甲状腺过氧化物酶抗体在自身免疫性甲状腺疾病中的表现

甲状腺功能亢进（甲亢）、甲状腺功能低下（甲低）和亚临床甲低患者甲状腺过氧化物酶抗体（TPOAb）、甲状腺球蛋白抗体（TGAb）和甲状腺微粒体抗体（TMAb）的阳性率和阳性患者的抗体水平均高于正常对照组，TPOAb阳性率在各组中又明显高于同组的TGAb和TMAb阳性率。甲状腺功能恢复正常的复诊组TPOAb阳性患者的抗体水平明显低于甲亢组、甲低组和亚临床甲低组。提示TPOAb对自身免疫性甲状腺疾病的诊断、治疗及预后评估具有一定的临床意义。     

甲状腺功能减退症患者血清甲状腺刺激阻断性抗体随访研究

目的　研究临床甲状腺功能减退症(甲减)患者血清甲状腺刺激阻断性抗体(TSBAb)与甲减病因、甲状腺功能、碘营养状态及病情预后的关系。方法　检测三个不同碘摄入量地区39例临床甲减患者的血清TSBAb、甲状腺刺激性抗体(TSAb)、甲状腺过氧化物酶抗体(TPOAb)和甲状腺球蛋白抗体(TgAb),两年后随访。TSBAb和TSAb采用重组人促甲状腺素受体(rhTSHR) 中国仓鼠卵巢细胞生物法测定。结果　自身免疫甲减组TSBAb活性为(48. 9±21. 1)%, 高于非自身免疫甲减组且显著高于对照组(P<0. 01); 自身免疫甲减组TSBAb阳性率40. 0%, 显著高于非自身免疫甲减组(0% )和对照组(均P<0. 05)。甲减患者TSBAb活性随地区碘摄入量的升高而增强(9. 3±18. 8)%、(41. 7±23. 1)%和(53. 8±13. 4)% (P<0. 01)。尿碘浓度>600μg/L组的TSBAb活性显著高于<300μg/L组[ (55. 4±19. 7)% vs(34. 9±24. 3)%,P<0. 05 ]。TPOAb>500U/ml者甲状腺功能恢复不明显, TPOAb<500U/ml者血清TSH和FT4显著恢复(均P<0. 05),同时TSBAb活性由初访(56. 0±16. 1)%降至随访(46. 0±4. 6)%。结论　TSBAb是自身免疫甲减的特异性标志物。临床甲减患者TSBAb活性与碘摄入量有关。在预测临床甲减转归中TPOAb具有重要意义。当TPOAb未达强阳性时,患者甲状腺功能恢复与TSBAb     

关于促甲状腺素受体抗体的研究

促甲状腺素受体抗体（TRAb）是针对促甲状腺素受体（TSHR）的自身抗体，与Grawes病（GD）和自身免疫性甲状腺功能减退症（甲减）的发病密切相关。TRAb主要包括甲状腺刺激性抗体（TSAb）和甲状腺刺激阻断性抗体（TSBAb），可与TSHR分子上不同位点作用产生不同生物学效应。     

促甲状腺素受体抗体检测的临床意义

促甲状腺素受体抗体 (TRAb)与多种自身免疫性甲状腺疾病的发病密切相关 ,是临床诊断这些疾病的重要指标。TRAb在功能上可分为甲状腺刺激性抗体 (TSAb)和甲状腺刺激阻断性抗体(TSBAb) ,可与促甲状腺素受体分子上不同位点结合产生不同生物学效应。其中TSAb可引起Graves病 (GD)患者甲状腺功能亢进和弥漫性甲状腺肿的发生 ,而TSBAb则可导致自身免疫性甲状腺功能减退症 (甲减 )患者甲减的发生。本文将对TRAb检测在GD鉴别诊断、辅助制定GD治疗方案、抗甲状腺药物疗效及预测复发、筛查自身免疫性甲减等方面的临床价值作一全面综述。     

