Figure 3
Figure 3. ITP patients had similar glycocalicin levels but higher glycocalicin indicies (GCI) than controls with an inverse correction between GCI and A-IPF, and higher glycocalicin and A-IPF values for patients treated with TPO-A. (A) Plasma glycocalicin levels for patients with ITP compared with healthy controls. The y-axis represents plasma glycocalicin levels; and the x-axis, individual samples. There was no statistically significant difference between the mean (± SE) glycocalicin levels for ITP patients (n = 17) and controls (n = 8): 1.86 ± 0.25 versus 1.60 ± 0.21 μg/mL (P = .144). (B) GCIs for patients with ITP and healthy controls. The y-axis represents GCIs; and the x-axis, individual samples. There was a significant and large difference between the mean (± SE) GCI for ITP patients (n = 17) and controls (n = 8): 31.36 ± 13.28 versus 1.75 ± 0.24 (P = .001). (C) Correlative analysis of GCI and A-IPF for ITP patients. The y-axis represents GCI; and the x-axis, A-IPF. There was a negative correlation between GCI and A-IPF (r2 = −0.578, P = .015). This demonstrates that platelet destruction is equivalent to platelet production. (D) Paired correlative analyses of plasma glycocalicin levels and A-IPF with platelet counts for ITP patients receiving thrombopoieitin receptor agonists and IVIG and/or prednisone. One line graph has a y-axis of A-IPF, and the other represents plasma glycocalicin levels, divided into those patients treated with TPO-A and those treated with IVIG and/or prednisone. The x-axis represents the platelet count. There were positive trends for A-IPF with platelet count for those patients treated with TPO-A (r2 = 0.503, P = .216) and IVIG and/or prednisone (r2 = 0.829, P = .058). This is shown in conjunction with negative trends for plasma glycocalicin levels with platelet count for those treated with TPO-A (r2 = −0.611, P = .115) and for those treated with IVIG and/or prednisone (r2 = −0.543, P = .297). Patients treated with TPO-A had greater A-IPF and plasma glycocalicin levels than those treated with IVIG and/or prednisone.

ITP patients had similar glycocalicin levels but higher glycocalicin indicies (GCI) than controls with an inverse correction between GCI and A-IPF, and higher glycocalicin and A-IPF values for patients treated with TPO-A. (A) Plasma glycocalicin levels for patients with ITP compared with healthy controls. The y-axis represents plasma glycocalicin levels; and the x-axis, individual samples. There was no statistically significant difference between the mean (± SE) glycocalicin levels for ITP patients (n = 17) and controls (n = 8): 1.86 ± 0.25 versus 1.60 ± 0.21 μg/mL (P = .144). (B) GCIs for patients with ITP and healthy controls. The y-axis represents GCIs; and the x-axis, individual samples. There was a significant and large difference between the mean (± SE) GCI for ITP patients (n = 17) and controls (n = 8): 31.36 ± 13.28 versus 1.75 ± 0.24 (P = .001). (C) Correlative analysis of GCI and A-IPF for ITP patients. The y-axis represents GCI; and the x-axis, A-IPF. There was a negative correlation between GCI and A-IPF (r2 = −0.578, P = .015). This demonstrates that platelet destruction is equivalent to platelet production. (D) Paired correlative analyses of plasma glycocalicin levels and A-IPF with platelet counts for ITP patients receiving thrombopoieitin receptor agonists and IVIG and/or prednisone. One line graph has a y-axis of A-IPF, and the other represents plasma glycocalicin levels, divided into those patients treated with TPO-A and those treated with IVIG and/or prednisone. The x-axis represents the platelet count. There were positive trends for A-IPF with platelet count for those patients treated with TPO-A (r2 = 0.503, P = .216) and IVIG and/or prednisone (r2 = 0.829, P = .058). This is shown in conjunction with negative trends for plasma glycocalicin levels with platelet count for those treated with TPO-A (r2 = −0.611, P = .115) and for those treated with IVIG and/or prednisone (r2 = −0.543, P = .297). Patients treated with TPO-A had greater A-IPF and plasma glycocalicin levels than those treated with IVIG and/or prednisone.

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