Human herpes virus-6 (HHV-6) is a DNA virus with two known subtypes A and B. It is unique as its genome integrates into that of humans and is transmitted through the germ cells to the progeny, which is the major mode of vertical transmission (86%) compared to transplacental transmission (14%). 1 Chromosomally integrated HHV-6 (ciHHV-6) is diagnosed by the detection of HHV-6 DNA in hair follicles and/or nail clippings while it will be absent in transplacental infection. 2 We present a neonate who presented in shock after birth, was diagnosed with ciHHV-6Aassociated myocarditis and was successfully treated with artesunate, an antimalarial drug with antiviral properties.

Objectives: The aim of the study was to estimate the time required for normalization of hypothyroxinemia of prematurity in neonates below 34 weeks of gestation. Material and Methods: A retrospective study was conducted in neonates born below 34 weeks of gestation, between January 2015 and December 2016. Data were collected on free thyroxine (fT4) and thyroid-stimulating hormone (TSH) levels, tested on days 3, 14, 28, and 42. Gestational age, birth weight, use of antenatal steroids, mechanical ventilation, and various preterm morbidities, along with development at 18 months of corrected age, were comparatively analyzed in neonates with and without hypothyroxinemia. The median time for normalization of fT4 in all these variables was estimated. Results: On day 3, low fT4 was noted in 69 (37.7%) out of 183 neonates born below 34 weeks of gestation; all had normal TSH levels. Hypothyroxinemia showed statistically significant association with gestational age, birth weight, antenatal steroid use, respiratory distress syndrome, invasive ventilation, shock, sepsis, patent ductus arteriosus (PDA), anemia during stay in neonatal intensive care unit, and development at 18 months. Median time for normalization was 14 days in most of the neonates, and 28 days in those with <28 weeks of gestational age, weight of <1000 g and with shock, anemia, and PDA. Two infants with hypothyroxinemia received therapy with levothyroxine at 6 weeks for a short duration, as TSH was high. Conclusion: Hypothyroxinemia of prematurity takes 14–28 days to normalize based on maturity, weight, and illnesses. This study recommends serum fT4 testing at 2 weeks of life, provided congenital hypothyroidism was ruled out by 3–4 days of life, using direct blood spot card metabolic screening.

Introduction: Coronavirus disease 2019 (COVID-19), an extremely contagious pandemic, caused by the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), originated from Wuhan, Hubei province, in China in December 2019. From April 2020, pediatric epicenters in Europe and the USA reported a new clinical spectrum called “pediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2” or “multisystem inflammatory syndrome in children,” respectively. The unique feature was immune-mediated multiorgan dysfunction in response to previous COVID exposure. This case series aims to prospectively analyze the incidence, severity, and patterns of cardiac involvement in sick neonates exposed to perinatal SARS-CoV-2 in India. Methods: Twelve neonates presenting with very early-onset multi-inflammatory syndrome in neonates (MIS-N) at two tertiary care centers in India were included. Their clinical profiles, echocardiography findings, and treatment details were recorded. Results: Clinical presentations varied from loss of fetal movement, perinatal depression, prematurity, unusual respiratory distress syndrome, cardiogenic shock, arrhythmias, and multi-organ dysfunction. Echocardiographic markers were severe pulmonary hypertension, significant valvular regurgitation, cardiomegaly, biventricular dysfunction, neonatal coronary artery aneurysms, intracardiac thrombus, pericardial effusion, and arrhythmias. All babies, except one, had positive COVID IgG antibody and high inflammatory markers. Two mothers had antenatal primary contact with COVID patients 4–6 weeks prior to delivery, while 3 (25%) had documented mild COVID infection. All neonates were started on immunosuppressive therapy. Clinical stabilization and declining inflammatory markers were observed within 48–96 h of targeted therapy. All neonates (except one) recovered and were discharged in a stable condition. Follow-up available up to 9 months demonstrated persistent clinical, laboratory, and echocardiographic recovery in all survivors. Conclusion: Infection of pregnant mothers during community transmission during the two COVID-19 waves in India appears to have caused significant immune dysregulation and cardiac damage in neonates. Echocardiography detected significant damage to coronary arteries, pulmonary arterial hypertension, intracardiac thrombus, ventricular dysfunction, and incompetence of valve apparatus in MIS-N. Aggressive immunomodulators with antiplatelet drugs proved lifesaving. Echocardiography is an inexpensive, readily available imaging modality. It should be utilized to save this fragile, extremely special cohort.

A 27 year old multigravida, presented with giant left ventricular cardiac rhabdomyoma at the 23rd gestational week. A previous bad obstetric history prompted amniocentesis. A heterozygous, pathogenic, missense variant in exon 40 of the Tuberous Sclerosis (TSC 2) gene with autosomal dominant inheritance was extracted from fetal DNA by targeted gene capture. Sanger's sequencing confirmed the same. This fetus highlighted the need for genetic assessment in every cardiac rhabdomyoma and a paradigm shift in fetal counseling protocol. We retrospectively reviewed our personal, multi-centric 13 years (2008-2020) database of cardiac rhabdomyomas in the fetal and pediatric cohort. Cardiac rhabdomyoma preceded extra-cardiac manifestations of Tuberous Sclerosis in 87.5% of our cohort. This article underscores this forgotten ominous association. We propose a paradigm shift in fetal counseling in such a scenario, remembering the heterogeneous timing and presentations of this widely variable genetic lesion.