Graves甲亢合并白细胞减少与甲状腺自身抗体相关性研究

目的对Graves甲亢合并白细胞减少患者的白细胞与甲状腺自身抗体[甲状腺过氧化酶抗体（TPOAb）、甲状腺球蛋白抗体（TGAb）]进行相关性分析,探讨TPOAb、TGAb与Graves甲亢合并白细胞减少的关系。方法采用放射免疫法检测20例Graves甲亢合并白细胞减少患者及20例白细胞正常的Graves甲亢患者的TPOAb、TGAb水平,并将白细胞数与TPOAb、TGAb水平进行相关性分析。结果 Graves甲亢合并白细胞减少患者的TPO-Ab、TGAb水平略高于白细胞正常的Graves甲亢患者,但无统计学差异。线性回归分析显示,Graves甲亢患者的白细胞数与TPOAb、TGAb之间没有相关性。结论 TPOAb、TGAb水平与Graves甲亢并白细胞减少无关。     

促甲状腺素受体抗体检测的临床意义

促甲状腺素受体抗体(TRAb)与多种自身免疫性甲状腺疾病的发病密切相关,是临床诊断这些疾病的重要指标.TRAb在功能上可分为甲状腺刺激性抗体(TSAb)和甲状腺刺激阻断性抗体(TSBAb),可与促甲状腺素受体分子上不同位点结合产生不同生物学效应.其中TSAb可引起Graves病(GD)患者甲状腺功能亢进和弥漫性甲状腺肿的发生,而TSBAb则可导致自身免疫性甲状腺功能减退症(甲减)患者甲减的发生.本文将对TRAb检测在GD鉴别诊断、辅助制定GD治疗方案、抗甲状腺药物疗效及预测复发、筛查自身免疫性甲减等方面的临床价值作一全面综述.     

促甲状腺素受体抗体检测的临床意义

促甲状腺素受体抗体(TRAh)与多种自身免疫性甲状腺疾病的发病密切相关，是临床诊断这些疾病的重要指标。TRAb在功能上可分为甲状腺刺激性抗体(TSAb)和甲状腺刺激阻断性抗体(TSBAb)，可与促甲状腺素受体分子上不同位点结合产生不同生物学效应。其中TSAb可引起Graves病(GD)患者甲状腺功能亢进和弥漫性甲状腺肿的发生，而TSBAb则可导致自身免疫性甲状腺功能减退症(甲减)患者甲减的发生。本文将对TRAb检测在GD鉴别诊断、辅助制定GD治疗方案、抗甲状腺药物疗效及预测复发、筛查自身免疫性甲减等方面的临床价值作一全面综述。     

甲状腺功能亢进症患者甲状腺刺激及刺激阻断性抗体共存现象的探讨

在自身免疫性甲状腺疾病中,甲状腺刺激抗体(thyroid-stimulating antibody,TSAb)是甲状腺功能亢进症(简称甲亢)的病因,而甲状腺刺激阻断性抗体(thyroid stimulation-blocking antibody,TSBAb)则阻断TSH或TSAb与TSH受体结合,使刺激TSH受体的活动减弱,导致甲减。目前国内有关TSBAb测定的报道甚少。本文介绍用FRTL-5细胞以cAMP作为终点的测定方法,同时测定患者同一份血样的TSAb和TSBAb。现将2例Graves甲亢和1例桥本甲亢TSAb和TSBAb共存的情况作一探讨。     

多囊卵巢综合征患者血清甲状腺特异抗体检测及临床意义

目的探讨自身免疫性甲状腺炎（AIT）与多囊卵巢综合征（PCOS）的关系。。方法72例PCOS患者为观察组,68例健康体检的育龄期妇女为对照组。测定两组血清甲状腺特异抗体[包括甲状腺过氧化物酶抗体（TPOAb）、甲状腺球蛋白抗体（TGAb）]水平;比较观察组特异抗体阳性（指TPOAb及TGAb均阳性;诊断为AIT）与阴性（TPOAb及TGAb均阴性）者促卵泡素（FSH）／黄体生成素（LH）值及流产率。结果观察组及对照组特异抗体阳性率分别为23．6％、4．4％,P〈0．05。观察组特异抗体阳性者LH／FSH显著高于阴性者（P〈0．05）;特异抗体阳性者与阴性者流产率分别为23．5％、10．2％,但差异无统计学意义。结论PCOS患者AIT发病率显著高于正常人群,与雌、孕激素水平失衡有关;对PCOS患者应注意筛查甲状腺特异抗体,避免误诊误治。     

