Morgan K, Schiffman S, Feinstein D
Thromb Haemost. 1984 Jul 29;51(3):371-5.
Two patients with hereditary factor XI deficiency developed inhibitors following plasma transfusions. Neither had severe spontaneous bleeding. The patients' plasmas neutralized both factor XI in plasma, purified factor XI, and purified factor XIa. The inhibitor in both patients' plasmas adsorbed to Protein A-Sepharose. The inhibitors eluted from Protein A-Sepharose were partially neutralized by kappa and lambda light chain antisera indicating that they were polyclonal IgG antibodies. Both inhibitors markedly decreased adsorption of factor XI to glass surfaces. The cleavage of factor XI by trypsin was unaffected by the inhibitors. The lack of severe spontaneous bleeding in both of these patients strongly suggests that an alternate coagulation mechanism bypassing factor XI must compensate for this severe defect.
两名遗传性因子XI缺乏症患者在输注血浆后产生了抑制剂。两人均无严重自发性出血。患者血浆中和了血浆中的因子XI、纯化的因子XI和纯化的因子XIa。两名患者血浆中的抑制剂均吸附于蛋白A-琼脂糖。从蛋白A-琼脂糖上洗脱的抑制剂被κ和λ轻链抗血清部分中和,表明它们是多克隆IgG抗体。两种抑制剂均显著降低因子XI对玻璃表面的吸附。抑制剂不影响胰蛋白酶对因子XI的裂解。这两名患者均无严重自发性出血,强烈提示存在一种绕过因子XI的替代凝血机制来弥补这一严重缺陷。