Serum total sialic acid (TSA) has gained medical interest, particularly as a cardiovascular risk factor and it has been hypothesized that serum levels relate to serum acute phase proteins, some of which are sialylated. We assayed serum TSA and also lipid associated sialic acid (LASA) in 50 normal individuals (24 male) and 15 subjects (12 male) who had experienced a myocardial infarct. The mean serum TSA in the normal individuals was 2.05 SD 0.38 mmol/L (range 1.16-2.74) and the mean serum LASA was 0.70 SD 0.19 mmol/L (range 0.23-1.03). We also measured five serum acute phase proteins and found a good correlation between these and serum TSA: C-reactive protein, r = 0.52, P < 0.001, alpha-1-antichymotrypsin, r = 0.79, P < 0.0001, alpha-2-macroglobulin, r = 0.38, P < 0.01 and alpha-1-acid glycoprotein, r = 0.32, P < 0.05. A significant correlation between plasma TSA and plasma C-reactive protein (r = 0.47, P < 0.04) and also fibrinogen (r = 0.53, P < 0.04) was noted on day one following the myocardial infarction, whereas a significant correlation between plasma TSA and plasma alpha-1-antichymotrypsin (r = 0.51, P < 0.03) and also plasma alpha-1-acid glycoprotein (r = 0.64, P < 0.05) was found on day two following the infarction. Thus it would seem that serum TSA is at least in part related to some of the acute phase proteins in both healthy individuals and those having had a myocardial infarction.
Plasma total sialic acid (TSA) and lipid-associated sialic acid (LASA) were measured in 19 patients with a myocardial infarction (MI) on days 1, 2, and 5 and in 19 normal subjects. On each day plasma TSA was elevated in the MI patients as compared with that of normal subjects, although no significant difference was seen in the plasma LASA between the two groups. The following plasma acute-phase proteins were also assayed in the MI patients and the normal subjects: C-reactive protein (CRP), alpha-1 acid glycoprotein (AGP), alpha-1 antichymotrypsin (ACT), alpha-2 macroglobulin (AMG), and fibrinogen (FIB). Significantly elevated plasma concentrations were found in the MI patients as compared with normal subjects. Furthermore, a significant correlation was found between some of these plasma acute-phase proteins (ACT, AMG, and FIB) and plasma TSA in the MI patients and also in normal subjects (ACT, AMG, CRP, and FIB). However, no significant difference was noted in any of the plasma acute-phase proteins, or plasma TSA, or plasma LASA between survivors and patients who died of their MI.
Serum total sialic acid has gained recent interest äs a cardiovascular risk factor. We measured serum total sialic acid and three acute phase proteins; C-reactive protein, a r antichymotrypsin and
Total serum sialic acid (TSA), recently shown to be a cardiovascular risk factor, was measured in 15 patients with severe hypertriglyceridaemia (fasting triglyceride > 2.3 mmol l-1) and 15 age and sex matched normal control subjects. To test the hypothesis that serum TSA is related in some way to serum acute phase proteins we also measured five acute phase proteins, namely alpha-1-antichymotrypsin (ACT), alpha-1-acid-glycoprotein (AGP), alpha-2-macroglobulin (AMG), C-reactive protein (CRP) and haptoglobin (HAP) in both groups. Of note was the significantly elevated serum TSA in the severely hypertriglyceridaemic group as compared to normal subjects. Serum TSA being 71.9 +/- 11.7 mg dl-1 and 59.6 +/- 10.2 mg dl-1 respectively (P < 0.01 Mann-Whitney test). Serum CRP was significantly elevated in the type IV patients as compared to controls (6.4 +/- 4.5 mg l-1 vs. 3.3 +/- 1.9 mg l-1 P < 0.05 Mann Whitney test) as was serum AMG (2.1 +/- 0.89 g l-1 vs. 1.5 +/- 0.53 g l-1 P < 0.05 Mann Whitney test). There was no correlation between serum TSA and lipoprotein (a) in either the normal or severely hypertriglyceridaemic subjects. We suggest that serum TSA could in part be related to hypertriglyceridaemia and serum acute phase proteins but that its property as a cardiovascular risk factor is not related to serum lipoprotein (a) concentrations.
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