Discussion
Previous cases of bone marrow suppression related to SARS-CoV-2 infection described in literature included a 33-year-old female patient who underwent extensive evaluation for myelodysplasias including bone marrow biopsy and ultimately received granulocyte colony-stimulating factor (G-CSF) for severe neutropenia 11 days following acute COVID-19 infection.6 Additionally, a 5-month-old was noted to have severe neutropenia treated with G-CSF following recent SARS-CoV-2 infection. The child was diagnosed with MIS-C in the setting of 36-hour history of persistent fever, perineal cellulitis, and lip ulceration with a negative SARS-CoV-2 PCR but positive IgG and IgM antibodies. No previous clinical symptoms occurred for which an acute COVID-19 infection was suspected.7 Lastly, a 23-day-old and a 39-day-old neonate with mild COVID-19 infection were noted to have severe neutropenia that resolved without intervention, thought to be related to postinfectious transient neutropenia associated with viral infections in infancy.1 Of note, our patient did not undergo further evaluation with a bone marrow biopsy due to the rapid recovery of her cell lines. The true extent of viral induced bone marrow failure is not completely understood, especially as it relates to SARS-CoV-2. For example, the influenza virus and the hepatitis virus families are thought to induce thrombocytopenia by the uptake of platelets by viral particles facilitating hepatic clearance.8, 9 Enterovirus infections have been described as profoundly altering the relative proportions of different cell populations in the bone marrow, depleting hematopoietic progenitor cells, and markedly reducing the restorative capacity of specific subsets of progenitor cells in the bone marrow.10Ebstein-Barr virus, cytomegalovirus, and human herpesvirus 6 can cause neutropenia through increased neutrophil adherence to the endothelium, enhanced neutrophil utilization, and anti-neutrophil antibody formation.11 Overall, bone marrow suppression secondary to infections by well-known viruses could explain the hematological manifestations of SARS-CoV-2; however, the presence of leukopenia, thrombocytopenia, and severe neutropenia remain novel findings. Our patient’s laboratory abnormalities in the setting of COVID-19 are noteworthy as rapid bone marrow response occurred without therapeutic intervention or clinical complications. Bone marrow biopsy may not be indicated in patients with COVID-19 infection and pancytopenia given the transient nature of hematological manifestations even in patients with trisomy 21.