Table 1.
Platelet desialylation of different groups [M (P 25, P 75)]
| Age | Gender (M/F) | PLT (×109/L) | RCA-1 (%) | ECL (%) | |
|---|---|---|---|---|---|
| ITP (n = 61) | 43 ± 18 | 18/43 | 16.0 ± 12.5 | 1.60 (0.50,8.50) | 1.30 (0.30,5.05) |
| Efficacy grouping (n = 61) | |||||
| CR (n = 26) | 36 ± 16 | 4/22 | 16.1 ± 15.3 | 1.10 (0.30,2.05) | 0.85 (0.28,1.90) |
| R (n = 21) | 44 ± 19 | 10/11 | 17.2 ± 10.5 | 1.80 (0.65,5.75) | 1.00 (0.30,2.05) |
| NR (n = 14) | 52 ± 17 | 4/10 | 13.9 ± 9.7 | 32.95 (4.40,62.20) | 20.60 (2.83,34.68) |
| Antibody grouping (n = 33) | |||||
| Anti-GPIbα (+) (n = 9) | 39 ± 14 | 2/7 | 10.7 ± 5.3 | 2.50 (0.55,24.15) | 2.20 (0.45,13.85) |
| Single anti-GPIIbIIIa (+) (n = 14) | 35 ± 16 | 3/11 | 16.0 ± 14.5 | 0.55 (0.18,1.70) | 0.35 (0.10,1.90) |
| Double negative (n = 10) | 41 ± 17 | 5/5 | 14.9 ± 9.7 | 0.65 (0.10,5.50) | 1.15 (0.10,2.15) |
| CTD (n = 10) | 43 ± 20 | 3/7 | 20.3 ± 20.0 | 5.15 (1.63,28.85) | 2.20 (0.90,14.25) |
| MDS (n = 10) | 51 ± 27 | 3/7 | 29.3 ± 18.4 | 8.75 (1.30,14.03) | 5.60 (2.08,16.85) |
| AA (n = 6) | 31 ± 11 | 4/2 | 28.2 ± 9.6 | 0.75 (0.18,18.3) | 0.95 (0.10,3.05) |
| AML (n = 8) | 49 ± 19 | 4/4 | 19.4 ± 18.6 | 0.20 (0.13,0.80) | 0.03 (0.01,0.50) |
| Healthy control (n = 20) | 41 ± 12 | 10/10 | 197.7 ± 61.7 | 0.10 (0.10,0.30) | 0.00 (0.00,0.10) |
The platelets of primary ITP patients were collected prior to treatment. Fluorescin-conjugated lectins RCA-1 and ECL were used to detect desialylated galactose and β-GlcNAc residues on platelets via flow cytometry. Platelets from healthy blood donors (controls) and secondary ITP and non-ITP thrombocytopenic patients were also studied. Normal distribution measurement data is presented as mean ± SEM; skewed distribution measurement data is presented as M (P 25, P 75), in which M represents the median, P 25 and P 75 represent the 25th percentile and 75th percentile, respectively. Kruskal-Wallis rank sum test showed platelet desialylation is significantly higher in ITP patients as compared to that in healthy blood donors (RCA-1 Z = −4.918, p < 0.001; ECL Z = −5.512, p < 0.001). The course of therapies was independent from the platelet desialylation assays. The RCA-1 and ECL-positive platelets in non-responder (NR) group are significantly higher than those in complete responder (CR) and responder (R) groups (RCA-1 χ2 = 10.581, p < 0.01; ECL χ2 = 13.741, p < 0.005). No significant difference was observed between CR and R groups (p > 0.05). Correlation analysis indicated that as platelet desialylation increases, the efficacy of therapy decreases. Higher platelet desialylation in ITP patients with anti-GPIbα antibodies was observed as compared with other ITP patients although statistical difference was not reached (RCA-1 χ2 = 3.729, 0.16 > p > 0.05; ECL χ2 = 3.864, 0.15 > p > 0.05). Higher levels of platelet desialylation were also observed in patients of CTD (systemic lupus erythematosus, n = 6; sicca syndrome, n = 4) with thrombocytopenia; MDS and AA as compared with healthy controls (RCA-1 χ2 = 33.790, p < 0.001; ECL χ2 = 42.992, p < 0.001). There is no statistical difference in platelet desialylation between the AML patients and healthy donors (p > 0.05)