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Letters |
a Author for correspondence.
Dept. of Clin. Pathol., Jichi Med. School Yakushiji, Minamikawachi, Tochigi 329-04, Japan
Dept. of Lab. Med., Niigata Univ., Niigata 951, Japan
To the Editor:
Serum amyloid A (SAA), an apolipoprotein found in HDL, is a sensitive acute-phase reactant, its concentration in serum increasing up to 1000-fold in inflammatory disorders. Recently, greater attention has been paid to the roles of SAA in lipoprotein metabolism and atherogenesis under inflammatory conditions. Findings have shown that (a) SAA maintains the reverse cholesterol transport system (1), (b) cells in the artery walls are able to express SAA (2), and (c) SAA is present in atherosclerotic lesions (3). However, there are no data regarding serum concentrations of SAA in the atherosclerotic diseases. Because the development of atherosclerotic lesions is accompanied by inflammation-like events, including release of cytokines capable of inducing SAA synthesis from cells in the artery walls (4), a slight increase in serum concentrations of SAA seems possible.
Currently, a well-established latex agglutination nephelometric immunoassay is used to determine SAA (5). The antibodies used in the assay system have no apparent cross-reactivity with a recently discovered constitutive isotype of SAA. This method has shown SAA to be a useful marker for viral infections, in which acute-phase reactants are not remarkably increased (6). Here, we report our examination of serum SAA concentrations in patients with coronary atherosclerosis.
We studied 24 patients (17 men, 7 women; ages 39–90) believed, on the basis of symptoms, stress electrocardiogram, and echocardiogram, to have angina pectoris or myocardial infarction. Stenosis in branches of the coronary artery was finally confirmed by angiography. These patients were followed-up conservatively as outpatients; serum samples were obtained during their regular appointments, when no apparent symptoms were noted.
The SAA values of the patients ranged from 1.5 to 5.1 mg/L. The number of affected coronary artery branches did not affect the SAA concentrations. The concentrations of HDL cholesterol were reduced (mean 30% lower) in these patients, but the SAA values were not related to the HDL cholesterol concentrations.
Using this method in a previous study (7), we had also measured SAA in a large number of healthy subjects (n = 452, ages 16–70 years). In 95% of these healthy subjects, SAA values were <8.0 mg/L, and 85% showed concentrations <5.0 mg/L. Thus, the SAA concentrations in coronary atherosclerosis are indistinguishable from those seen physiologically. This suggests that local atherosclerotic changes as inflammatory stimuli may not reach the liver, the central organ of SAA synthesis; alternatively, perhaps locally produced SAA does not appear in the circulation.
References
The following articles in journals at HighWire Press have cited this article:
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H.A. Alhadi and K.A.A. Fox Do we need additional markers of myocyte necrosis: the potential value of heart fatty-acid-binding protein QJM, April 1, 2004; 97(4): 187 - 198. [Abstract] [Full Text] [PDF]
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