Kamińska Teresa, Szuster-Ciesielska Agnieszka, Wysocka Alicja, Marmurowska-Michałowska Halina, Dubas-Slemp Halina, Kandefer-Szerszeń Martyna
Department of Virology and Immunology, Maria Curie-Skłodowska University, Lublin, Poland.
Med Sci Monit. 2003 Jul;9(7):CS71-5.
There have been few publications concerning the role of the immune system in neuroleptic intolerance. Some studies have shown that in neuroleptic malignant syndrome (NMS), associated with disseminated intravascular coagulation (DIC), the serum level of tumor necrosis factor alpha (TNF-alpha) increases significantly, which is thought to trigger the onset of DIC.
A 23-year-old woman suffering from catatonic schizophrenia developed hypersensitivity to neuroleptics. One month before being referred to the present authors, she had a haloperidol-induced NMS episode in another psychiatric hospital, with high temperature, CPK activity, muscle rigidity and leukocytosis. On admission to our clinic and after treatment with promazine, laboratory tests showed an increase in serum CPK activity and mild leukocytosis. Neuroleptic treatment was discontinued, and the serum level of CPK and white blood cell count was monitored daily for 7 days, as well as the serum level of some cytokines and the production of reactive oxygen species (ROS) by blood neutrophils. The serum levels of interleukin 1 alpha (IL-1), IL-6 and TNF-alpha changed significantly over the observation period, forming waves with peak activity of IL-6 and TNF-alpha exceeding normal levels. The level of IL-1 alpha was within the control range. ROS production by the patient's blood neutrophils was also increased, as well as catalase serum activity.
Some proinflammatory cytokines may participate in the mechanisms leading to the development of neuroleptic intolerance in schizophrenic patients. Cytokine-stimulated ROS production may participate in tissue injury and increase CPK serum activity.
关于免疫系统在抗精神病药物不耐受中的作用,相关出版物较少。一些研究表明,在与弥散性血管内凝血(DIC)相关的抗精神病药物恶性综合征(NMS)中,肿瘤坏死因子α(TNF-α)的血清水平显著升高,这被认为会引发DIC的发作。
一名患有紧张型精神分裂症的23岁女性对抗精神病药物产生超敏反应。在被转诊至本文作者处的一个月前,她在另一家精神病医院发生了一次由氟哌啶醇诱发的NMS发作,伴有高热、肌酸磷酸激酶(CPK)活性升高、肌肉强直和白细胞增多。在我院门诊就诊并接受丙嗪治疗后,实验室检查显示血清CPK活性升高和轻度白细胞增多。停用抗精神病药物治疗,并连续7天每日监测血清CPK水平和白细胞计数,以及一些细胞因子的血清水平和血液中性粒细胞产生的活性氧(ROS)。在观察期内,白细胞介素1α(IL-1)、IL-6和TNF-α的血清水平发生了显著变化,形成了波峰,其中IL-6和TNF-α的活性峰值超过正常水平。IL-1α水平在对照范围内。患者血液中性粒细胞产生的ROS以及过氧化氢酶血清活性也增加。
一些促炎细胞因子可能参与了导致精神分裂症患者出现抗精神病药物不耐受的机制。细胞因子刺激产生的ROS可能参与组织损伤并增加血清CPK活性。