促甲状腺激素受体抗体和甲状腺过氧化物酶抗体检测对Gravse病的诊断意义

目的探讨促甲状腺激素受体抗体（ThyrotropinReceptorAntibody,TRAb）和甲状腺过氧化物酶抗体（ThyroidPer．oxidaseAntibody,TPOAb）测定对格雷夫斯病（Gravse病,GD）的诊断价值。方法用放射受体分析法（RadioReceptorAs—say,RRA）对75例初诊GD患者,99例未控制的GD患者,112例经抗甲状腺药物治疗缓解的GD患者,23例GD复发患者,56例健康体检者分别进行TRAb和TPOAb的测定。结果GD初诊组、未控制组、复发组TRAb水平和阳性率均显著高于GD控制组（P〈0．05）,GD控制组TRAb水平和阳性率显著高于正常对照组（P〈0．05）,差异均有统计学意义。GD患者各组TPOAb水平和阳性率均显著高于正常对照组（P〈0．05）。结论检测血清TRAb和TPOAb水平在GD发病、进展及复发具有重要的临床意义。     

Thyroid response, especially to thyrotropin-binding inhibitory immunoglobulins, in euthyroid relatives of patients with Graves' disease: a clinical follow-up

Three hundred and fifty-three euthyroid relatives of Graves' disease patients were tested for TSH binding inhibitory immunoglobulins (TBII). Eighteen had elevated levels of TBII, and 232 who had negative TBII levels also agreed to be followed for a period of 6-30 months. TBII was chosen as the critical screening measurement for this study, rather than thyroid-stimulating antibodies (TSAb) and thyroid-stimulating blocking antibodies (TSBAb), because of the availability and ease of use of TBII RIA kits. Eleven of the 18 subjects with elevated TBII were T3 nonsuppressible (group I), and 10 of the 11 were TRH unresponsive. Nine of these 10 subjects showed TSH levels below 0.05 mU/L. The remaining 7 subjects were T3 suppressible and TRH responsive (group II). Alterations in thyroid status occurred in 8 of the 11 subjects in group I during follow-up. One developed hypothyroidism, and 7 became hyperthyroid. The hypothyroid subject had initial titers of TBII, TSAb, and TSBAb that were markedly elevated, and TSAb disappeared when she became hypothyroid. Six of the 7 subjects who developed hyperthyroidism had elevated TSAb and negative TSBAb titers while they were euthyroid. All 7 subjects in group II remained euthyroid during the follow-up period. Only 2 of the 232 relatives who initially had negative TBII titers became hyperthyroid during the follow-up period. The results indicate that euthyroid relatives with a family history of Graves' disease who have elevated TBII levels and suppressed basal serum TSH concentrations have a much higher potential to develop hyperthyroidism than those who have normal or negative TBII levels.     

Autoimmune thyroid disease accompanied by recurring episodes of painful thyroid ameliorated by thyroidectomy

A 71-yr-old female initially presented with clinical and biochemical hyperthyroidism with high TSH binding inhibitory immunoglobulin (TBII) and anti-thyroid peroxidase antibody (TPOAb) titers. Histological findings of the thyroid revealed hyperplasia with a focal germinal center, indicating Graves' disease and mild focal chronic thyroiditis. Four episodes of painful and tender thyroid occurred over the next 2 yr accompanied by acute inflammatory reactions. The first episode that developed while the patient was in a hyperthyroid state was soon followed by hypothyroidism associated with further increases in anti-thyroglobulin antibody (TGAb) and TPOAb titers. The subsequent 3 episodes occurred during the hypothyroid state, when the TGAb titer progressively increased with each episode. We performed subtotal thyroidectomy to prevent further episodes. Specimens obtained at thyroidectomy showed that extreme fibrosis had replaced the thyroid parenchyma with collapsed follicles and moderate lymphocyte infiltration. No further episodes occurred after thyroidectomy, and during a 3-yr follow-up period, TBII and thyroid-stimulating antibody (TSAb) disappeared and TGAb and TPOAb titers decreased. This case report provides further evidence supporting the notion that thyroid epithelial destruction progresses during relatively short periods of recurrent painful thyroid and that thyroidectomy helps patients affected by this condition that are unresponsive to other treatment strategies.     

