BACKGROUND: Human alpha2-HS glycoprotein (alpha2-HSG) is synthesized and secreted by the liver into circulation. Plasma concentrations of alpha2-HSG decrease significantly following infection, inflammation and malignancy. Since increased plasma concentrations of C-reactive protein are observed in patients with acute myocardial infarction (AMI), we hypothesized that plasma concentrations of alpha2-HSG would decrease during the initial phase of AMI and begin to increase in the recovery phase. METHODS: Twenty patients diagnosed with AMI were recruited for the study. A sensitive and specific ELISA was developed to assay alpha2-HSG concentrations in plasma. RESULTS: In AMI patients, plasma alpha2-HSG concentrations were decreased (281.3+/-25.8 mg/l, ranging from 132 to 489 mg/l on admission) compared to healthy individuals (312.3+/-9.9 mg/l, ranging from 210 to 450 mg/l) (P= 0.142). Interestingly, 40% of AMI patients demonstrated alpha2-HSG concentrations below 200 mg/l compared to none in the healthy control group. During the recovery period, alpha2-HSG concentrations begin to increase, with a mean+/-SEM of 290.1+/-22.1 mg/l. Regression analysis comparing plasma alpha2-HSG concentrations on admission to concentrations on discharge showed a significant positive correlation in matched-pair patient samples (P<0.01, r=0.45). CONCLUSIONS: We conclude that, in contrast to C-reactive protein, alpha2-HSG functions as a negative acute phase protein in AMI patients. Plasma alpha2-HSG concentrations start to decrease within a few hours after the onset of AMI and return to near normal concentrations during the recovery period (5-7 days after AMI).
BACKGROUND:Humanalpha2-HS glycoprotein (alpha2-HSG) is synthesized and secreted by the liver into circulation. Plasma concentrations of alpha2-HSG decrease significantly following infection, inflammation and malignancy. Since increased plasma concentrations of C-reactive protein are observed in patients with acute myocardial infarction (AMI), we hypothesized that plasma concentrations of alpha2-HSG would decrease during the initial phase of AMI and begin to increase in the recovery phase. METHODS: Twenty patients diagnosed with AMI were recruited for the study. A sensitive and specific ELISA was developed to assay alpha2-HSG concentrations in plasma. RESULTS: In AMI patients, plasma alpha2-HSG concentrations were decreased (281.3+/-25.8 mg/l, ranging from 132 to 489 mg/l on admission) compared to healthy individuals (312.3+/-9.9 mg/l, ranging from 210 to 450 mg/l) (P= 0.142). Interestingly, 40% of AMI patients demonstrated alpha2-HSG concentrations below 200 mg/l compared to none in the healthy control group. During the recovery period, alpha2-HSG concentrations begin to increase, with a mean+/-SEM of 290.1+/-22.1 mg/l. Regression analysis comparing plasma alpha2-HSG concentrations on admission to concentrations on discharge showed a significant positive correlation in matched-pair patient samples (P<0.01, r=0.45). CONCLUSIONS: We conclude that, in contrast to C-reactive protein, alpha2-HSG functions as a negative acute phase protein in AMI patients. Plasma alpha2-HSG concentrations start to decrease within a few hours after the onset of AMI and return to near normal concentrations during the recovery period (5-7 days after AMI).