Suppressed pediatric asthma hospitalizations during the COVID-19 pandemic in Japan, from a national survey.

BACKGROUND: Acute asthma exacerbation in children is often caused by respiratory infections. In this study, a coordinated national surveillance system for acute asthma hospitalizations and causative respiratory infections was established. We herein report recent trends in pediatric acute asthma hospitalizations since the COVID-19 pandemic in Japan. METHODS: Thirty-three sentinel hospitals in Japan registered all of their hospitalized pediatric asthma patients and their causal pathogens. The changes in acute asthma hospitalization in children before and after the onset of the COVID-19 pandemic and whether or not COVID-19 caused acute asthma exacerbation were investigated. RESULTS: From fiscal years 2010-2019, the median number of acute asthma hospitalizations per year was 3524 (2462-4570), but in fiscal years 2020, 2021, and 2022, the numbers were 820, 1,001, and 1,026, respectively (the fiscal year in Japan is April to March). This decrease was observed in all age groups with the exception of the 3- to 6-year group. SARS-CoV-2 was evaluated in 2094 patients from fiscal years 2020-2022, but the first positive case was not detected until February 2022. Since then, only 36 of them have been identified with SARS-CoV-2, none of which required mechanical ventilation. Influenza, RS virus, and human metapneumovirus infections also decreased in FY 2020. In contrast, 24% of patients had not been receiving long-term control medications before admission despite the severity of bronchial asthma. CONCLUSION: SARS-CoV-2 was hardly detected in children with acute asthma hospitalization during the COVID-19 pandemic. This result indicated that SARS-CoV-2 did not induce acute asthma exacerbation in children. Rather, infection control measures implemented against the pandemic may have consequently reduced other respiratory virus infections and thus acute asthma hospitalizations during this period. However, the fact that many hospitalized patients have not been receiving appropriate long-term control medications is a major problem that should be addressed.

Novel mutation of early, perinatal-onset, myopathic-type very-long-chain acyl-CoA dehydrogenase deficiency.

A male neonate demonstrated fetal distress, neonatal asphyxia, and transient hyper-creatine kinase-emia (8400IU/L), followed by repeated episodes of rhabdomyolysis 1-2 times/year during infancy and early childhood. At age 6 years, decreased levels of total and free carnitine in serum, and mild fiber size variation and increased fatty droplets in muscle, were confirmed. Both blood and serum fatty-acid analysis demonstrated elevated 5-tetradecenoate levels, and the acyl-CoA dehydrogenase activity of the palmitoyl-CoA/octanoyl-CoA ratio decreased in skin fibroblasts. The sequenced clone analysis of a complimentary DNA fragment revealed a compound heterozygote mutation of exon 9 (A790G) and exon 10 (997 ins T), which is a novel mutation of a myopathic-type very-long-chain acyl-CoA dehydrogenase deficiency. The patient has reached age 13 years. By treatment with an avoidance of fasting, feeding with a high-carbohydrate and low-fat diet, and intravenous drip infusion soon after every onset of rhabdomyolysis, his physical and mental development has stayed within the normal range. Patients with a perinatal onset of myopathic-type very-long-chain acyl-CoA dehydrogenase deficiency have not yet been reported. His novel mutation might be related to his clinical characterization.