The role of thyroid stimulating antibody (TSAb) in the thyroid function of patients with post-partum hypothyroidism

OBJECTIVE: We investigated the association between thyroid function and the biological activities of thyroid stimulating antibodies (TSAb) and thyroid stimulation blocking antibodies (TSBAb) in patients with post-partum hypothyroidism. DESIGN: A prospective study. PATIENTS: We studied 25 patients with post-partum hypothyroidism who visited our thyroid clinic during the period from 1985 to 1990. MEASUREMENTS: We measured TSH binding inhibitory immunoglobulin (TBII) and TSAb activity at the initial presentation of each of the 25 patients. Women found to have elevated TSAb activity were followed up. Upon finding negative TSAb activity along with positive TBII activity in the serum at the initial presentation, we measured TSBAb activity. Women found to have elevated levels of TSBAb at the initial presentation were also followed up. RESULTS: Elevated TBII activity was found in six of the 25 patients, as was high TSAb activity (205-2651%, normal 55.0-145.0%) in five of these six and in one other patient at the initial presentation. Markedly elevated TSBAb activity (89%) was found in one TBII positive patient. We were able to follow up serially five TSAb positive patients and the TSBAb positive patient over periods ranging from 11.5 to 26.5 months post-partum. The maximal value of TSAb activity was observed at the initial presentation in all TSAb positive patients, following which the activities gradually decreased. One of these patients developed Graves' hyperthyroidism associated with high TSAb activity (1223%) at 10.5 months post-partum. One of the other patients was restored to euthyroid with elevated TSAb activity (279%), but thereafter developed hypothyroidism in conjunction with the disappearance of TSAb activity at 26.5 months post-partum. In the other two patients, normalization of thyroid function was observed with elevated TSAb activity. Thereafter, thyroid function remained within the normal range even with the disappearance of TSAb activity. In the other patient, normalization of thyroid function was observed at 11.5 months post-partum, 3 months after the disappearance of TSAb activity. In the TSBAb positive patient, TSBAb activity decreased to 21% by 17.5 months post-partum associated with normalization of thyroid function. CONCLUSION: The present study demonstrates the presence of elevated levels of TSAb activity in some patients with post-partum hypothyroidism. In these patients, Graves' hyperthyroidism may be induced by TSAb activity, and hypothyroidism may reoccur with the disappearance of the TSAb activity. Furthermore, post-partum hypothyroidism may be due to increased TSBAb activity in some patients.     

Role of thyrotropin receptor antibodies in the development of hyperthyroidism: follow-up studies on nine patients with Graves' disease

TSH binding inhibitor immunoglobulin (TBII) and thyroid-stimulating antibody (TSAb) activities were measured serially for 4-32 months in nine patients before and during development of hyperthyroidism due to Graves' disease. Initially, all were euthyroid, seven had thyroid enlargement, one had proptosis, and seven had high serum titers of antithyroid microsomal antibodies. The occurrence of hyperthyroidism was preceded by detection of both TBII and TSAb in four patients and detection of TSAb alone in four patients. One patient had neither TBII nor TSAb when euthyroid. The mean initial TBII and TSAb activities were 10.2 +/- 15.2% (+/- SD) and 2677 +/- 4620%, respectively, when these patients were euthyroid. When they became hyperthyroid, both TBII and TSAb activities increased in all patients. At that time, TBII was detected in all but one (eight of nine subjects; 88.9%), with a mean activity of 58.8 +/- 23.4% (+/- SD), and TSAb was detected in all nine patients, with a mean value of 4508 +/- 4429%. These findings not only indicate the crucial role of TSH receptor antibodies in the development of hyperthyroidism due to Graves' disease, but also suggest that a certain period of subclinical Graves' disease exists before the onset of overt hyperthyroidism in most patients, in the sense that they have TSH receptor antibodies, especially TSAb, in their serum even though they are euthyroid.     

