Background :Inflammation plays a role in atherogenesis, plaque vuluerability and the development of coronary artery disease. Activated macrophages contribute to both atherosclerotic plaque disruption and intracoronary thrombus formation. Neopterin, a pteridine derivative, produced by activated macrophages enhances inflammatory process within vulnerable plaques. Interleukin-10 (IL-10), a potent anti-inflammatory cytokine, seems to be involved in atherogenesis. It has a protective role in both atherosclerotic lesion formation and stabilization. The present study was designed to assess the levels of the inflammatory markers (neopterin and C- reactive protein), and anti-inflammatory marker (interleukin-10) in patients with coronary artery disease and to assess its relations to the early coagulation markers (Ddimer and thrombus precursor protein) . A total of 43 patients with coronary artery disease were enrolled. Of these, 20 patients had chronic stable angina with stable symptoms over 3 months (SA group) and 23 patients had acute myocardial infarction (AMI group). Twenty two healthy subjects were taken as a control group. Serum C- reactive protein (CRP), neopterin, interleukin -10 (IL-10), plasma D-dimer and plasma thrombus precursor protein (TpP) were measured for all subjects. High levels of inflammatory markers (neopterin and CRP) were observed in all patients with coronary artery disease as well as positive correlation between these indexes was present. Moreover, the increase in inflammatory indexes was more prominent in AMI group than in SA group. Serum IL-10 levels showed significant increase in all patients but surprisingly, AMI group had low levels of IL-10 as compared to SA group. Significant negative correlation was observed between neopterin and IL-10 in all patients. Ddimer showed significant increase in AMI group as compared either to SA group or to the controls. Significant elevations of TpP were present in AMI and SA group with higher values in AMI group than in SA group. D-dimer did not correlate with serum neoprterin in AMI and SA groups but correlated negatively to serum IL-10 only in SA group. Meanwhile, TpP correlated positively with serum neopterin and negatively with IL-10 in both patient’s group. In conclusion, inflammation has a pivotal role in the course of coronary artery disease. Neopterin can be considered as a marker of coronary artery disease as well as of adverse coronary events. TpP is more reliable than D-dimer as a marker of coagulation activation. It may be tempting to speculate that therapeutic intervention that increase the endogenous IL-10 serum levels or even an exogenous administration of IL-10 may represent novel therapeutic methods to improve the clinical outcome in patients with coronary artery disease.