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Muscle involvement in SARS‐CoV‐2 infection.

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Title: Muscle involvement in SARS‐CoV‐2 infection.
Authors: Pitscheider, Lea (AUTHOR), Karolyi, Mario (AUTHOR), Burkert, Francesco R. (AUTHOR), Helbok, Raimund (AUTHOR), Wanschitz, Julia V. (AUTHOR), Horlings, Corinne (AUTHOR), Pawelka, Erich (AUTHOR), Omid, Sara (AUTHOR), Traugott, Marianna (AUTHOR), Seitz, Tamara (AUTHOR), Zoufaly, Alexander (AUTHOR), Lindeck‐Pozza, Elisabeth (AUTHOR), Wöll, Ewald (AUTHOR), Beer, Ronny (AUTHOR), Seiwald, Stefanie (AUTHOR), Bellmann‐Weiler, Rosa (AUTHOR), Hegen, Harald (AUTHOR), Löscher, Wolfgang N. (AUTHOR)
Source: European Journal of Neurology. Oct2021, Vol. 28 Issue 10, p3411-3417. 7p.
Subjects: Influenza, SARS-CoV-2, COVID-19, Creatine kinase
Abstract: Background and Purpose: Since the outbreak of the severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) pandemic, several reports indicated neurological involvement in COVID‐19 disease. Muscle involvement has also been reported as evidenced by creatine kinase (CK) elevations and reports of myalgia. Methods: Creatine kinase, markers of inflammation, pre‐existing diseases and statin use were extracted from records of Austrian hospitalised COVID‐19 patients. Disease severity was classified as severe in case of intensive care unit (ICU) admission or mortality. COVID‐19 patients were additionally compared to an historical group of hospitalised influenza patients. Results: Three hundred fifty‐one patients with SARS‐CoV‐2 and 258 with influenza were included in the final analysis. CK was elevated in 27% of COVID‐19 and in 28% of influenza patients. CK was higher in severe COVID‐19 as were markers of inflammation. CK correlated significantly with inflammation markers, which had an independent impact on CK when adjusted for demographic variables and disease severity. Compared to influenza patients, COVID‐19 patients were older, more frequently male, had more comorbidities, and more frequently had a severe disease course. Nevertheless, influenza patients had higher baseline CK than COVID‐19, and 35.7% of intensive care unit (ICU)‐admitted patients had CK levels >1,000 U/L compared to only 4.7% of ICU‐admitted COVID‐19 patients. Conclusions: HyperCKemia occurs in a similar frequency in COVID‐19 and influenza infection. CK levels were lower in COVID‐19 than in influenza in mild and severe disease. CK levels strongly correlate with disease severity and markers of inflammation. To date, it remains unclear whether hyperCKemia is due to a virus‐triggered inflammatory response or direct muscle toxicity. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neurology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Muscle involvement in SARS‐CoV‐2 infection.
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  Data: <searchLink fieldCode="AR" term="%22Pitscheider%2C+Lea%22">Pitscheider, Lea</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Karolyi%2C+Mario%22">Karolyi, Mario</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Burkert%2C+Francesco+R%2E%22">Burkert, Francesco R.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Helbok%2C+Raimund%22">Helbok, Raimund</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wanschitz%2C+Julia+V%2E%22">Wanschitz, Julia V.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Horlings%2C+Corinne%22">Horlings, Corinne</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Pawelka%2C+Erich%22">Pawelka, Erich</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Omid%2C+Sara%22">Omid, Sara</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Traugott%2C+Marianna%22">Traugott, Marianna</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Seitz%2C+Tamara%22">Seitz, Tamara</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zoufaly%2C+Alexander%22">Zoufaly, Alexander</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Lindeck‐Pozza%2C+Elisabeth%22">Lindeck‐Pozza, Elisabeth</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wöll%2C+Ewald%22">Wöll, Ewald</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Beer%2C+Ronny%22">Beer, Ronny</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Seiwald%2C+Stefanie%22">Seiwald, Stefanie</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bellmann‐Weiler%2C+Rosa%22">Bellmann‐Weiler, Rosa</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Hegen%2C+Harald%22">Hegen, Harald</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Löscher%2C+Wolfgang+N%2E%22">Löscher, Wolfgang N.</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neurology%22">European Journal of Neurology</searchLink>. Oct2021, Vol. 28 Issue 10, p3411-3417. 7p.
– Name: Subject
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  Data: <searchLink fieldCode="DE" term="%22Influenza%22">Influenza</searchLink><br /><searchLink fieldCode="DE" term="%22SARS-CoV-2%22">SARS-CoV-2</searchLink><br /><searchLink fieldCode="DE" term="%22COVID-19%22">COVID-19</searchLink><br /><searchLink fieldCode="DE" term="%22Creatine+kinase%22">Creatine kinase</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background and Purpose: Since the outbreak of the severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) pandemic, several reports indicated neurological involvement in COVID‐19 disease. Muscle involvement has also been reported as evidenced by creatine kinase (CK) elevations and reports of myalgia. Methods: Creatine kinase, markers of inflammation, pre‐existing diseases and statin use were extracted from records of Austrian hospitalised COVID‐19 patients. Disease severity was classified as severe in case of intensive care unit (ICU) admission or mortality. COVID‐19 patients were additionally compared to an historical group of hospitalised influenza patients. Results: Three hundred fifty‐one patients with SARS‐CoV‐2 and 258 with influenza were included in the final analysis. CK was elevated in 27% of COVID‐19 and in 28% of influenza patients. CK was higher in severe COVID‐19 as were markers of inflammation. CK correlated significantly with inflammation markers, which had an independent impact on CK when adjusted for demographic variables and disease severity. Compared to influenza patients, COVID‐19 patients were older, more frequently male, had more comorbidities, and more frequently had a severe disease course. Nevertheless, influenza patients had higher baseline CK than COVID‐19, and 35.7% of intensive care unit (ICU)‐admitted patients had CK levels >1,000 U/L compared to only 4.7% of ICU‐admitted COVID‐19 patients. Conclusions: HyperCKemia occurs in a similar frequency in COVID‐19 and influenza infection. CK levels were lower in COVID‐19 than in influenza in mild and severe disease. CK levels strongly correlate with disease severity and markers of inflammation. To date, it remains unclear whether hyperCKemia is due to a virus‐triggered inflammatory response or direct muscle toxicity. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of European Journal of Neurology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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