Background: Short stature can be a normal variant or secondary to an underlying disorder. It is necessary to evaluate short stature to differentiate a normal from pathological short stature and thus decide the further treatment needed. This study was conducted at a tertiary care hospital to find out the various etiologies of short statureMethods: An observational study was conducted on 49 children in age of 2-12 years with short stature. They were grouped as normal variants and pathological short stature depending on upper-lower segment ratio the study group was later divided into proportionate and disproportionate short stature. They were further investigated to find out the etiology of the short stature. The bone age of all groups was compared with the chronological age to calculate the bone age retardation.Results: Out of 49 children 26.5% were normal variants and 73.4% as pathological type. 77.7% of pathological short stature were proportionate type. The male:female ratio was 1:1.4. Chronic systemic disorders were detected in 24.48% while malnutrition and endocrine disorders constituted 12% each. The bone age retardation in endocrine disorders was 0.47.Conclusions: Chronic systemic disorders were commonest cause of pathological short stature in this study. Females were predominantly affected in all groups and bone age retardation was maximum in endocrine disorders, thus indicating that early diagnosis and management of these disorders is necessary to decrease the growth retardation in these children. An understanding of short stature not only permits to differentiate a normal variant from an underlying disorder but also helps in modifying the course by means of early intervention.
Multisystem inflammatory syndrome (MIS-C) in children (MIS-C) associated with severe acute respiratory syndrome coronavirus-2 (SARS-CoV2) is well recognised in children, however, rarely reported in newborns. It usually presents as fever and multiorgan involvement, with blood investigations showing increased inflammatory markers weeks after exposure to SARS-CoV-2. Unlike older children, the mechanism is unique in neonates as COVID-19 infection and the subsequent inflammatory reaction leading to MIS-C occur in two different individuals. We reviewed the perinatal history, clinical features, and outcomes of 3 neonates with features consistent with MIS-N related to maternal SARS-CoV-2, from August 2021 to December 2021. Anti-SARS-CoV-2 IgG and IgM antibodies were tested in all neonates. Clinical picture comprised multiorgan dysfunction (gastrointestinal, cardiorespiratory, haematological and dermatological), positive inflammatory markers, high ferritin and high D-dimer levels, elevated Cardiac enzymes. Blood cultures were sterile. Positive anti-SARS-CoV-2 IgG in both the mother and the infant, along with epidemiological evidence of maternal contact with COVID-19, clinched the diagnosis of MIS-C. Immunomodulatory drugs (intravenous immunoglobulin and systemic steroids) were administered. Multisystem inflammatory syndrome should be considered as a differential diagnosis in all critically ill neonates, particularly with maternal history of COVID-19 infection or epidemiological contact. This neonatal presentation is the reflection of fetal inflammatory response syndrome associated with maternal SARS-CoV-2 infection. Having no fever throughout the course of illness, in some neonates, suggests that neonates respond differently compared with children.
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