Figure 7
Figure 7. Elevations in circulating VEGF and Ang2 correlate with progression of an acute SCLS episode and induction of endothelial permeability. (A-B) Clinical course of a patient with a severe SCLS crisis characterized by hypotension, hemoconcentration (elevated Hgb; A) and a 20-kg weight gain in 3 days (B). (C) Serum and plasma VEGF and Ang2 in serial samples taken during the course of the illness were measured by ELISA. Baseline values were obtained 130 days before the episode during an asymptomatic period and at the beginning of the leak (admission to intensive care) and postleak (diuresis) phases as indicated by arrows. (D-E) Serum obtained at the peak of symptoms (“peak”) but not serum from the postleak resolution phase (“resolved”) induces endothelial permeability as assessed by decreased TEER (D) and reorganization of adhesive junctions and cell retraction (E); **P = .003, paired t test.

Elevations in circulating VEGF and Ang2 correlate with progression of an acute SCLS episode and induction of endothelial permeability. (A-B) Clinical course of a patient with a severe SCLS crisis characterized by hypotension, hemoconcentration (elevated Hgb; A) and a 20-kg weight gain in 3 days (B). (C) Serum and plasma VEGF and Ang2 in serial samples taken during the course of the illness were measured by ELISA. Baseline values were obtained 130 days before the episode during an asymptomatic period and at the beginning of the leak (admission to intensive care) and postleak (diuresis) phases as indicated by arrows. (D-E) Serum obtained at the peak of symptoms (“peak”) but not serum from the postleak resolution phase (“resolved”) induces endothelial permeability as assessed by decreased TEER (D) and reorganization of adhesive junctions and cell retraction (E); **P = .003, paired t test.

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