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.