Comparison of Clinical Manifestations of Kawasaki Disease According to SARS-CoV-2 Antibody Positivity

Background@#Kawasaki disease (KD) is the most common cause of acquired heart disease in paediatric patients, with infectious agents being the main cause. This study aimed to determine whether there are differences in the clinical manifestations of KD between patients with and without severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibodies. @*Methods@#From January 1, 2021 to August 15, 2022, 82 patients with analysable echocardiographic data were diagnosed with KD. Twelve patients with multisystem inflammatory syndrome in children were excluded. Serologic tests were performed by chemiluminescence immunoassay for both the nucleocapsid (N) and the spike (S) proteins in blood samples. Among the 70 patients diagnosed with KD at Jeonbuk University Children’s Hospital, the SARS-CoV-2 antibody test was performed in 41 patients. @*Results@#The SARS-CoV-2 antibody test results for the N antigen were positive in 12 patients, while those for S protein were positive in 14 patients. N antigen SARS-CoV-2 antibodypositive KD was different from N antigen SARS-CoV-2 antibody-negative KD in terms of sex (male predominance in the positive group, 83.3% vs. female predominance in the negative group 62.1%, P = 0.008) and the incidence of refractory KD (41.7% vs. 10.3%, P = 0.034). The pro-B-type natriuretic peptide level was lower in the N-antigen SARS-CoV-2 antibody-positive KD group than that in the negative group (518.9 ± 382.6, 1,467.0 ± 2,417.6, P = 0.049). No significant differences in the echocardiographic findings between both groups were noted. In the multi-variable analysis, SARS-CoV-2 antibody (N antigen) was the only predictor of refractory KD (odds ratio, 13.70; 95% confidence interval, 1.63–115.44; P = 0.016). @*Conclusion@#High incidence of intravenous immunoglobulin-refractory KD may occur in up to 40% of the patients having recent history of coronavirus disease 2019. For patients having KD with N-type SARS-CoV-2 antibody positivity, adjunctive treatment, such as corticosteroids, can be considered as the first line of treatment.

Two Case Reports of Life-Threatening Croup Caused by the SARS-CoV-2 Omicron BA.2 Variant in Pediatric Patients

Croup is a common upper airway infection characterized by a barking cough, stridor, and hoarseness. It is usually caused by viral infection. A small number of croup caused by coronavirus disease 2019 (COVID-19) has been reported in children before the omicron variant surge. Previously reported cases indicated that croup caused by COVID-19 can be treated in the same manner as those with other viral causes. We describe two cases (9-monthold girl and 11-month-old boy) of previously healthy infants who presented with a barking cough and chest retraction and required endotracheal intubation and cardiopulmonary resuscitation. Despite receiving dexamethasone and nebulized racemic epinephrine (NRE) treatment for croup in the emergency department, these patients still developed acute respiratory failure. Reverse transcription polymerase chain reaction (RT-PCR) of nasopharyngeal samples revealed severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) omicron BA.2 variant (Stealth omicron) and no other common respiratory viral pathogens. Both patients were treated with mechanical ventilation, dexamethasone, and NRE in the pediatric intensive care unit. The duration of intubation was 112 hours and 80 hours, respectively. Both patients were discharged without complications. To the best of our knowledge, this is the first report of life-threatening croup produced by the omicron BA.2 variant and confirmed by RT-PCR. We suggest that this SARS-CoV-2 variant may cause severe croup that may not improve with conventional treatment, even in children without underlying diseases.

A Case Report for Using Methylprednisolone for Severe ARDS Caused by SARS-CoV-2 Delta Variant in a Pediatric Patient With Lennox-Gastaut Syndrome

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in the coronavirus disease 2019 (COVID-19) pandemic. COVID-19 can result in fatal comorbidities, including acute respiratory distress syndrome (ARDS). Several reports suggest that children have milder illness, though severe cases have still been reported. We report a 9-year-old boy with ARDS caused by the SARS-CoV-2 delta (B.1.617.2) variant. He was admitted to our hospital and carefully observed due to underlying Lennox-Gastaut syndrome. He developed intractable seizures with a high fever. Although the seizures were controlled, his respiratory condition deteriorated to severe ARDS. High-dose methylprednisolone was administered with high positive end-expiratory pressure and low tidal volume. After ARDS treatment, oxygenation improved sufficiently to permit extubation. This case suggests that close observation is required in pediatric patients with neurologic comorbidities because of an increased risk for severe COVID-19.

A Case of Myocarditis Presenting With a Hyperechoic Nodule After the First Dose of COVID-19 mRNA Vaccine

Myocarditis and/or pericarditis have been reported as adverse events following coronavirus disease 2019 (COVID-19) messenger RNA vaccination, with most cases occurring within 1 week after the second dose. We report a rare case of myocarditis after the first dose of the BNT162b2 (Pfizer-BioNTech) COVID-19 vaccine in a 17-year-old boy. Here, we describe the laboratory, electrocardiographic, and imaging findings of myocarditis.

