IL-8 is a cytokine and a potent chemoattractant for neutrophils.
Infiltration of the myocardium by nettirophils is observed in patients with
coronary artery disease. IL-8 regulate and activate neutrophils in acute
inflammation. Also, IL-8 has a regulatory role in ischemic and reperfused
myocardium. To evaluate the usefulness of IL-8 for early detection of A.MI
and to detect the effect of thrombolytic therapy on the level of IL-8. We
measure serum CK-MB, total leukocytic count and serum IL-8 levels in group I
(14 patients with AMI who have received streptokinase), group 11 (13 patients
with AMI who have not received thrombolytic therapy) at 0, 3, 12 and 24 hours
after admission and group III (15 halthy control subjects, serum IL-8
concentration measured by enzyme linked immunosorbent assay (ELISA)
maximal level of IL-8 in the 27 patients with AMI (349 1: 291 pg/ml)
significantly (P < 0.01) exceeded those in the control group (4.4 ± 2.2 pg/ml).
Peak of serum level of IL-8 reached earlier. Than total leukocytic count
and serum level of CK-MB in all patients with AMI (27) (5.5, 16.5, 15 hrs
respectively). IL-8 is an early markers of AMI.
There was highly significant differences between group I (patients with
A.MI who have received thrombolytic therapy) and group II (patients with
AMI who have not received thrombolytic therapy) as regard maximal serum
level of CK-MB and total leukocytic count (119.0 -I- 11.2 1U/L VS 93.0 a' 17.5)
(P < 0.01) and 14.1 at 2.3 x 103/mm3 VS 12-2.3 (Pc 0.05) respectively.
However there was no signcant difference between group (I) therapy
and group (II) as regard maximal level ofIL-8 (380 ±308 VS 318 .1- 275 pg/ml,
P > 0.05 respectively, but there was significant difference between group land
II as regard time of maximal rise of IL-8 (4.5 ±1.2 VS 6.5 ±3.2 hrs) (Pc
0.05) respectively.
Conclusion IL-8 may be an early diagnostic tool for detection AMI, also
thrombolytic therapy cause earlier and higher peaking and repaid decrease of
serum IL-8 in patients with AMI. |