INTRODUCTION:
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS- CoV2) associated
with multisystem inflammatory syndrome in children (MIS-C) has been
reported widely across the world [1, 2]. The exact pathogenesis for
MIS-C remains indefinable. Post-infectious Virus-induced immune
dysregulation appears to play a predominant role [3]. The immature
Immune system in neonates may not produce adequate SARS-CoV-2
antibodies. However, a large study cohort has demonstrated recently
regarding efficient transplacental transfer of immunoglobulin (IG-G)
antibodies from mother to fetus [4]. These immunoglobulins are
generally protective against SARS-CoV-2 infection, but the
transplacental transfer of immunoglobulin along with in-utero transfer
of other inflammatory cytokines might imitate a process to MIS-C,
causing immune activation and featuring as a multisystem inflammatory
syndrome in neonates (MIS-N) [5]. Sero conversion response to
SARS-CoV-2 infection has been seen within 2–3weeks of symptomatic
infection, with both immunoglobulins (IG-M and IG-G) levels depicted in
plasma [6, 7].
Neonates who had perinatal SARS-CoV-2 infection can also cause an
antibody response, and there is suspicion that there may be a late-onset
manifestation with a presentation same as MIS-C seen in children
[8]. This condition has been reported in the neonates, presenting
with fever and multisystem involvement especially myocarditis clinically
or with raised biomarkers such as LDH and ProB-type natriuretic peptide
(proBNP) [9].The possible manifestations in neonates presenting with
MIS-N has only been reported in a small number of cases [5, 10–16].
In this study we present a clinical spectrum of 98 neonate’s cohort
presenting with MIS-N with multi system involvement.