| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
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| Research Abstract |
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
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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
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