淋巴细胞被prokainamide改变:与药物诱导的红斑狼综合征的关系
Lancet (London, England)
|October 20, 1979
概括
胺胺诱导的狼患者经常产生冷反应性淋巴细胞毒性抗体. 在停止服用普罗卡因胺后,抗体水平下降,这表明药物和狼发育之间存在直接联系.
科学领域:
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
- 类风湿病学 类风湿病学
背景情况:
- 普罗卡因胺是一种用于治疗心律障碍的药物.
- 药物诱导性红斑狼是一种模仿全身性红斑狼的疾病.
- 普罗卡因胺在狼发病中的作用尚未完全理解.
研究的目的:
- 为了调查冷反应性淋巴细胞毒性抗体的存在和重要性,在患有前因胺胺诱导的狼的患者中.
- 探索普罗卡因胺在淋巴细胞功能上的体外影响.
主要方法:
- 来自新诊断的普罗卡因胺诱导性狼患者,长期接受普罗卡因胺治疗但没有狼的患者和正常个体的血清被测试了淋巴细胞毒性抗体.
- 淋巴细胞增殖试验是使用在不同度的普罗卡因胺存在时的植物血凝激活进行的.
主要成果:
- 感冒反应性淋巴细胞毒性抗体被检测到在65%的新诊断的procainamide诱导狼患者中,与对照人群相比,度更高.
- 抗体水平下降后,普罗卡因胺提取,与临床改善相关.
- 在体外,普罗卡因胺在高度下抑制了由植物血凝激发的淋巴细胞增殖,但在较低度下增强了淋巴细胞增殖.
结论:
- 普罗卡因胺可以通过直接改变淋巴细胞功能或产生针对淋巴细胞膜结构的自身抗体来诱导狼.
- 寒冷反应性淋巴细胞毒性抗体的存在可能作为益卡因胺诱导狼的生物标志物.
- 需要进一步的研究,以阐明益卡因胺的免疫调节作用背后的精确机制.
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