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Macrophage Migration Inhibitory Factor (Mif) as a Biomarker in the Assessment of Pulmonary Arterial Hypertension and Interstitial Lung Disease: a Preliminary Study

K. Omonuwa

Arunabh Talwar

M. Hu

X. Lin

P. Berkowki

Sophy Dedopoulos

E. J. Miller


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Conference: 2008 International PHA Conference and Scientific Sessions

Release Date: 06.20.2008

Presentation Type: Abstracts

Omonuwa K., Talwar A., Hu M., Lin X., Berkoski P., Dedopoulos S., Miller E.J.

North Shore University Hospital, Manhasset, NY, USA

BACKGROUNDMacrophage migration inhibitory factor (MIF) has been well described as a pro-inflammatory cytokine and regulator of neuro-endocrine function. As lungs can synthesize and release MIF, we sought to investigate potential role of MIF as a biomarker in assessment of patients with pulmonary arterial hypertension (PAH) with and without interstitial lung disease (ILD).

METHODSStudy involved 20 patients; 9 with PAH {mean pulmonary artery pressure > 25mmHg and pulmonary capillary wedge pressure <18mmHg}, 5 with ILD, and 6 with PAH associated with ILD. Venous blood samples, drawn before and after exercise oximetry on treadmill were centrifuged, plasma separated and stored at -80oC for MIF analysis. The pre- and post exercise plasma MIF concentrations and percentage increases were then compared in the three subject groups with PAH, ILD, and PAH with ILD.

RESULTS: Significantly more MIF accumulated in plasma of patients with PAH associated with ILD following exercise (4.4 ± 2.8ng/ml) than in patients with ILD (1.4 ± 0.7 ng/ml) alone (p=0.04). While there was a wide variance in pre-exercise MIF plasma concentrations, the percentage increase in plasma MIF post-exercise was significantly greater (p=0.02) in patients with  PAH associated with ILD (215.4 ± 223.5%) than in the presence of either single disease alone (PAH -19.1 ± 40.4; ILD 84.1 ± 103.0%) .

CONCLUSIONOur preliminary data show for the first time, the release of MIF in patients with PAH associated with ILD. In addition, our data are consistent with the lung as a source of MIF, a phenomenon only recently reported. While more patients are presently been recruited, our early findings however suggest that MIF may be, at the very least, a biomarker for the assessment of PAH associated with ILD.