Hepcidin is a key regulator of iron metabolism and a mediator of
anemia in inflammation. Recent in vitro studies recognized
prohepcidin as a type II acute phase protein regulating via
interleukin-6. The aim of the present study was to investigate the
time course of plasma prohepcidin after a large cardiac surgery in
relation to IL-6 and other inflammatory parameters. Patients with
chronic thromboembolic hypertension (n=22, males/females
14/8, age 51.9±10.2 years) underwent pulmonary
endarterectomy using cardiopulmonary bypass and deep
hypothermic circulatory arrest were included into study. Arterial
concentrations of prohepcidin, IL-1β, IL-6, IL-8, tumor necrosis
factor-α, and C-reactive protein were measured before/after
sternotomy, after circulatory arrest, after separation from bypass,
and then 12, 18, 24, 36, 48 h and 72 h after the separation from
bypass. Hemodynamic parameters, hematocrit and markers of
iron metabolism were followed up. Pulmonary endarterectomy
induced a 48 % fall in plasma prohepcidin; minimal
concentrations were detected after separation from
cardiopulmonary bypass. Prohepcidin decline correlated with an
extracorporeal circulation time (p<0.01), while elevated IL-6
levels were inversely associated with duration of prohepcidin
decline. Postoperative prohepcidin did not correlate with markers
of iron metabolism or hemoglobin concentrations within a 72-h
period after separation from CPB. Prohepcidin showed itself as a
negative acute phase reactant during systemic inflammatory
response syndrome associated with a cardiac surgery. Results
indicate that the evolution of prohepcidin in postoperative period
implies the antagonism of stimulatory effect of IL-6 and
contraregulatory factors inhibiting prohepcidin synthesis or
increasing prohepcidin clearance.
Cardiac surgery with deep hypothermic circulatory arrest produces less systemic inflammatory response than low-flow cardiopulmonary bypass in newborns