Development of primary hypothyroidism with the appearance of blocking-type antibody to thyrotropin receptor in Graves' disease in late pregnancy.

Spontaneous remission of Graves' disease with a decrease of thyroid stimulating antibody (TSAb) activity is commonly observed in pregnancy. In this article, however, a Graves' patient who developed primary hypothyroidism with an appearance of thyroid stimulation-blocking antibody (TSBAb) activity in late pregnancy is reported. A 25-year-old woman presented with clinical and biochemical hyperthyroidism with an elevation of 99mTcO4- thyroid uptake (4.7%; normal range, 0.7%-3.0%) and mildly elevated activity of thyrotropin-binding inhibitory immunoglobulin (TBII; 30.4%). She was euthyroid with normal TBII (8.0%) and TSAb (126%) before pregnancy, when the patient was taking a 5-mg daily dose of methimazole (MMI). MMI was stopped by the patient when she became pregnant. Subsequently, the patient progressed into primary hypothyroidism with a marked elevation of TBII activity (78.4%) in the third trimester of the pregnancy (at that time, TSAb activity was not detected). TSBAb measured 2 weeks later was detected at the activity of 85.0%. Replacement therapy was initiated with levothyroxine (LT4) (0.05-0.1 mg/day), which was discontinued on the 55th day postpartum because of the onset of mild thyrotoxicosis followed by short-term euthyroid state despite high TSBAb activity. Subsequently, because the patient developed primary hypothyroidism 5 months after delivery, replacement therapy with LT4 (0.1-0.125 mg/day) was readministered. Thus, it is suggested that the development of hypothyroidism with the appearance of TSBAb in Graves' patients can occur even in late pregnancy.     

Clinical results of anti-inflammatory therapy in Graves' ophthalmopathy and association with thyroidal autoantibodies

OBJECTIVE: Graves' ophthalmopathy (GO) is clinically associated with autoimmune thyroid disease, and autoantibodies to thyroidal antigens, especially to the TSH-receptor (TRAb), might be involved in the disease process. While there is mounting evidence that TRAb are associated with GO at the onset of the disease, so far no studies have looked at the association between thyroidal autoantibodies and the clinical outcome of GO therapy. The aim of this retrospective study was to evaluate whether TSH binding inhibitory immunoglobulins (TBII) and thyroid stimulating antibodies (TSAb) are still associated with the clinical activity and severity of GO after the completion of anti-inflammatory therapy. In addition, we wanted to elucidate whether thyroid peroxidase (TPO) or thyroglobulin (TG) autoantibodies (TPOAb and TGAb) are in any way related to GO. DESIGN PATIENTS AND MEASUREMENTS: Clinical activity score (CAS) and the severity of GO (modified NOSPECS score) were assessed in 108 patients with GO after steroid therapy and, if indicated, orbital irradiation. Patients were grouped according to their clinical presentation and autoantibody levels (TBII, TSAb, TPOAb and TGAb) were measured. After therapy for hyperthyroidism, all patients were clinically euthyroid but showed clear heterogeneity for GO 4-12 months after the end of anti-inflammatory therapy. Fifty-two patients had inactive GO, 41 had moderately active and 15 still had very active (non-responsive) GO. Concerning severity, 27 patients had mild GO, 64 moderately severe and 17 severe GO. RESULTS: TBII titres were still positive in 14 (93%) of 15 patients in the non-responsive group (CAS > 6) compared to 22 (42%) of 52 patients (P < 0.001) with post-therapeutic inactive GO (CAS 相似文献   

