Introduction <p>SARS-CoV-2 and influenza viruses can lead to liver involvement, although the extent and clinical significance remain unclear. We aimed to study liver involvement among children with pneumonia associated with SARS-CoV-2 and Influenza viruses.</p> Methods <p>Pediatric patients who were diagnosed with pneumonia due to COVID-19 or influenza infection in our hospital were enrolled. Liver function tests were evaluated at admission and during the disease course.</p> Results <p>A total of 117 children were included: 69 with SARS-CoV-2 pneumonia and 48 with influenza pneumonia. Liver injury at admission was observed in 37.6% of SARS-CoV-2 cases and 29.2% of influenza cases (<i>p</i> = 0.429). During the disease course, liver injury increased to 55.1% and 37.5%, respectively (<i>p</i> = 0.09). Among children with normal liver function at admission, mild to moderate reversible liver injury developed in 30.2% of SARS-CoV-2 and 23.5% of influenza pneumonia cases (<i>p</i> = 0.6). CRP and LDH levels were significantly higher in COVID-19 patients, whereas hepatotoxic drug exposure and comorbid conditions contributed to the variability in liver injury patterns (<i>p</i> = 0.005 and <i>p</i> = 0.012, respectively). Mortality occurred only in the SARS-CoV-2 pneumonia group (14.4% vs. 0%, <i>p</i> = 0.005). Pulmonary, neurometabolic, and malignant comorbidities were independently associated with hepatotoxic progression, while shock and moderate-to-severe liver injury at admission were significant predictors of mortality.</p> Conclusion <p>COVID-19 is associated with more frequent liver involvement and higher mortality than influenza (<i>p</i> = 0.005). The interplay between viral infection, systemic inflammation, shock, and drug-related hepatotoxicity likely contributes to the observed hepatic dysfunction. Further research is warranted to clarify the mechanisms of viral-induced liver injury.</p>

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Hepatitis is an underestimated complication among children with pneumonia associated with SARS-CoV-2 and influenza: a single center study

  • Kubra Aykac,
  • Osman Oguz Demir,
  • Mehmet Can Sari,
  • Aylin Irmak Kuruc,
  • Ozdenur Demiray,
  • Hayriye Hizarcioglu-Gulsen,
  • Ersin Gumus,
  • Sevilay Karahan,
  • Ali Bülent Cengiz,
  • Yasemin Ozsurekci

摘要

Introduction

SARS-CoV-2 and influenza viruses can lead to liver involvement, although the extent and clinical significance remain unclear. We aimed to study liver involvement among children with pneumonia associated with SARS-CoV-2 and Influenza viruses.

Methods

Pediatric patients who were diagnosed with pneumonia due to COVID-19 or influenza infection in our hospital were enrolled. Liver function tests were evaluated at admission and during the disease course.

Results

A total of 117 children were included: 69 with SARS-CoV-2 pneumonia and 48 with influenza pneumonia. Liver injury at admission was observed in 37.6% of SARS-CoV-2 cases and 29.2% of influenza cases (p = 0.429). During the disease course, liver injury increased to 55.1% and 37.5%, respectively (p = 0.09). Among children with normal liver function at admission, mild to moderate reversible liver injury developed in 30.2% of SARS-CoV-2 and 23.5% of influenza pneumonia cases (p = 0.6). CRP and LDH levels were significantly higher in COVID-19 patients, whereas hepatotoxic drug exposure and comorbid conditions contributed to the variability in liver injury patterns (p = 0.005 and p = 0.012, respectively). Mortality occurred only in the SARS-CoV-2 pneumonia group (14.4% vs. 0%, p = 0.005). Pulmonary, neurometabolic, and malignant comorbidities were independently associated with hepatotoxic progression, while shock and moderate-to-severe liver injury at admission were significant predictors of mortality.

Conclusion

COVID-19 is associated with more frequent liver involvement and higher mortality than influenza (p = 0.005). The interplay between viral infection, systemic inflammation, shock, and drug-related hepatotoxicity likely contributes to the observed hepatic dysfunction. Further research is warranted to clarify the mechanisms of viral-induced liver injury.