Clinical Significance of the Bacille Calmette-Guérin Site Reaction in Kawasaki Disease Patients Aged Less than 18 Months

PURPOSE: The purpose of this study was to investigate the clinical significance of Bacille Calmette-Guérin (BCG) site reaction in terms of diagnosis and outcome prediction in young children with Kawasaki disease (KD). METHODS: The incidence of BCG site reaction in the respective age ranges was investigated in 1,058 patients who were admitted at Asan Medical Center between January 2006 and February 2017. The 416 patients under 18 months of age were enrolled as subjects for the analysis of the association between BCG site reaction and other laboratory and clinical findings. The analysis was performed separately in complete and incomplete KD groups. RESULTS: The incidence rate of BCG site reaction was peaked at 6–12 months (83%) and decreased with increasing age after 12 months in 1,058 patients (P < 0.001). The incidence rate was above 70% in KD aged less than 18 months and more frequent than those of cervical lymphadenopathy. The logistic regression analyses showed that the principal clinical findings including conjunctivitis (P=0.781), red lips/oral mucosa (P=0.963), rash (P=0.510), cervical lymphadenopathy (P=0.363), changes in extremities (P=0.283) and the coronary artery aneurysm (P=0.776) were not associated with the BCG site reaction. CONCLUSIONS: The BCG site reaction could be a useful diagnostic tool independent to principal clinical findings in KD developing in children aged < 18 months, who underwent BCG vaccination. Outcome of KD patients was not different between groups with or without the BCG site reaction in both complete KD and incomplete KD.

Virus-associated Rhabdomyolysis in Children

PURPOSE: Virus-associated rhabdomyolysis is very rare. We report 15 patients with rhabdomyolysis caused by various viruses. METHODS: Fifteen patients who were diagnosed with rhabdomyolysis and a viral infection were included in this study. Clinical, laboratory, and radiologic findings were evaluated through retrospective chart reviews. RESULTS: Chief complaints were severe bilateral lower leg pain and leg weakness. The median age was 5.7 years. The male:female ratio was 2:5. The viral infections were caused by influenza virus B, parainfluenza virus, and rhinovirus. One patient with influenza virus B had coinfection with coronavirus. Median initial laboratory values and ranges were as follows:serum creatinine, 0.4 (0.1-0.5) mg/dL; serum aspartate transaminase, 124 (48-1,098) IU/L; serum alanine transaminase, 30 (16-1,455) IU/L; serum creatine kinase, 2,965 (672-16,594) IU; serum lactate dehydrogenase, 400 (269-7,394) IU/L; serum myoglobin, 644 (314-3,867) ng/mL; urine myoglobin, 3 (3-10,431) ng/mL. All patients recovered without complications. CONCLUSION: This is the first report of the simultaneous occurrence of rhabdomyolysis caused by various viruses. This is also the first report of rhinovirus-associated rhabdomyolysis.

Virus-associated Rhabdomyolysis in Children

PURPOSE: Virus-associated rhabdomyolysis is very rare. We report 15 patients with rhabdomyolysis caused by various viruses. METHODS: Fifteen patients who were diagnosed with rhabdomyolysis and a viral infection were included in this study. Clinical, laboratory, and radiologic findings were evaluated through retrospective chart reviews. RESULTS: Chief complaints were severe bilateral lower leg pain and leg weakness. The median age was 5.7 years. The male:female ratio was 2:5. The viral infections were caused by influenza virus B, parainfluenza virus, and rhinovirus. One patient with influenza virus B had coinfection with coronavirus. Median initial laboratory values and ranges were as follows:serum creatinine, 0.4 (0.1-0.5) mg/dL; serum aspartate transaminase, 124 (48-1,098) IU/L; serum alanine transaminase, 30 (16-1,455) IU/L; serum creatine kinase, 2,965 (672-16,594) IU; serum lactate dehydrogenase, 400 (269-7,394) IU/L; serum myoglobin, 644 (314-3,867) ng/mL; urine myoglobin, 3 (3-10,431) ng/mL. All patients recovered without complications. CONCLUSION: This is the first report of the simultaneous occurrence of rhabdomyolysis caused by various viruses. This is also the first report of rhinovirus-associated rhabdomyolysis.

Two cases of TSC2/PKD1 contiguous gene deletion syndrome

Tuberous sclerosis complex (TSC, MIM#191100) is an autosomal dominant neurocutaneous syndrome caused by mutation or deletion of TSC1 encoding hamartin or TSC2 encoding tuberin and characterized by seizure, mental retardation, and multiple hamartomas or benign tumors in the skin, brain, retina, heart, kidney, and lungs. The TSC2 gene on chromosome 16p13.3 lies adjacent to the PKD1 gene which is responsible for autosomal dominant polycystic kidney disease (MIM#173900). The TSC2/PKD1 contiguous gene syndrome (TSC2/PKD1 CGDS, MIM#600273) is caused by deletion of both TSC2 and PKD1 gene. We recently experienced a 15 month-old boy and a 26 month-old girl with TSC2/PKD1 CGDS confirmed by multiplex ligation-dependent probe amplification (MLPA) analysis. They showed not only typical neurologic manifestations of TSC such as epilepsy, subependymal nodules, and subcortical tubers, but also polycystic kidney disease. The contiguous gene syndrome involving PKD1 and TSC2 should be suspected in children with enlarged polycystic kidneys and TSC. MLPA analysis is a useful method for the genetic confirmation of TSC2/PKD1 CGDS.