STUDIES ON THYROTROPHIN RECEPTOR ANTIBODIES IN PATIENTS WITH EUTHYROID GRAVES'' DISEASE

Thyroid stimulating antibodies (TSAb) and TSH-binding inhibitor immunoglobulins (TBII) were assessed in 30 patients with euthyroid Graves' disease. TSAb were detected in 24 cases (80.0%), the incidence being not significantly different from that in hyperthyroid Graves' disease (29/30, 97.6%). On the other hand, the incidence of TBII in patients with euthyroid Graves' disease (12/30, 40.0%) was significantly lower than that in patients with hyperthyroid Graves' disease (30/30, 100.0%). The mean TSAb and TBII activities in the euthyroid patients were significantly lower than in the hyperthyroid patients (P less than 0.005 and P less than 0.001, respectively). Both TBII and, more closely, TSAb activities correlated with T3-nonsuppressibility and inhibition of serum TSH response to TRH stimulation. The findings supported the stimulation in vivo of the thyroid by these antibodies. Both antithyroglobulin and antimicrosomal antibody titres in euthyroid Graves' disease were significantly lower than in hyperthyroid Graves' disease (P less than 0.05, P less than 0.01, respectively). Goitre size was significantly smaller (P less than 0.001), and 99mTc thyroid uptake was significantly lower (P less than 0.001) in the euthyroid than in the hyperthyroid group. Thus, the reduced mass of thyroid tissues responding to the stimulators was considered to be one of the factors responsible for the euthyroidism despite the presence of TSAb. The high incidence of TSAb and relatively low incidence of TBII in euthyroid Graves' disease indicate that the presence of TSAb does not necessarily lead to hyperthyroidism and that the development of overt thyrotoxicosis may require augmentation of both TSAb and TBII.     

Immunoglobulins of untreated Graves' patients with or without thyrotropin receptor antibody (determined by porcine thyrocytes) universally elicit potent thyroid hormone-releasing activity in cultured human thyroid follicles.

Thyrotropin receptor antibody (TRAb), comprising thyrotropin binding inhibitor immunoglobulin (TBII) and thyroid-stimulating antibody (TSAb), both of which are conventionally determined using porcine thyrocytes in Japan, is not always positive in patients with untreated Graves' disease. To elucidate whether immunoglobulin G (IgG) obtained from TBII/TSAb-positive (+) or negative (-) Graves' disease patients are responsible for hyperthyroidism, we investigated the thyroid hormone-releasing activity (THRA) of these IgGs in human thyroid follicles in suspension culture, in which bovine thyrotropin (bTSH) is detectable even at 0.1 microU/mL. Human thyroid follicles, obtained from Graves' disease patients by subtotal thyroidectomy, were cultured in serum-free F-12/RPMI-1640 medium supplemented with bTSH or purified Graves' IgGs. After preculturing for 3 days, 125I was added, and after an additional 3 days of culture, 1251 incorporated into the thyroid follicles and organic 125I released into the culture medium (mainly 1251 -T4 + 125I-T3) were counted. Seventy TBII(+)/TSAb( + )-, 3 TBII( + )/TSAb( - )-, and 3 TBII( - )/TSAb( + )- patients with untreated Graves' disease were all positive for THRA, which became undetectable in spontaneous remission obtained after several years of medical treatment. The THRA was equivalent to 0.8-230 microU/mL bTSH. Furthermore, 2 TBII(-)/TSAb(-) patients were significantly positive for THRA. This TBII(-)/TSAb(-)IgG stimulated human thyrocytes to produce cyclic adenosine monophosphate (cAMP), and this was partially inhibited by antihuman IgG antibody. The THRA induced by TBII(+)/TSAb(+) IgGs as well as TBII(-)/TSAb(-) IgG was inhibited by blocking-type TRAb obtained from TBII(+) patients with myxedema. There was a significant correlation between THRA and TSAb. These in vitro findings suggest that all IgGs obtained from untreated Graves' patients (n = 78) elicit potent THRA in human thyroid follicles in suspension culture. Because the TBII(-)/TSAb(-) IgGs can stimulate cAMP production in human but not in porcine thyrocytes, they probably recognize epitope(s) of TSH-binding sites specific to the human thyrotropin (hTSH) receptor. Furthermore, we have demonstrated that the thyroid gland of hyperthyroid Graves' patients is stimulated by IgG(s) equivalent to at least 0.8 microU/mL bTSH (about 5 microU/mL hTSH) in vitro.     

