Alarcón-Segovia D, Fishbein E, Cetina J A, Raya R J, Barrera E
Clin Exp Immunol. 1973 Dec;15(4):543-8.
A few patients have been reported who developed systemic lupus erythematosus (SLE) in the course of prolonged treatment with chlorpromazine. Patients on this drug have also been found to have antinuclear antibodies (ANAs) although they do not develop lupus. We have studied the antigenic specificity of ANAs in fifty-four patients on longterm chlorpromazine treatment and compared our findings with those on 175 patients on anticonvulsants, 215 patients on isoniazid, 109 SLE patients and fifty-four healthy subjects, sex and age matched to the chlorpromazine patients. Thirty-nine per cent of patients on chlorpromazine had ANAs which were most frequently directed to single stranded (s)DNA. In contrast, patients on anticonvulsants as well as those on isoniazid had ANA directed to soluble nucleoprotein (sNP) most frequently and none of the patients on isoniazid had ANA to sDNA. The mechanisms by which chlorpromazine, isoniazid or anticonvulsant intake results in ANAs probably differ. Our findings suggest that development of ANAs in patients on chlorpromazine may be initiated by interaction of the drug with denatured DNA.
有报道称,少数患者在长期服用氯丙嗪的过程中患上了系统性红斑狼疮(SLE)。服用这种药物的患者也被发现有抗核抗体(ANA),尽管他们没有患上狼疮。我们研究了54名长期接受氯丙嗪治疗的患者体内ANA的抗原特异性,并将我们的研究结果与175名服用抗惊厥药的患者、215名服用异烟肼的患者、109名SLE患者以及54名年龄和性别与氯丙嗪患者相匹配的健康受试者进行了比较。39%服用氯丙嗪的患者有ANA,其中最常见的是针对单链(s)DNA。相比之下,服用抗惊厥药的患者以及服用异烟肼的患者最常见的是针对可溶性核蛋白(sNP)的ANA,而异烟肼治疗的患者中没有针对sDNA的ANA。服用氯丙嗪、异烟肼或抗惊厥药导致ANA产生的机制可能不同。我们的研究结果表明,氯丙嗪治疗患者中ANA的产生可能是由药物与变性DNA的相互作用引发的。