Costello P B, Green F A
J Rheumatol. 1986 Oct;13(5):882-6.
In previous in vitro studies of normal human blood and in vivo canine studies an intracellular erythrocyte (RBC) esterase was identified which controlled the rate of aspirin (ASA) hydrolysis and thus modulated the duration of intact ASA survival and availability for transacetylations required for some therapeutic effects. In whole blood from 30 patients with systemic lupus erythematosus (SLE), 10 normal subjects, and 40 patients with active seropositive rheumatoid arthritis (RA), there were negative correlations between the hematocrit level and the ASA half-life in vitro: r = -0.50, -0.83, and -0.61, respectively. When ASA hydrolysis rates were normalized to approximate whole blood esterase content (k/Hb [min-1 X g-1 X dl] X 10(-4) the mean rate was most rapid in patients with RA (24.2 +/- 2.8) and lowest in patients with SLE (18.6 +/- 3.1), especially in those with recently active disease. To differentiate intracellular and extracellular factors, ASA hydrolysis rates were measured in washed RBC suspensions from similar groups. The mean ASA hydrolysis rate (k/10(6) RBC X 10(-3) was significantly lower in SLE RBC (7.72 +/- 0.81). In RBC from patients with RA the average rate (8.50 +/- 0.85) lay between the SLE group and controls (9.08 +/- 1.04). Thus, an erythrocyte esterase defect in SLE patients resulted in reduced ASA hydrolyzing capacity. In blood from patients with RA a small reduction in esterase activity was compensated by extracellular factors increasing ASA accessibility to the esterase.
在先前对正常人血液的体外研究以及对犬类的体内研究中，发现了一种细胞内红细胞（RBC）酯酶，它控制着阿司匹林（ASA）的水解速率，从而调节完整ASA的存活时间以及某些治疗效果所需的转乙酰化反应的可用时间。在30例系统性红斑狼疮（SLE）患者、10名正常受试者和40例活动性血清学阳性类风湿关节炎（RA）患者的全血中，体外血细胞比容水平与ASA半衰期之间呈负相关：相关系数（r）分别为-0.50、-0.83和-0.61。当将ASA水解速率标准化以近似全血酯酶含量时（k/Hb [分钟-1×克-1×分升]×10-4），RA患者的平均水解速率最快（24.2±2.8），SLE患者最慢（18.6±3.1），尤其是那些近期病情活动的患者。为了区分细胞内和细胞外因素，在来自相似组别的洗涤红细胞悬液中测量了ASA水解速率。SLE患者红细胞（RBC）的平均ASA水解速率（k/106 RBC×10-3）显著较低（7.72±0.81）。RA患者红细胞的平均水解速率（8.50±0.85）介于SLE组和对照组（9.08±1.04）之间。因此，SLE患者的红细胞酯酶缺陷导致ASA水解能力降低。在RA患者的血液中，酯酶活性的小幅降低被细胞外因素所补偿，这些因素增加了ASA与酯酶的接触机会。
