Previous studies described the clinical features of Covid-19 in adults and infants under 1 year of age. Little is known about features, outcomes and intrauterine transmission potential in newborn babies aged 28 days or less. Through systematical searching, we identified 4 infections in newborn babies in China as of March 13. The age range was 30 hours to 17 days old. Three were male. Two newborn babies had fever, 1 had shortness of breath, 1 had cough and 1 had no syndromes. Supportive treatment was provided for all 4 newborn babies. None required intensive unit care or mechanical ventilation. None had any severe complications.Three newborn babies recovered by the end of this study and had been discharged with 16, 23, and 30 days of hospital stay. All 4 mothers were infected by SARS-CoV-2, 3 showing symptoms before and 1 after delivery. Cesarean section was used for all 4 mothers, 3 at level Ⅲ hospitals and 1 at a level Ⅱ hospital. Three newborn babies were separated from mothers right after being born and were not breastfed. In summary, newborn babies are susceptible to SARS-CoV-2 infection. The symptoms in newborn babies were milder and outcomes were less severe as compared to adults. Intrauterine vertical transmission is possible but direct evidence is still lacking.

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Background: Familial hypomagnesemia with secondary hypocalcemia (HSH) is a rare autosomal recessive disease characterized by severe hypomagnesemia and hypocalcemia associated with neurological symptoms, including generalized seizures, tetany and muscle spasms, which are refractory to anticonvulsant treatment. The pathophysiological hallmarks of HSH are the impaired intestinal absorption of magnesium accompanied by renal magnesium wasting as a result of a reabsorption defect in the distal convoluted tubule. Mutations in TRPM6, the gene encoding the transient receptor potential cation channel subfamily member 6, have been found to be responsible for this disease. In the present study, we report a Chinese family with 2 sisters affected with severe HSH, and elucidate the characteristics of TRPM6 gene mutations in these 2 patients. Methods: We evaluated the clinical, laboratory, and radiographic findings. All 39 TRPM6 exons and flanking exon-intron junctions from genomic DNA were amplified and sequenced in 2 affected members suffering from HSH and their family. Results: We found two novel mutations in the family, one frameshift mutation (c.1196delC) and one non-sense mutation (c.4577G>A). These mutations were predicted to result in a complete loss of function of TRPM6. Both of the sisters were compound heterozygotes for these mutations. Conclusion: Our results suggested that the compound heterozygous mutations in TRPM6 were responsible for HSH in the Chinese family.