Novel coronavirus infection and rhabdomyolysis

Abstract

Influenza A virus subtype is associated with several viruses, including H1N1 and SARS-CoV-1. It has been reported in the literature that some patients with severe acute respiratory syndrome or H1N1 infection show mild to moderate increases in serum CK levels. Similarly, in many case reports in the literature, a case of SARS-CoV-2 associated rhabdomyolysis has been reported. Haroun et al. showed that rhabdomyolysis is associated with increased mortality in patients with COVID-19. Gang et al. reported that rhabdomyolysis was associated with in-hospital mortality in their study in hospitalized patients. The mechanism of muscle damage in viral infections, especially SARS-CoV-2, is not fully understood. Possible explanations suggested including direct and indirect mechanisms. The most important possible explanation is that the virus directly causes muscle damage. The presence of angiotensin converting enzyme 2, which is defined as the functional receptor for SARS-CoV and SARS-CoV-2, in skeletal muscles is one of the data supporting this theory in the literature. However, in postmortem examinations SARS-CoV was not detectable in skeletal muscle, and it is therefore unclear whether SARS-CoV-2 directly infects muscle. The second plausible explanation postulates that the cytokine storm-like immune response may lead to skeletal muscle damage. The muscle pain seen in patients during viremia and the accompanying high CK levels support the first explanation. Late rhabdomyolysis seen in hospitalized patients support the second explanation.

Keywords

• COVID-19
• coronavirus infections
• rhabdomyolysis
• SARS-CoV-2

References

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