Gilhus N E, Lea T
Department of Neurology, University of Bergen, Norway.
Epilepsia. 1988 May-Jun;29(3):317-20. doi: 10.1111/j.1528-1157.1988.tb03726.x.
IgG subclass concentrations were determined in sera from 20 epileptic patients before carbamazepine therapy and after 6 weeks of treatment. Subclass-specific monoclonal antibodies were used in an ELISA technique. Carbamazepine reduced the IgG2 concentration in 13 patients, and the mean value fell from 3.21 to 2.47 g/L during the carbamazepine treatment (p less than 0.01). This IgG2 decrease was maintained after 4 and 12 months of carbamazepine therapy. IgG1, IgG3, and IgG4 concentrations did not change. IgG2 deficiency was not seen. The reduction in IgG2 was not related to the carbamazepine serum concentration within the therapeutic range, to the type of epilepsy, or to the age of the patient. The carbamazepine-induced reduction of IgG2 in serum may indicate an altered immune response to certain antigens, preferentially to carbohydrates.
测定了20例癫痫患者在卡马西平治疗前及治疗6周后的血清IgG亚类浓度。采用酶联免疫吸附测定(ELISA)技术,使用亚类特异性单克隆抗体。卡马西平使13例患者的IgG2浓度降低,在卡马西平治疗期间,平均值从3.21g/L降至2.47g/L(p<0.01)。在卡马西平治疗4个月和12个月后,IgG2的降低仍持续存在。IgG1、IgG3和IgG4浓度未发生变化。未发现IgG2缺乏。IgG2的降低与治疗范围内的卡马西平血清浓度、癫痫类型或患者年龄无关。卡马西平引起的血清IgG2降低可能表明对某些抗原,尤其是对碳水化合物的免疫反应发生了改变。