Validation of the Urticaria Control Test (UCT) in Children With Chronic Urticaria.

BACKGROUND: Few validated tools exist to evaluate chronic urticaria (CU) control in children. Although the Urticaria Control Test (UCT) exhibits favorable clinometric properties in adult CU, it is not yet validated in children. OBJECTIVE: To evaluate the validity of the UCT for the assessment of pediatric CU. METHODS: Children presenting with CU were consecutively recruited and completed both the UCT and the Children's Dermatology Life Quality Index (CDLQI) at study entry. Using the CDLQI as an anchor, we assessed the internal consistency, convergent and known-groups validity, and screening accuracy of the UCT at study entry and at follow-up. RESULTS: A total of 52 children with CU were recruited. The UCT exhibited respectable internal consistency in the evaluation of CU (Cronbach's α, 0.73; 95% CI, 0.62-0.85). UCT and CDLQI scores strongly correlated (r = -0.74; P < .01). The UCT distinguished between different strata of disease severities established by the CDLQI (P < .01). Screening accuracy of the UCT was excellent in the discrimination of poorly controlled CU (area under the curve, 0.82). An optimal cutoff of less than or equal to 10 was determined for defining poorly controlled CU (sensitivity, 95.5%; specificity, 63.3%). Data at follow-up were consistent with data at study entry. Subgroup analyses of patients with chronic spontaneous urticaria were consistent with overall estimates of validity. CONCLUSIONS: The UCT is a valid tool for the assessment of pediatric CU and chronic spontaneous urticaria, as evidenced by the acceptable internal consistency, convergent and known-groups validity, and screening accuracy at multiple time points.

A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohistiocytosis genes' interactions points to Neutrophil extracellular traps as mediators of thrombosis in COVID-19.

Abnormal coagulation and an increased risk of thrombosis are features of severe COVID-19, with parallels proposed with hemophagocytic lymphohistiocytosis (HLH), a life-threating condition associated with hyperinflammation. The presence of HLH was described in severely ill patients during the H1N1 influenza epidemic, presenting with pulmonary vascular thrombosis. We tested the hypothesis that genes causing primary HLH regulate pathways linking pulmonary thromboembolism to the presence of SARS-CoV-2 using novel network-informed computational algorithms. This approach led to the identification of Neutrophils Extracellular Traps (NETs) as plausible mediators of vascular thrombosis in severe COVID-19 in children and adults. Taken together, the network-informed analysis led us to propose the following model: the release of NETs in response to inflammatory signals acting in concert with SARS-CoV-2 damage the endothelium and direct platelet-activation promoting abnormal coagulation leading to serious complications of COVID-19. The underlying hypothesis is that genetic and/or environmental conditions that favor the release of NETs may predispose individuals to thrombotic complications of COVID-19 due to an increase risk of abnormal coagulation. This would be a common pathogenic mechanism in conditions including autoimmune/infectious diseases, hematologic and metabolic disorders.