Zucker S, Zarrabi M H, Romano G S, Miller F
Br J Haematol. 1978 Nov;40(3):447-57. doi: 10.1111/j.1365-2141.1978.tb05816.x.
In this report we have described three patients with chronic schizophrenia on long-term chlorpromazine therapy who developed asymptomatic IgM inhibitors of the intrinsic phase of blood coagulation. The anticoagulant resulted in decreased measurements of all of the plasma clotting factors in the intrinsic pathway (factors VIII, IX, XI, XII, Fletcher factor and Fitzgerald factor). Using crude coagulation reagents, the serum of these patients interfered with the clot promoting activity of contact product. To determine the relationship between drug therapy and these IgM inhibitors, we have studied nine additional schizophrenic patients on long-term chlorpromazine therapy. All nine chlorpromazine-treated patients had significantly increased levels of serum IgM and asymptomatic inhibitors of coagulation. We conclude that long-term high-dose chlorpromazine treatment of schizophrenic patients results in an increased concentration of IgM which has inhibitory activity in the contact phase of blood coagulation.
在本报告中，我们描述了三名长期接受氯丙嗪治疗的慢性精神分裂症患者，他们出现了无症状的凝血内源性阶段IgM抑制剂。这种抗凝剂导致内源性途径中所有血浆凝血因子（因子VIII、IX、XI、XII、弗氏因子和菲氏因子）的测量值降低。使用粗制凝血试剂时，这些患者的血清会干扰接触产物的促凝活性。为了确定药物治疗与这些IgM抑制剂之间的关系，我们研究了另外九名长期接受氯丙嗪治疗的精神分裂症患者。所有九名接受氯丙嗪治疗的患者血清IgM水平和无症状凝血抑制剂均显著升高。我们得出结论，对精神分裂症患者进行长期大剂量氯丙嗪治疗会导致IgM浓度升高，而IgM在血液凝固的接触阶段具有抑制活性。
