XIE Ke-jian,ZHANG Qi,XIA Yu-xiang.Dynamic study on the influence of 131I treatment on the circulating sFas levels in patients with Graves′disease[J].Chinese Journal of Radiological Medicine and Protection,2006,26(5):493-495
Dynamic study on the influence of 131I treatment on the circulating sFas levels in patients with Graves′disease
Received:November 18, 2005  
DOI:
KeyWords:Graves disease  sFas  131I therapy
FundProject:浙江省教育厅科研基金资助项目(20041050);温州市“新世纪551人才工程”基金资助项目(2004-551-2)
Author NameAffiliationE-mail
XIE Ke-jian School of Laboratory Medical Science Wenzhou Medical College, Wenzhou 325035, China wzzhangqi@126@.com 
ZHANG Qi 325035, 温州医学院检验医学院核医学室  
XIA Yu-xiang School of Laboratory Medical Science Wenzhou Medical College, Wenzhou 325035, China  
徐云弟 325035, 温州医学院检验医学院核医学室  
管瑜 School of Laboratory Medical Science Wenzhou Medical College, Wenzhou 325035, China  
李焕斌 325035, 温州医学院检验医学院核医学室  
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Abstract::
      Objective To study the influence of 131I treatment on the circulating sFas levels of patients with Graves′disease(GD) before and after treatment with 131I. Methods Using the method of enzyme-linked immunosorbent assay(ELISA) and radioimmunoassay, the levels of sFas in serum and thyroid hormone of GD 52 patients were measured before and after 131I therapy while 30 healthy subjects with age and sex matched served as controls, and the results were compared with that of the control group. Results The sFas levels in serum of GD patients were significantly higher than that of the control group(P<0.01). The serum sFas level tended to decrease after the medication of 131I at 180 d, but still higher than that of the normal controls(P<0.05). The concentration of serum sFas was positively correlated with the titers of anti-hyrotropin(TSH) receptor antibody (r= 0.595,P<0.01), but not with the other clinical parameters(FT3, FTT4 and TSH). Conclusions Abnormal concentration of sFas in serum can be observed in patients with GD. 131I therapy would suppress the auto-immune status in GD patients, and the circulating sFas may play a role in the pathogenesis of GD.
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