Fears R, Ferres H, Glasgow E, Standring R, Hogg K J, Gemmill J D, Burns J M, Rae A P, Dunn F G, Hillis W S
SmithKline Beecham Pharmaceuticals, Great Burgh, Epsom, Surrey.
Br Heart J. 1992 Aug;68(2):167-70. doi: 10.1136/hrt.68.8.167.
To examine the induction of antistreptokinase antibodies after giving streptokinase or anistreplase to patients with acute myocardial infarction.
Patients were randomly allocated to receive either 1.5 x 10(6) IU, streptokinase or 30U anistreplase in a double blind study. Blood samples were collected immediately before treatment and subsequently at intervals up to 30 months; plasma samples were assayed for streptokinase resistance titre (functional assay) and streptokinase binding by IgG (microradioimmunoassay).
Cardiology department in a general hospital.
128 consecutive eligible patients. Samples were collected for up to one year according to a prospective design: a subsection of 47 patients was selected for intensive study over the first 14 days. After one year, all available patients (67) were sampled on one further occasion.
Antibody responses to streptokinase and anistreplase were similar. Streptokinase resistance titres exceeded pretreatment concentrations five days after dosing, and values peaked at 14 days. By 12 months after dosing, 92% of resistance titres (n = 84) had returned to within the pretreatment range. Antistreptokinase IgG concentrations also exceeded baseline concentrations within five days and peaked at 14 days. Half of the individual values had returned to within the pretreatment range by 12 months (n = 84) and 89% by 30 months (n = 18).
Although we cannot be sure of the clinical significance, because of the increased likelihood of resistance due to antistreptokinase antibody, streptokinase and anistreplase may not be effective if administered more than five days after an earlier dose of streptokinase or anistreplase, particularly between five days and 12 months, and increased antistreptokinase antibody may increase the risk of allergic-type reactions.
研究急性心肌梗死患者接受链激酶或茴香酰化纤溶酶原链激酶激活剂治疗后抗链激酶抗体的诱导情况。
在一项双盲研究中,患者被随机分配接受1.5×10⁶IU链激酶或30U茴香酰化纤溶酶原链激酶激活剂治疗。在治疗前即刻及随后长达30个月的时间间隔内采集血样;检测血浆样本中的链激酶抵抗滴度(功能测定)以及IgG对链激酶的结合情况(微量放射免疫测定)。
一家综合医院的心脏病科。
128例连续符合条件的患者。根据前瞻性设计,样本采集长达一年:选取47例患者的一个亚组在最初14天进行深入研究。一年后,对所有可获得的患者(67例)再进行一次采样。
对链激酶和茴香酰化纤溶酶原链激酶激活剂的抗体反应相似。给药后5天,链激酶抵抗滴度超过治疗前浓度,14天时达到峰值。给药后12个月,92%的抵抗滴度(n = 84)恢复到治疗前范围以内。抗链激酶IgG浓度在5天内也超过基线浓度,14天时达到峰值。到12个月时,一半的个体值(n = 84)恢复到治疗前范围以内,到30个月时89%(n = 18)恢复到该范围以内。
尽管由于抗链激酶抗体导致抵抗增加,我们无法确定其临床意义,但如果在较早剂量的链激酶或茴香酰化纤溶酶原链激酶激活剂给药后超过5天给药,尤其是在5天至12个月之间,链激酶和茴香酰化纤溶酶原链激酶激活剂可能无效,并且抗链激酶抗体增加可能会增加过敏样反应的风险。