry, coagulation function evaluation, humoral and cellular immune response assessment, cytokine analysis and evaluation for any coexisting infection (including bacteria, fungi and other respiratory viruses). The other respiratory viruses included influenza A virus, influenza B virus, respiratory syncytial virus, adenovirus, coxsackievirus. Patients were also evaluated for mycoplasma and chlamydia. Patients with SARS-CoV-2 infection received antiviral treatment with arbidol (200 mg, three times daily, oral), oseltamiv
Keywords Extracted from PMC Text: glucocorticoid Wuhan alanine aminotransferase 8.0–9.0 Wuhan, Thirty‐nine influenza A virus day−1 193.5 U L−1 first‐line Throat swab specimens eye erythrocyte person‐to‐person Lymphocyte chest 11.0–23.0 intravenous glucocorticoids cardiac Glucocorticoids eosinophil interleukin‐6 patients lymphocytes × coronavirus LDH one‐way cellular immune response assessment FDP kidney cellular inhaled high‐dose glucocorticoids [11, 15] Writing‐review T‐cell WDRY2020‐K137 blood oxygen chi‐square SAA 1.0–6.0 11.25–25.75 inpatients human interferon alpha (rIFN‐α) (50 μg L−1 [IQR RT‐PCR 1.6–4.3] COVID‐19 cases[14 aminotransferase lung coronavirus disease 2019 226.75–320.25 immune cells 55/113 Oral glucocorticoids laboratory‐confirmed COVID‐19 aspartate aminotransferase virus–cell serum amyloid A leucocyte patient intravenous MODS [12] [2, 4, 11, 13] D‐dimer ganciclovir birds IL‐6 α‐HBDH SARS‐CoV‐2 infections oxygen coxsackievirus SARS‐CoV moxifloxacin ritonavir IFN‐α 262.5 U L−1 [ 5.0–13.25 SARS‐CoV‐2 [6 methylprednisolone 1.0–2.0] 's ribavirin oral interleukin‐10 humans neutrophil CRP 5.25–14.25 immunoglobulin Vero cells human immunodeficiency virus 207.0 U L−1 [IQR 45/114 serum ferritin Patients AST lopinavir levofloxacin lymphocyte Oxygen COVID‐19 lactate dehydrogenase pulmonary [7] 15.5–23.0 hepatic enteral blood ALT serum fibrinogen adenovirus cephalosporins chest CT U‐test malignant tumour Wuhan, China [1, 2, 3, alpha‐hydroxybutyrate dehydrogenase throat high‐risk
Extracted PMC Text Content in Record: First 5000 Characters:Since December 2019, an increasing number of coronavirus disease 2019 (COVID‐19) cases have occurred in Wuhan, China [1, 2, 3, 4]. Initially, most of the patients diagnosed with pneumonia of unknown aetiology shared a history of exposure to the Huanan Seafood Market [1]. The pathogen was a novel coronavirus named severe acute respiratory coronavirus 2 (SARS‐CoV‐2) and discovered in samples of the lower respiratory tract from patients with COVID‐19 by deep sequencing analysis [5]. Similar to most coronaviruses, SARS‐CoV‐2 can infect various mammals (including humans) and birds and can cause respiratory, hepatic enteral and neurological diseases [5]. COVID‐19 emerged and rapidly spread amongst susceptible populations due to the high pathogenicity of SARS‐CoV‐2. A family cluster associated with COVID‐19 confirmed person‐to‐person transmission of SARS‐CoV‐2 [6]. As of 30 March 2020, 82447 SARS‐CoV‐2 infection cases (including 3310 deaths) in China and 693282 SARS‐CoV‐2 infection cases (including 33106 deaths) worldwide have been confirmed [7]. As a high‐risk population, healthcare workers perform their clinical activities in the hospital and are more likely to be exposed to respiratory pathogens. Up to 11 February 2020, 1716 confirmed COVID‐19 cases (including 5 deaths) have been observed amongst Chinese medical staff [8]. It has been confirmed that 8358 Italian health workers tested positive for SARS‐CoV‐2 and 61 doctors died in this pandemic until 30 March 2020, which aggravated the shortage of medical workers [9]. However, clinical manifestations of healthcare workers with COVID‐19 have not been reported. In this study, we described the epidemiological and clinical characteristics of COVID‐19 amongst healthcare workers in Wuhan, China. Multivariable linear regression analysis was applied to explore predictors of reducing the duration of viral shedding and optimizing treatment options. This study focused on healthcare workers hospitalized between 16 January 2020 and 27 February 2020 with COVID‐19 in Union Hospital of Tongji Medical College, Huazhong University of Science and Technology and Renmin Hospital of Wuhan University (Wuhan, China). This research was approved by the Ethics Committee of Renmin Hospital of Wuhan University (WDRY2020‐K137). All healthcare workers with COVID‐19 enrolled were diagnosed according to the interim guidance from the World Health Organization (WHO) [10]. Severe cases are defined as those with resting blood oxygen saturation level below 93%, resting respiratory rate greater than 30 breaths per minute, or lung infiltration of over 50% within 24–48 h on pulmonary imaging [8], and nonsevere group included mild and moderate cases. Oral informed consent was obtained, and written consent was waived. The information was obtained from the available electronic medical records of patients. Clinical outcomes were followed until 31 March 2020. We collected epidemiological, demographic, clinical, laboratory, radiological, treatment and outcome data. The data were analysed and checked by two clinicians. For unclear records, we directly contacted the involved doctors or other healthcare providers for clarification. The date of illness onset was defined as the date of initial symptom. Histories of exposure to patients with confirmed or suspected SARS‐CoV‐2 infection were tracked within two weeks before the onset of illness. The duration of viral shedding was defined as the duration from the illness onset to two consecutive negative results of real‐time RT‐PCR in lower respiratory samples collected at least one day apart. Fitness for discharge was based on abatement of fever for at least three days, significant relief of respiratory symptoms, improvement in chest computed tomography (CT) evidence and viral clearance. The durations from onset of disease to chest CT confirmation of viral pneumonia, aetiological diagnosis, hospital admission, improvement in chest CT evidence, treatment and the end of viral shedding were recorded. Throat swab specimens were obtained from all patients after admission every three days and every 1–2 days after the first negative result of SARS‐CoV‐2 or the patient's subjective symptoms improved. SARS‐CoV‐2 was confirmed by real‐time RT‐PCR using a previously described protocol [11]. Laboratory tests included a complete blood count, evaluation of infection‐related biomarkers, evaluation of serum biochemistry, coagulation function evaluation, humoral and cellular immune response assessment, cytokine analysis and evaluation for any coexisting infection (including bacteria, fungi and other respiratory viruses). The other respiratory viruses included influenza A virus, influenza B virus, respiratory syncytial virus, adenovirus, coxsackievirus. Patients were also evaluated for mycoplasma and chlamydia. Patients with SARS‐CoV‐2 infection received antiviral treatment with arbidol (200 mg, three times daily, oral), oseltamivir (75 mg, twice daily, oral), lopinavir and ritonavir
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