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Critical Care

Open Access

Macrophage migration inhibitory factor (MIF), C-reactive protein (CRP) and C3a serum levels following coronary artery bypass graft surgery (CABG)

  • HTF Mendonça F°1,
  • HCC Faria Neto1,
  • P Bozza1,
  • R Novaes1,
  • F Bozza1,
  • RV Gomes1,
  • LA Campos1,
  • MA Fernandes1,
  • PM Nogueira1 and
  • HF Dohmann1
Critical Care20015(Suppl 3):P21

Published: 26 June 2001


Coronary Artery Bypass GraftMigration Inhibitory FactorMacrophage MigrationAnesthesia InductionMacrophage Migration Inhibitory Factor


MIF was first described in the late 1960s as a T lymphocyte derived product implicated on random migration of macrophages. In the last decade it has been 'rediscovered' as a pituitary hormone as well as a macrophage product in response to stress. Experimental models have demonstrated correlation between MIF administration and inflammatory reaction. Additionally, anti-MIF treatment was associated with clear improvement of survival in certain models. As CRP, C3a and other substances with inflammatory properties, MIF has been studied specifically in the infectious setting. Results of these studies are extrapolated but not frequently applied to surgical trauma models. Trauma related to CABG in the noninfectious setting could promote sequential alterations on serum levels of CRP, C3a and MIF.


Thirty-seven consecutive patients undergoing CABG had serum levels of MIF (measured by sandwich ELISA), CRP and C3a (measured by nephelometric technique) determined at anesthesia induction and 3, 6 and 24 h after the end of cardiopulmonary bypass (CPB). Patients operated in the emergency setting, in the course of acute illness, and those with missing samples or data were excluded. Multiple organ dysfunction score (MOD) was registered until 96 h postoperative. Applying analysis of variance (ANOVA) for repeated measures, we tested sequential variability along observed moments. Bonferroni test determined differences between measurements.


In this series, it was noted a relatively homogeneous distribution concerning to organ dysfunction at 72 h postoperative (MOD = 2.98 ± 1.7). Serum levels of C3a (mg/dl) presented a slight, but significant decrease from 116 ± 5.46 at baseline to 91.19 ± 4.55 at 3 h, and 93.97 ± 5.91 at 6 h post-CPB (P < 0.05). CRP (mg/dl) showed a progressive increase until 24 h postoperative, from 1.57 ± 0.41 at baseline to 3.24 ± 0.72, 4.01 ± 0.65 and 11.23 ± 1.04 at 3, 6 and 24 h post-CPB, respectively (P < 0.05). MIF (ng/ml) also progressively increased from 162.94 ± 16.51 at baseline to 287.80 ± 35.14 at 6 h post-CPB, decreasing thereafter (P < 0.05).


Alterations in C3a levels were not impressive, although statistically significant, acutely after CABG. In contrast, MIF and CRP serum levels showed a remarkable increase associated with CABG. Our results may implicate MIF as a new and useful marker for response to CABG-related trauma.

Authors’ Affiliations

Hospital Pró-Cardíaco, Surgical Intensive Care Unit, PROCEP, Brazil


© The Author(s) 2001