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Despite rapidly evolving knowledge about COVID 19 infection, routes of perinatal COVID 19 transmission and viral load in mother neonate dyad remain uncertain. Data were analysed to describe the clinicodemographic profile and viral load in neonates born to COVID 19 positive mothers. Of 2947 deliveries, 69 mothers were COVID 19 positive (2.3%), with 1 abortion, 2 macerated stillbirths and 2 fresh stillbirths as pregnancy outcomes. Of 65 tested neonates, 10.7% (7) were confirmed COVID 19 positive by RTPCR (reverse transcriptase-polymerase chain reaction). Viral load (cycle threshold, Ct of E, RDRp) in neonates was comparable with the Ct reported from adults; however, neonates had milder clinical manifestations. All 7 neonates who tested positive for COVID 19 were subsequently discharged. Six of the 7 neonates were asymptomatic and 1 neonate needed respiratory support (indication being prematurity) which resolved after 48 h. Maternal and neonatal comparison of Ct of E and RdRp gene was statistically non-significant (25.97 vs 19.68, p = 0.34 and 26.5 vs 25.0, p = 0.84). Viral loads of mothers with COVID 19 positive neonates compared with mothers with COVID 19 negative neonates for E and RdRp gene were also statistically non-significant (25 vs 27.19, p = 0.63 and 19.6 vs 27.6, p = 0.08). The majority (93%) of neonates tested later than 48 h (roomed in with mother and breastfed) tested negative. Conclusion: The study supports milder manifestation in COVID 19 positive neonates. Risk of transmission from COVID 19 positive mother to neonate by rooming-in and breastfeeding is low. In this study on a limited number of neonates, maternal viral load was not found to be associated with the positivity status or severity of the illness of neonate.

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The increasing incidence of obesity, leading to metabolic complications is now recognized as a major public-health problem. Insulin resistance is a central abnormality of the metabolic syndrome, or syndrome X, originally hypothesized by Reaven Insulin resistance is more strongly linked to intra abdominal fat than to fat in other depots. Adipose tissue secretes numerous factors (adipokines) known to markedly influence lipid and glucose/insulin metabolism, oxidative stress, and cardiovascular integrity. Some of these adipokines have been shown to directly or indirectly affect insulin sensitivity through modulation of insulin signaling and the molecules involved in glucose and lipid metabolism. A pilot study was conducted with 80 healthy subjects who were non diabetic, non hypertensive and having no family history of hypertension, the aim was to evaluate the correlation of adiponectin and leptin levels with obesity and insulin resistance markers in healthy north Indian adult population. Serum leptin, adiponectin and insulin was estimated by sandwich ELISA method. In our study, Leptin correlated significantly with BMI (P value of 0.0000), WC (P value = 0.007), and HC (P value = 0.000). leptin showed significant positive correlation with fasting insulin (P value 0.002), post prandial insulin (P value = 0.000) and HOMA-IR (P value = 0.002). Adiponectin showed significant positive correlation with triglycerides (P value = 0.038), strong negative correlation with HDL-cholesterol (P value = 0.017). Serum concentrations of leptin are associated with central body fat distribution. Insulin resistance and adiponectin is associated with dyslipidemia and these all disorders may ultimately lead to metabolic syndrome.