Influence of serum amyloid A on the decrease of high density lipoprotein-cholesterol in active sarcoidosis

Objective: We have previously observed low levels of high density lipoprote in (HDL) cholesterol in active sarcoidosis. The aim of this study was to an alyze the role of serum amyloid A (SAA) on this lipid disorder. Methods: Ei ghty five untreated sarcoid patients, 40 with active disease and 45 with in active disease, were recruited. Sarcoidosis activity was evaluated by means of clinical, chest X-ray, gallium-67 scan, serum angiotensin converting en zyme (peptidyl-dipeptidase A) values, and pulmonary function tests. Analysi s of lipoprotein metabolism included: serum cholesterol, low density lipopr otein (LDL)-cholesterol, HDL-cholesterol, HDL,-cholesterol, HDL,-cholestero l, apolipoprotein A-I (apo A-I), apolipoprotein B (apo B), and triglyceride concentrations. Serum amyloid A protein and lecithin-cholesterol acyltrans ferase (LCAT) activity were measured. Results: In active sarcoidosis we fou nd significantly reduced levels of HDL-cholesterol (1.17 +/- 0.36 vs. 1.44 +/- 0.39 mmol/l, P = 0.002), HDL3-cholesterol (0.78 +/- 0.23 vs. 1.02 +/- 0 .21 mmol/l, P < 0.0001), and apo A-I (1.36 +/- 0.29 vs. 1.61 +/- 0.27 g/l, P < 0.0001) and significantly increased levels of triglyceride (1.51 +/- 0. 64 vs. 1.03 +/- 0.46 mmol/l, P < 0.0001), and apo B (1.14 +/- 0.25 vs. 0.99 +/- 0.27 g/l, P = 0.012) versus inactive sarcoidosis. Serum amyloid A conc entrations were significantly increased in the patients with active disease (155.45 +/- 154.01 mg/ml) compared to the inactive sarcoid patients (89.70 +/- 65.36 mg/ml) (P = 0.011). There were no significant differences in cho lesterol, LDL-cholesterol, HDL,-cholesterol or LCAT values between groups. Multivariate logistic regression analysis showed that HDL-cholestrrol (regr ession coefficient b = - 1.96; S.E. = 0.87; P = 0.02) and SAA (regression c oefficient b = 0.01; S.E. = 0.004; P = 0.01) were the two variables indepen dently associated with disease activity. Moreover, a significant negative c orrelation was observed between SAA levels and both HDL-cholesterol (r = - 0.39; P = 0.01) and apo A-I (r = - 0.35; P = 0.03) levels, in the active sa rcoid group. Conversely, no correlation was found in the inactive sarcoid g roup. Conclusion: The low HDL-cholesterol and apo A-I concentrations seen i n active sarcoid patients are associated with a significant increase of SAA levels. We suggest that the displacement of apo A-I by SAA on HDL accounts for the lower level of HDL-cholesterol seen in active sarcoidosis. (C) 200 0 Elsevier Science Ireland Ltd. All rights reserved.