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）是一种以女性为主的疾病。这些女性患者的考虑是在怀孕期间或更年期和双侧病例观察到几乎一半的这些患者。然而，特发性ctss的病因尚不清楚。因此，我们认为cts的考虑与女性激素有关；Estrogene。因此，我们通过免疫学和内分泌学的研究来探讨雌激素作为特发性ct的潜在致病因素的作用。首先，用放射免疫法测定特发性ct患者血清总雌激素水平。对照组为正常健康女性（年龄50-65岁）血清。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。绝经前患者血清总雌激素水平为122.16 * 47.0 pg/ml，绝经后患者血清总雌激素水平为77.29 * 30.2pg/ml。从这些数据来看，患者血清雌激素水平低于健康对照组。我们认为ct局部滑膜生长与雌激素分泌减少有关。然后，我们在培养的滑膜细胞和韧带细胞上检测雌激素受体。术中获得滑膜或韧带组织，将这些组织切碎，在添加10%FCS的RPMI-1640培养基中培养。两周后，对生长细胞进行tripsin （0.1% tripsin和0.05% EDTA）处理，洗涤后培养。三次传代后，清洗细胞，用受体法检测雌激素受体。雌激素受体；窦细胞KD值7.3X10^<-10> M， KD值；韧带细胞检测到7.3X10^<-8> M。雌激素受体对窦细胞的亲和力明显高于对韧带细胞的亲和力。此外，多余的非标记雌激素抑制标记雌激素与雌激素受体的结合。这些结果表明我们检测到的受体对雌激素具有特异性。为了研究鼻腔组织生长的原因，我们用ELISA法检测血清中生长因子的水平。患者体内的tgf - β和碱性fgf比健康对照组高得多。从这些数据来看，窦组织的生长在某种程度上与这些生长因子有关。此外，与健康对照组相比，患者外周血淋巴细胞功能明显下降，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IL-2的表达得到改善。我们认为cts侧化与雌激素分泌低有关，这些患者由于雌激素分泌抑制而具有较高的雌激素受体亲和力。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