Background Acute myocarditis (AMC) can cause poor outcomes or even death in children. We aimed to identify AMC risk factors and create a mortality prediction model for AMC in children at hospital admission. Methods This was a single-center retrospective cohort study of AMC children hospitalized between January 2016 and January 2020. The demographics, clinical examinations, types of AMC, and laboratory results were collected at hospital admission. In-hospital survival or death was documented. Clinical characteristics associated with death were evaluated. Results Among 67 children, 51 survived, and 16 died. The most common symptom was digestive disorder (67.2%). Based on the Bayesian model averaging and Hosmer–Lemeshow test, we created a final best mortality prediction model (acute myocarditis death risk score, AMCDRS) that included ten variables (male sex, fever, congestive heart failure, left-ventricular ejection fraction < 50%, pulmonary edema, ventricular tachycardia, lactic acid value > 4, fulminant myocarditis, abnormal creatine kinase-MB, and hypotension). Despite differences in the characteristics of the validation cohort, the model discrimination was only marginally lower, with an AUC of 0.781 (95% confidence interval = 0.675–0.852) compared with the derivation cohort. Model calibration likewise indicated acceptable fit (Hosmer‒Lemeshow goodness-of-fit, P¼ = 0.10). Conclusions Multiple factors were associated with increased mortality in children with AMC. The prediction model AMCDRS might be used at hospital admission to accurately identify AMC in children who are at an increased risk of death.
Premature ovarian insufficiency (POI) is a heterogeneous disease affecting the physical and mental health of millions of women worldwide. The contribution of genetic factors in the pathogenesis of POI has increased, with quite a few of causative genes involved in meiosis. ZMM proteins are a group of conserved proteins participating in meiotic synapsis and crossover maturation. Here, by screening the variations of ZMM genes in our in‐house WES database of 1030 idiopathic POI patients, one novel homozygous variation in SPO16 (c.160 + 8A > G) was firstly identified in one patient. The variation was verified to disturb mRNA splicing by minigene assay, produced a non‐functional SPO16 protein, and was classified as pathogenetic according to American College of Medical Genetics guideline. During meiotic prophase I, SHOC1 binds to branched DNA and recruits SPO16 and other ZMM proteins to facilitate crossover formation. Together with our recent identified bi‐allelic variations of SHOC1 in a published work, this study highlighted the essential roles of ZMM genes in the maintenance of ovarian function and expanded the POI gene spectrum.
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