Immunological and endocrinological studies on Carpal Tunnel Syndrome -Development of New Immunological Therapy-

特发性腕管综合征（Idiopathic Carpel Tunnel Syndrome，C.T.S）是一种女性多于男性的疾病。这些女性患者的考虑是在怀孕或绝经期间，在这些患者中几乎一半的患者中观察到双侧病例。尽管如此，特发性C.T.S.is病因不明。因此，我们推测C.T.S.的出现与女性激素--雌激素有关。因此，我们从免疫学和内分泌学角度探讨雌激素在特发性C.T.S.发病中的作用。首先，采用放射免疫法测定特发性C.T.S.患者血清总雌激素水平。作为对照，使用来自正常健康女性（年龄; 50-65）的血清。正常对照组绝经前血清雌激素水平为185.5 × 112.5pg/ml，绝经后为203.3 × 168.3pg/ml。血清总雌激素水平绝经前为122.16 × 47.0pg/ml，绝经后为77.29 × 30.2pg/ml， 关于我们 usal。从这些数据来看，患者的血清雌激素水平低于健康对照组。我们推测，局部滑膜生长在C.T.S.与减少雌激素的产生。在体外培养的滑膜或韧带细胞上检测雌激素受体。手术时取滑膜或韧带组织，将这些组织切碎并在添加10%FCS的RPMI-1640培养基中培养。两周后，将生长细胞用胰蛋白酶处理（0.1%胰蛋白酶和0.05%EDTA），洗涤，然后培养。细胞传代3次后，洗涤细胞，用受体分析法检测细胞雌激素受体。雌激素受体：<-10>在窦细胞上检测到KD值7.3X10^ M，<-8>在韧带细胞上检测到KD值7.3X10^ M。窦腔细胞雌激素受体的亲和力明显高于韧带细胞。过量的未标记雌激素抑制标记雌激素与雌激素受体的结合。这些结果表明，我们所检测到的受体是雌激素的特异性受体。为了研究窦组织生长的原因，我们用ELISA法测定了血清中生长因子的水平。从这些数据来看，鼻窦组织的生长与这些生长因子有关。此外，与健康对照组相比，患者的外周淋巴细胞功能显著降低，因此，我们确定生长因子的产生与淋巴细胞功能低下有关。这种淋巴细胞功能的下调通过IL-2的激活而得到改善。我们认为CT扫描异常与雌激素分泌低下有关，这些患者由于雌激素分泌低下而具有高亲和力的雌激素受体。此外，高血清生长因子可诱导窦组织生长。少

Idiopathic Carpel Tunnel Syndrome (C.T.S) is the desease, which occurs mainly female compared with male. The sideration of these female patients were during the period of pregnancy or menopause and bilateral cases are observed in almost half of these patients. Nevertheless, etiology of Idiopathic C.T.S.is unknown. Therefore, We supposed that sideration of C.T.S.was related with female hormone ; Estrogene. So, we carried out immunological and endocrinological study to investigate the effect of estrogen as a potential causative factor for idiopathic C.T.S.At first, serum total estrogen level in the idiopathic C.T.S.patients was measured by radioimmunoassay. As controls, serum from normal healthy female ( age ; 50-65 ) were used. Serum level of estrogen in healthy controls were 185.5 * 112.5pg/ml at premenopausal and 203.3 * 168.3pg/ml at post menopausal. On the other hand, serum lrvel of total estrogen in patients were 122.16 * 47.0 pg/ml at premenopausal, 77.29 * 30.2pg/ml at postmenopa … More usal. From these data, serum estrogen level in patients was lower than that in healthy controls. We supposed that local synovial growth in C.T.S.was related with decrease of estrogen production. Then, we detected estrogen receptor on cultured synovial or ligamental cells. Synovial or ligamental tissues were obtained at operation, and these tissues were minced and cultured in RPMI-1640 added 10%FCS , medium. After two weeks, growth cells were tripsinized ( 0.1% tripsin and 0.05% EDTA), washed and then cultured. After three times passage, cells were washed and detected estrogen receptors by receptor assay. Estrogen receptor ; KD value 7.3X10^<-10> M was detected on sinovial cells and KD value ; 7.3X10^<-8> M was detected on ligamental cells. Affinity of estrogen receptors on sinovial cells was much higher than those on ligament cells. Moreover, surplus non-labeled estrogen inhibited labeled estrogen binding to estrogen receptor. These results suggests that receptor detected by us was specific for estrogen. To investigate why sinovial tissue was grown, we assayed serum level of growth factor by ELISA.TGF-beta and basic-FGF were much higher in patients than healthy controls. From this data, growth of sinovial tissue was somewhere related with these growth factors . Moreover, peripheral lymphocyte function in patients was significantly decreased compared with healthy controls, so, we decided that production of growth factors were related with low lymphocyte function. This downregulation of lymphocyte function was improved by acklition of IL-2. We decided that C.T.S sidelation is related with low estrogen production, and these patients have high affinity of estrogen receptor because of depression of estrogen production. Moreover, high serum growth factors may induce growth of sinovial tissue. Less