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

特发性心电隧道综合征是指以女性为主，男性居多的疾病。这些女性患者在怀孕或更年期期间被考虑，其中几乎一半的患者观察到双侧病例。然而，特发性CTS的病因尚不清楚。因此，我们推测C.T.S.的偏向与雌激素--雌激素有关。因此，我们开展了免疫学和内分泌学方面的研究，以探讨雌激素作为特发性甲状腺癌潜在致病因素的作用。首先，采用放射免疫法测定了特发性甲状腺癌患者血清总雌激素水平。以正常健康女性(年龄50~65岁)血清为对照。健康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。更具随意性。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CTS局部滑膜生长与雌激素分泌减少有关。然后，我们检测了培养的滑膜或韧带细胞上的雌激素受体。术中取滑膜或韧带组织，在添加10%胎牛血清的RPMI-1640培养液中培养。两周后，取生长细胞(0.1%Tripsin和0.05%EDTA)，洗涤后培养。传代3次后，洗涤细胞，用受体分析法检测雌激素受体。雌激素受体Kd值7.3X10^&lt；-10&gt；M出现在鼻窦细胞上，Kd值为7.3X10^&lt；-8&gt；M出现在韧带细胞上。雌激素受体在鼻窦细胞上的亲和力远高于韧带细胞。此外，过剩的非标记雌激素抑制了标记雌激素与雌激素受体的结合。这些结果表明，我们检测到的受体是雌激素特异性的。为了探讨鼻窦组织生长的原因，我们用ELISA法检测了患者血清中生长因子的水平。患者血清中的转化生长因子-β和碱性成纤维细胞生长因子明显高于健康对照组。根据这些数据，鼻窦组织的生长在某种程度上与这些生长因子有关。此外，患者的外周血淋巴细胞功能明显低于健康对照组，因此，我们认为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抑制IL-2而得到改善。我们认为CTS侧化与低雌激素产生有关，这些患者由于雌激素产生抑制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鼻窦组织生长。较少

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