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. 2015 Feb 26;11(2):e1004619. doi: 10.1371/journal.ppat.1004619

Table 1. Numbers and cellular origin of microvesicles containing Stx2 in plasma from patients and controls.

Platelet-derived microvesicles (x103/mL) Monocyte-derived microvesicles (x103/mL) Neutrophil-derived microvesicles (x103/mL) RBC-derived microvesicles (x103/mL)
Stx2-positive Stx2-positive Stx2 positive Stx2 positive
HUS Acute phase (n = 13) 1697 (315–3900)*** 453 (57–855)*** 603 (99–1509)** 187 (30–354)** 517 (45–1794)*** 135 (38–222)*** 543 (240–1182) a 51 (12–120)* a
Recovery (n = 12) 154 (63–241) 0 43 (6–212) 0 13 (3–91) 0 114 (90–618) b 0 b
HC (n = 5) 215 (108–574) 0 (0–212) c 102 (35–489) 0 (0–99) c 94 (25–324) 0 (0–72) c NA NA
Controls (n = 10) d 123 (80–171) 0 42 (21–56) 0 28 (15–38) 0 5 (0–8) 0
Renal failure controls (n = 2) 130–282 0 31–96 0 58–133 0 NA NA

Samples from pediatric HUS patients (1–12) were available during the acute phase of disease and after recovery whereas samples from patient 13 and patients with hemorrhagic colitis (15–19) were only available during the acute phase of disease. Data are expressed as median and (range) of circulating microvesicles positive for each membrane specific marker (CD42b for platelets, CD38 for monocytes and CD66 for neutrophils). *** Denotes P value <0.001, ** P<0.01 and *P<0.05 when comparing microvesicles in plasma from HUS patients with recovery.

a, HUS patients analyzed for CD235a-positive red blood cells (RBC)-derived microvesicles (n = 6, not all patients were analyzed). Significantly higher levels were detected during the acute phase compared to controls (n = 6), P<0.001).

b, Recovery samples analyzed for RBC-derived microvesicles (n = 3).

c, Two of the patients with HC had detectable levels of microvesicles containing Stx2.

d, Pediatric controls (n = 4) analyzed for platelet (CD42b), monocyte (CD38) and neutrophil (CD66)-derived microvesicles. Adult controls (n = 6) analyzed for RBC/CD235a-derived microvesicles. NA: not analyzed.