Objective
To provide a comprehensive and systematic analysis of demographic characteristics, clinical symptoms, laboratory findings and imaging features of coronavirus disease 2019 (COVID‐19) in pediatric patients.
Methods
A meta‐analysis was carried out to identify studies on COVID‐19 from December 25, 2019 to April 30, 2020.
Results
A total of 48 studies with 5829 pediatric patients were included. Children at all ages were at risk for COVID‐19. The main illness classification ranged as: 20% (95% CI: 14 to 26%, I
2
=91.4%) asymptomatic, 33% (95% CI: 23 to 43%, I
2
=95.6%) mild and 51% (95% CI: 42 to 61%, I
2
=93.4%) moderate. The typical clinical manifestations were fever 51% (95% CI: 45 to 57%, I
2
=78.9%) and cough 41% (95% CI: 35 to 47%, I
2
=81.0%). The common laboratory findings were normal white blood cell 69% (95% CI: 64 to 75%, I
2
=58.5%), lymphopenia 16% (95% CI: 11 to 21%, I
2
=76.9%) and elevated creatine‐kinase MB (CK‐MB) 37% (95% CI: 25 to 48%, I
2
=59.0%). The frequent imaging features were normal images 41% (95% CI: 30 to 52%, I
2
=93.4%) and ground‐glass opacity 36% (95% CI: 25 to 47%, I
2
=92.9%). Among children under 1‐year old, critical cases account for 14% (95% CI: 13 to 34%, I
2
=37.3%) that should be of concern. In addition, vomiting occurred in 33% (95% CI: 18 to 67%, I
2
=0.0%) cases that may also need attention.
Conclusions
Pediatric patients with COVID‐19 may experience milder illness with atypical clinical manifestations and rare lymphopenia. High incidence of critical illness and vomiting symptoms reward attention in children under 1‐year old.
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Naringin maintains bone mass in various osteoporosis models, while its effect on bone in disuse osteoporosis has not been reported. The present study explores whether naringin can prevent disuse osteoporosis induced by unilateral sciatic neurectomy (USN) and whether the Semaphorin 3A-induced Wnt/β-catenin signalling pathway is involved in the osteoprotection of naringin. Naringin dose-dependently prevented the deterioration of bone mineral density (BMD), trabecular structure and biomechanical strength in femur due to USN. Naringin increased bone formation but inhibited resorption, as indicated by bone-turnover markers in blood and urine and the histological staining of Osteocalcin (OCN) and tartrate-resistant acid phosphatase (TRAP) in femur. Semaphorin 3A (Sema3A) and active β-catenin protein decreased after USN and could be restored by naringin to the levels of the sham-operated rats. In addition, naringin in vitro promoted the differentiation of osteoblasts and inhibited osteoclastic differentiation. Our studies suggest that the down-regulation of Sema3A and the subsequent inactivation of Wnt/β-catenin signalling may be some of the mechanisms involved in USN-induced osteoporosis. Naringin could increase the expression of Sema3A and the activation of Wnt/β-catenin signalling to prevent disuse osteoporosis induced by denervation. Thus, naringin functions in bone maintenance and could be a promising therapeutic alternative in preventing disuse osteoporosis.
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