Acute liver failure and secondary TMA-like phenomenon following SARS-CoV-2 and Mycoplasma pneumoniae co-detection in...

In the post-pandemic era, the co-detection of SARS-CoV-2 and Mycoplasma pneumoniae (M. pneumoniae) is increasingly recognized in children, but its full clinical spectrum remains poorly characterized.

We describe a previously healthy 20-month-old girl who presented with sepsis, acute liver failure (ALT, 17,134 U/L), and extreme hyperinflammation (ferritin, 10,929.6 ng/mL; interleukin-6 [IL-6], 74 pg/ml) associated with SARS-CoV-2 and M. pneumoniae co-detection. Despite initial improvement in the liver function with glucocorticoid therapy, she subsequently developed a secondary thrombotic microangiopathy (TMA)-like phenomenon characterized by severe thrombocytopenia (52 × 10⁹/L), microangiopathic hemolysis, and acute kidney injury (creatinine, 181.5 μmol/L). A comprehensive etiological workup, including negative complement gene testing (whole-exome sequencing, whole-genome sequencing, and copy number variation analysis), supported a diagnosis of severe infection-associated secondary TMA-like phenomenon. The patient recovered after comprehensive supportive care, antimicrobial therapy, glucocorticoids, and prophylactic anticoagulation.

This case delineates a clinical sequence from acute liver failure to a secondary TMA-like phenomenon associated with SARS-CoV-2 and M. pneumoniae co-detection. The transient C3 consumption with spontaneous recovery, together with negative complement gene testing, was documented. This report highlights the importance of vigilant monitoring for a secondary TMA-like phenomenon in children with severe hyperinflammation and co-detection of viral and bacterial pathogens.