clinical characteristics and predictors of the duration of sarscov2 viral shedding CORD-Papers-2022-06-02 (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: 2020-09-21
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: patients lower respiratory samples kidney COVID-19 IL-10 6.75-12.5 Throat swab specimens lopinavir inpatients lung 55/113 interleukin-6 IL-6 serum amyloid A blood alanine aminotransferase intravenous eye birds SARS-CoV-2 [6 Fig. 2f cardiac Lymphocyte T-cell patient rIFN-alpha adenovirus ritonavir D-dimer Patients ribavirin lymphocytes levofloxacin immune cells fibrinogen humans rIFN-a aspartate aminotransferase cephalosporins cellular immune response assessment SARS-CoV-2 leucocyte SARS-CoV hepatic enteral chest lymphocyte Vero cells human immunodeficiency virus erythrocyte W. Liu Wuhan University WDRY2020-K137 SARS-CoV-2 infections IFN-a interleukin-10 FDP lactate dehydrogenase Wuhan Oxygen ALT Human-to-human oxygen LDH 45/114 AST Wuhan, throat Fisher's aminotransferase blood oxygen human interferon alpha inhaled SAA a-HBDH high-dose glucocorticoids [11, 15] neutrophil serum ferritin pulmonary [2, 4, 11, 13] , Table 3 cellular eosinophil coronavirus Glucocorticoid Glucocorticoids coronavirus disease 2019 CRP † intravenous glucocorticoids Oral C-reactive immunoglobulin chest CT Wuhan, China [1] [2] [3] [4 coxsackievirus methylprednisolone serum ganciclovir moxifloxacin oral glucocorticoid influenza A virus alpha-hydroxybutyrate dehydrogenase glucocorticoids 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: eye one‐way 1.0–6.0 chi‐square glucocorticoids immunoglobulin alpha‐hydroxybutyrate dehydrogenase first‐line Vero cells oxygen Throat swab specimens birds U‐test kidney glucocorticoid serum ferritin coronavirus hepatic enteral intravenous glucocorticoids pulmonary cardiac 's 11.25–25.75 226.75–320.25 levofloxacin SARS‐CoV α‐HBDH cellular LDH intravenous oral IL‐6 × lymphocyte serum blood methylprednisolone inhaled SARS‐CoV‐2 [6 CRP inpatients SARS‐CoV‐2 infections Wuhan, China [1, 2, 3, human immunodeficiency virus eosinophil Oral 1.6–4.3] blood oxygen coronavirus disease 2019 ganciclovir coxsackievirus L−1 [IQR IFN‐α Wuhan, fibrinogen moxifloxacin [2, 4, 11, 13] RT‐PCR Writing‐review 15.5–23.0 8.0–9.0 Thirty‐nine T‐cell Glucocorticoids day−1 neutrophil 5.0–13.25 patients malignant tumour lung lymphocytes chest CT Oxygen laboratory‐confirmed COVID‐19 [7] D‐dimer 45/114 lactate dehydrogenase 262.5 U L−1 [ cephalosporins 193.5 U L−1 immune cells lopinavir COVID‐19 cases[14 leucocyte SAA humans FDP 5.25–14.25 cellular immune response assessment virus–cell aminotransferase patient AST Patients adenovirus interleukin‐6 WDRY2020‐K137 erythrocyte Lymphocyte ritonavir aspartate aminotransferase 1.0–2.0] ALT interleukin‐10 Wuhan serum amyloid A alanine aminotransferase COVID‐19 throat chest human interferon alpha (rIFN‐α) (50 μg person‐to‐person ribavirin 207.0 U L−1 [IQR high‐risk influenza A virus high‐dose glucocorticoids [11, 15] MODS [12] 55/113 11.0–23.0
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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