Lea Pitscheider, Mario Karolyi, Francesco R Burkert, Raimund Helbok, Julia V Wanschitz, Corinne Horlings, Erich Pawelka, Sara Omid, Marianna Traugott, Tamara Seitz, Alexander Zoufaly, Elisabeth Lindeck-Pozza, Ewald Wöll, Ronny Beer, Stefanie Seiwald, Rosa Bellmann-Weiler, Harald Hegen, Wolfgang N Löscher
Author Information
Lea Pitscheider: Department of Neurology, Medical University Innsbruck, Innsbruck, Austria.
Mario Karolyi: 4th Medical Department with Infectious Diseases and Tropical Medicine, Kaiser Franz Josef Hospital, Vienna, Austria.
Francesco R Burkert: Department of Internal Medicine II, Infectious Diseases, Pneumology, Rheumatology, Medical University of Innsbruck, Innsbruck, Austria.
Raimund Helbok: Department of Neurology, Medical University Innsbruck, Innsbruck, Austria.
Julia V Wanschitz: Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. ORCID
Corinne Horlings: Department of Neurology, Medical University Innsbruck, Innsbruck, Austria.
Erich Pawelka: 4th Medical Department with Infectious Diseases and Tropical Medicine, Kaiser Franz Josef Hospital, Vienna, Austria.
Sara Omid: 4th Medical Department with Infectious Diseases and Tropical Medicine, Kaiser Franz Josef Hospital, Vienna, Austria.
Marianna Traugott: 4th Medical Department with Infectious Diseases and Tropical Medicine, Kaiser Franz Josef Hospital, Vienna, Austria.
Tamara Seitz: 4th Medical Department with Infectious Diseases and Tropical Medicine, Kaiser Franz Josef Hospital, Vienna, Austria.
Alexander Zoufaly: 4th Medical Department with Infectious Diseases and Tropical Medicine, Kaiser Franz Josef Hospital, Vienna, Austria.
Elisabeth Lindeck-Pozza: Department of Neurology, Kaiser Franz Josef Hospital, Vienna, Austria.
Ewald Wöll: Department of Internal Medicine, St. Vinzenz Hospital, Zams, Austria.
Ronny Beer: Department of Neurology, Medical University Innsbruck, Innsbruck, Austria.
Stefanie Seiwald: Department of Internal Medicine II, Infectious Diseases, Pneumology, Rheumatology, Medical University of Innsbruck, Innsbruck, Austria.
Rosa Bellmann-Weiler: Department of Internal Medicine II, Infectious Diseases, Pneumology, Rheumatology, Medical University of Innsbruck, Innsbruck, Austria.
Harald Hegen: Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. ORCID
Wolfgang N Löscher: Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. ORCID
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.
