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作 者:田民[1] 赵卫[1] 沈进[1] 杨慧英[2] 李红[2] 陆桂君[3] 余永忠[1] 易根发[1] 向述天[1] 李莉媛[1]
机构地区:[1]昆明医学院第一附属医院影像中心,昆明市延安医院650031 [2]昆明医学院第一附属医院内分泌科,650031 [3]昆明医学院第一附属医院病理科,650031
出 处:《介入放射学杂志》2007年第8期527-531,共5页Journal of Interventional Radiology
基 金:云南省科委重点项目(2002C012Z)
摘 要:目的观察Graves病(GD)栓塞前及栓塞后3年组织病理动态变化,了解栓塞后疗效的病理基础。方法38例GD患者行甲状腺动脉栓塞治疗,于术前、术后7d、6个月、3年分别测血清TT3、TT4、FT3、FT4、rT3、TSH、抗甲状腺球蛋白(TGAb)、抗甲状腺过氧化物酶抗体(TPOAb)、TSH受体抗体(TRAb)等指标,行甲状腺彩色超声检查。23例行甲状腺穿刺活检。结果栓塞后7d病理变化主要表现为急性缺血坏死。栓塞后6个月表现为缺血后的纤维组织增生和慢性炎症破坏为主。栓塞后3年主要表现为明显的间质纤维组织增生、淋巴细胞浸润和滤泡萎缩。栓塞术后3年组甲状腺刺激抗体(TGAb)、TPOAb较栓塞术前高,差异有统计学意义(P<0.05),FT3、FT4、TRAb栓塞治疗后6个月和3年均较栓塞术前低,差异有统计学意义(P<0.05)。栓塞后3年甲状腺损伤持续存在可能是造成TGAb、TPOAb栓塞术后3年组较栓塞术前、栓塞术后6个月组轻度升高的原因。栓塞术后3年组甲状腺刺激及抗体(TSAb)较栓塞术前、栓塞术后7d、栓塞术后6个月低,呈持续下降。栓塞后甲状腺腺体组织逐渐减少,淋巴细胞浸润也逐步减轻,这应该是栓塞后3年TRAb和甲状腺素均较术前明显下降的主要原因。结论①栓塞后动态病理变化提示病情中长期缓解的病理学基础是甲状腺组织减少,增生缓解。②栓塞后机体免疫功能有一定改善,其栓塞后机体免疫功能好转与病理改变相符。③甲状腺动脉栓塞使甲状腺腺体组织减少,甲状腺素分泌减少,免疫紊乱改善,对GD具有综合治疗作用。Objective To study the relation between change of thyroid tissues and thyroid autoantibody after thyroid arterial embolization in the treatment of hyperthyroidism caused by Graves' disease with observation on changes of histopathology and thyroid auto-antibody in 3 years after thyroid arterial embolization, and to understand the foundation of the therapeutic action after arterial embolization. Methods 1. Thirty-eight patients with Graves' disease treated by transeathter arterial embolization had been tested serum TT3, TY4, Fr3, FT4, rT3, TSH, TGAb, TPOAb, TRAb and followed up with color Doppler ultrasound respectively at different periods (before arterial embolization and 7 day, 6 month, 3 year after arterial embolization). 2. 23 patients underwem needle aspiration biopsy of the thyroid gland. Results Volume of thyroid gland instantly dwindled in size after thyroid arterial embolization or within a few days. The changes of histopathology mainly showed acute isehemie necrosis 7 days after thyroid arterial embolization and followed byfibrous hyperplasia mesenchymal proliferation and follicular atrophy occurring 6 months and 3 years afterward. TGAb, TPOAb at the 3rd year after thyroid arterial embolization were higher than those before the thyriod arterial embolization. FT3, FT4, TRAb at 6 month after thyroid arterial embolization were lower than those of the 3 years. Conclusion Maladjustment of immunity in GD patients would be improved through the treatment of thyroid arterial embolization, synchronously with the promotion in histopathology. The outcomings of the shrinkage of thyroid tissue, decrease of thyroxin secretion and improvement of immunity provide a combinationtherapy for GD.
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