Table 1 Studies evaluating CACs in burn patients

Gill et al., 2001 [12]

CD133⁺/KDR⁺/CD15⁻

No

Patients with > 15 % TBSA Burn → ↑VEGF systemically (at 6–12 h) which was followed by transient mobilization of CACs that peaked at 12 h and returned to baseline at 24–48 h.

Fox et al., 2008 [3]

CD45^dim/-/CD133⁺/CD144⁺/KDR⁺

Yes

All pts with burns exhibited a significant rise in CACs that peaked at 24 h and returned to baseline after 72 h. There was a positive correlation between level of CACs and percent TBSA of burn. CAC levels also correlated strongly with VEGF & SDF-1α levels.

Piatkowski et al., 2009 [25]

CD34⁺/KDR⁺/acLDL⁺/lectin⁺

Yes

Significantly lower CAC count in pts with extensive burns (>25 % TBSA) than those with smaller burns (10–24 %) on admission. CAC levels rose in all burn pts, with extensive burn pt CAC levels not reaching a significant level until day 5 except in pts who did not survive.

Groger et al., 2010 [26]

CD34⁺/KDR⁺/acLDL⁺

No (animal model)

All animals sustained 30 % TBSA burn. Observed significant CAC drop during burn insult followed by rapid increase to ½ baseline levels at 2 h that remained stable for 48 h.

Pan et al., 2010 [27]

CD31⁺/KDR⁺/acLDL⁺

Yes

Ex vivo analysis of burn fluid demonstrated stronger paracrine signaling for MNC recruitment and CAC differentiation in DPTB fluid when compared to SPTB fluid.

Zhang et al., 2010 [13]

acLDL⁺/lectin⁺

Yes (animal model)

↑CACs in all burn groups, but day and magnitude of mobilization inversely proportional to degree of burn insult.

Foresta et al., 2011 [2]

CD45⁺/CD34⁺/CD133⁺/KDR⁺

No

Significant drop in CACs in burn pts on admission compared to control. Significant release in CACs both at day 1 and 12 not observed in control group.