ABSTRACT
BACKGROUND AND AIM: Current data suggest little to no possibility of original COVID-19 transmission in pregnant women to the fetus during pregnancy or childbirth. Warning with Omicron new variants has decreased. CASE REPORT: A clinical case of a SARS-CoV-2 virus transplacental infection of a newborn, born at the end of 2022, from a mother who tested positive for Sars-covid-2 and positive IgM SARS-CoV-2 anti-virus. The newborn tested positive for SARS-CoV-2 12 hours after birth, and was clinically symptomatic after three days, an increase in IgM antibodies was not found, although the virus was identified in the urine samples through molecular tests. The insufficient time to determine the presence of antibodies and the immune system's state of immaturity can explain the lack of IgM in the newborn's blood at 14 days after birth. CONCLUSIONS: The Omicron SARS-CoV-2 keeps provoking infections among newborns, especially if the mother contracts it during the third trimester. The host response is most likely influenced by the newborn's peculiar state of immune immaturity. Just before birth, a positive nasal swab and the presence of a positive urine examination confirmed the diagnosis of intraplacental exposure. Research on the virus through molecular tests of urines can represent an additional technique when an aetiological framework of the infection is necessary and a distinction between congenital and post-natal forms.
Subject(s)
COVID-19 , Pregnancy Complications, Infectious , Infant, Newborn , Female , Pregnancy , Humans , SARS-CoV-2 , Pregnancy Complications, Infectious/diagnosis , Infectious Disease Transmission, Vertical , Immunoglobulin MABSTRACT
A 5-year-old girl was referred to the Department of Pediatrics and Neonatology, Guglielmo da Saliceto Hospital, Italy, because of growth retardation. Clinical and laboratory investigations showed pallor, hepatosplenomegaly, anemia and low/normal platelet count. Further investigations led to the diagnosis of Gaucher disease (GD). We believe this is the first report of growth hormone deficiency in a growth-retarded child with GD. After 1 year of imiglucerase replacement enzyme therapy, her bone age had normalized, linear growth rate had accelerated, and insulin growth factor-1 (IGF-1) and, perhaps more interestingly, growth hormone deficiency, had normalized. While the pathophysiological mechanisms underlying compromised growth in GD are poorly understood, the response to imiglucerase reported in this patient suggests that growth hormone deficiency is related to the underlying metabolic disorder in GD, rather than a primary endocrine pathology. Growth hormone deficiency adds to an already extensive list of possible clinical manifestations of this heterogeneous and complex disorder.