Characterization of thyroid-stimulating blocking antibodies that appeared during transient hypothyroidism after radioactive iodine therapy.

Hypothyroidism after radioactive iodine (RAI) therapy for Graves' disease can be transient or permanent. The cause for early transient hypothyroidism is unknown. We evaluated 11 patients who developed transient hypothyroidism within 6 months of RAI and 12 who remained euthyroid after RAI. Approximately equal numbers of patients in each group had thyroid-stimulating antibody (TSAb) that increased cyclic adenosine monophosphate (cAMP) levels in Chinese hamster ovary (CHO) cells transfected with the recombinant human thyrotropin receptor (TSHR) (WT cells). Approximately equal numbers of patients from both groups had an increase in TSAb activity post-RAI. All TSAbs had their dominant functional epitope on the N-terminus of the TSHR extracellular domain, requiring residues 90-165 for activity because they, but not TSH, completely lost stimulating activity in a receptor chimera, wherein TSHR residues 90-165 were substituted by equivalent residues of the lutropin/choriogonadotropin receptor (LH/CGR). Although equal numbers of patients in both groups had thyrotropin-binding inhibiting immunoglobulin activity (TBII), as measured by radioreceptor assay before RAI, patients with transient hypothyroidism had a surge in TBII activity and all except one became positive for thyroid-stimulating blocking antibodies (TSBAb), as measured by inhibition of TSH-stimulated cAMP from WT cells. When immunoglobulin G (IgGs) were epitope-mapped using TSHR/LH-CGR chimeras with different substitutions, 8 hypothyroid subjects had TSBAbs directed against residues 90-165 of the TSHR, as well as TSHR residues 261-370. Two had functional epitopes directed at residues 9-89 as well as TSHR residues 261-370. None of the euthyroid control patients developed TSBAbs and their TBII activity decreased post-RAI. When patients with transient hypothyroidism reverted to a euthyroid state, TSAb was still detectable in 5; however, TBII was present in all and TSBAb, although decreased, was still positive in 9. In summary, RAI therapy was associated with a change in thyroid antibody characteristics in most patients. Additionally, patients with a surge in TBII and the appearance of TSBAb developed transient hypothyroidism after RAI.     

河北某水源性高碘地区成人甲状腺疾病的流行病学调查

目的：调查水源性高碘地区－河北省黄骅市歧口村、高头村≥14岁人群甲状腺疾病的流行状况,方法：入户问卷调查4230人的基础上,采样调查1074人,所有采样调查对象均详细填与甲状腺疾病调查表,接受体检查和B超检查,测定血清促甲状腺激素（TSH）、甲状腺自身抗体（TAA）和甲状腺球蛋白（TG）,留取空腹尿样测量尿碘、TSH异常者测定甲状腺激素和TSH受体抗体（TRAb）。结果：采样人群的尿碘中位数为614．61μg/L。临床甲状腺功能亢进症（甲亢）和亚临床甲亢的患病率分别为1．21％和1．12％;临床甲亢中92．3％为Graves病所致,亚临床甲亢中75％TRAb阳性;回顾性分析普遍食盐碘化前后临床甲亢平均年发病率差异无显著性,临床甲状腺功能减低症（甲减）和亚临床甲减的患病率分别为1．96％和6．05％,患者TAA阳性率分别为85．71％和29．23％。采样人群甲状腺过氧化物酶抗体（TPOAb）和甲状腺球蛋白抗体（TGAb）阳性率分别为11．6％和9．3％。弥漫性甲状腺肿,结节性甲状腺肿、单发结节和多发结节的患病率分别为3．26％、2．61％、1．77％和6．4％。甲状腺癌病率为91．58／10万,结论：在尿磺中位数为614．61μg/L的碘营养状态下,甲状腺功能减退症和甲状腺癌患病率显著增高,提示这一碘摄入量并不安全。