Baseline Diameter of the Inferior Vena Cava Measured with Sonography in Euvolemic Children and its Relationship to Somatic Variables.

PURPOSE: To determine normative data for the inferior vena cava (VCI) diameter in euvolemic children and its correlation with different somatic parameters in a pediatric population at one center in Europe. MATERIALS AND METHODS: This prospective observational study enrolled healthy children aged 4 weeks to 18y that visited our outpatient clinic. Weight, height, body surface area, and age were recorded. The children were grouped according to weight, as follows (80 children/group): < 10 kg, 10-19.9 kg, 20-29.9 kg, 30-59.9 kg, and 60-90 kg. Children were placed in a supine position and, during quiet respiration, the maximum and minimum VCI diameters were measured with M-mode ultrasonography. The collapsibility index (CI) was also automatically calculated for each subject: CI = [VCI maximum (expiratory) diameter - VCI minimum (inspiratory) diameter]/VCI maximum (expiratory) diameter. RESULTS: From May 2016 through November 2018 we retrieved data for 415 children that underwent VCI diameter evaluations. 400 children were included (mean age: 7.8y ± 5.8, mean weight: 32 kg ±â€Š24.4, 46 % girls). The VCImax and the VCImin were significantly correlated with age (r = 0.867, p < 0.001, r = 0.797, p < 0.001), height (r = 0.840, p < 0.001, r = 0.772, p < 0.001), weight (r = 0.858, p < 0.001, r = 0.809, p < 0.001), and BSA (r = 0.878, p < 0.001, r = 0.817, p < 0.001). Correlations between the CI and age, weight, height, and BSA were not statistically significant. CONCLUSION: This prospective study provided reference values for sonographic measurements of VCI diameters in euvolemic children and might greatly assist in assessing fluid status in sick children.

Induction of autotaxin by the Epstein-Barr virus promotes the growth and survival of Hodgkin lymphoma cells.

A proportion of patients with Hodgkin lymphoma carry Epstein-Barr virus (EBV), an oncogenic herpesvirus, in their tumor cells. Although it is generally assumed that EBV contributes to the malignant phenotype of Hodgkin lymphoma cells, direct evidence in support of this is lacking. Here we show that EBV infection of Hodgkin lymphoma cells results in the induction of autotaxin, a secreted tumor-associated factor with lysophospholipase-D activity. Up-regulation of autotaxin increased the generation of lysophosphatidic acid (LPA) and led to the enhanced growth and survival of Hodgkin lymphoma cells, whereas specific down-regulation of autotaxin decreased LPA levels and reduced cell growth and viability. In lymphoma tissues, autotaxin expression was mainly restricted to CD30+ anaplastic large-cell lymphomas and Hodgkin lymphoma; in the latter, high levels of autotaxin were strongly associated with EBV positivity (P = .006). Our results identify the induction of autotaxin and the subsequent generation of LPA as key molecular events that mediate the EBV-induced growth and survival of Hodgkin lymphoma cells and suggest that this pathway may provide opportunities for novel therapeutic intervention.