抗甲状腺药物对131Ⅰ治疗甲状腺功能亢进症疗效的影响

^131Ⅰ是治疗甲状腺功能亢进症（甲亢）的主要药物之一，治疗前应用硫氧嘧啶类药物如丙硫氧嘧啶可能会降低^131Ⅰ治疗甲亢的治愈率，咪唑类药物如甲巯咪唑则不会影响其疗效。^131Ⅰ治疗甲亢后应用丙硫氧嘧啶或甲巯咪唑对^131Ⅰ疗效的影响尚有争议之处。抗甲状腺药物影响^131Ⅰ疗效的机理可能在于改变了^131Ⅰ的有效半衰期和（或）甲状腺对^131Ⅰ的摄取率。     

不同抗甲状腺药物对^131Ⅰ治疗Graves病近期疗效的比较

目的探讨Graves病患者使用不同抗甲状腺药物后再行^131Ⅰ治疗的疗效比较。方法随访Graves病经抗甲状腺药物治疗后再行^131Ⅰ治疗的患者98例,按治疗前分别使用丙基硫氧嘧啶、他巴唑、碳酸锂分为3组,前两组在^131Ⅰ治疗前停用抗甲亢药物15天,碳酸锂组使用至治疗当日,采用个性化^131Ⅰ治疗后6个月复查并评价治疗效果。结果使用丙基硫氧嘧啶组在^131Ⅰ治疗6月后仍有38％患者甲状腺功能亢进,使用他巴唑组甲亢比例为23％,而碳酸锂组仅为9．6％,3组间比较均有显著性差异（α〈0．05）;3组间发生甲减例数比较无显著性差异（P〉0．05）。结论在^131Ⅰ治疗Graves病前使用丙基硫氧嘧啶会降低^131Ⅰ治疗甲亢的疗效,其影响高于他巴唑组及碳酸锂组,3组中碳酸锂组对^131Ⅰ治疗甲亢的疗效影响最小。     

~（131）I治疗后Graves病突眼与甲亢病情转归相关分析

目的分析131I治疗后Graves病患者突眼与病情转归的关系。方法将进行131I治疗的Graves病患者分为突眼组和无突眼组,并分析两组131I治疗后甲亢及突眼病情转归情况。结果突眼组及无突眼组131I治疗有效率、永久性甲减发生率及治疗无效率相比均有统计学差异（P均〈0.05）。突眼组患者131I治疗后总有效率为73.5%（72/98例）,甲亢治疗有效的67例患者中,突眼治愈及好转者56例,占83.6%。突眼组促甲状腺受体抗体水平明显高于无突眼组（P〈0.05）。结论 131I是治疗Graves病患者甲亢及突眼的有效方法,突眼治疗效果与甲亢病情转归密切相关。131     

^131Ⅰ治疗甲亢后甲状腺声像图的探讨

我所用^131Ⅰ治疗甲已亢已20多年，治疗患者数千例，对这些患者治疗前后多次超声检查，发现部分患者^131Ⅰ治疗后的甲状腺声像图与治疗前差异较大。笔者对320例^131Ⅰ治疗甲亢后的患者进行3、6、12个月复查，探讨二维超声（2D）及彩色多普勒显像（CDFI）的特点，现报道如下。     

^131I治疗甲亢伴白细胞减少28例疗效观察

白细胞减少常见于甲状腺功能亢进症（甲亢）患者．可发生在甲亢治疗前或抗甲状腺药物（ATD）治疗后，治疗较为棘手。2000年1月-2004年1月，我们对28例甲亢伴白细胞减少患者采用^131I治疗，取得满意疗效。现报告如下。     

^131I治疗Graves病

放射性核素应用于临床治疗，已有60年的历史。自从1942年Hertz及Hamilton等介绍了^131碘(^131Ⅰ)治疗甲状腺功能亢进(甲亢)并获得成功后，经过几十年的发展，该方法不断得到改进，并被誉为是核素治疗学最成熟、应用最广泛的典范性治疗方法。^131Ⅰ、药物及手术均为治疗甲亢的有效方法，各具特色。然而，^131Ⅰ     

^131Ⅰ治疗甲亢对性腺和胰岛功能的影响

本文对^131Ⅰ治疗甲亢前后患者睾酮（T）、雌二醇（E2）、胰岛素（INS）、C-肽（C—P）含量进行了对比分析，探讨服用^131Ⅰ治疗甲亢对患者性腺和胰岛内分泌的影响。     

病毒性肝炎合并甲状腺功能亢进症11例临床分析

目的分析病毒性肝炎合并甲亢时的病情，探讨有效治疗方案。方法选择病毒性肝炎合并甲状腺功能亢进症11例，仅予护肝支持对症治疗9例，护肝和^131碘治疗2例。结果病毒性肝炎合并甲亢大多肝功损害明显，病情较重，其中重型肝炎5例，慢性肝炎重度4例，慢性肝炎中度2例。9例不抗甲亢治疗效果差，2例^131碘治疗病情好转。结论病毒性肝炎合并甲亢易造成肝损害及甲亢加重，不抗甲亢治疗预后差。     

影响^131I治疗甲状腺功能亢进症疗效的临床多因素分析

目的探讨^131I治疗甲状腺功能亢进症（甲亢）疗效的影响因素。方法对接受^131I治疗的100例弥漫性甲亢患者进行3、6个月跟踪随访,收集其临床资料、实验室检查结果,采用Logistic回归分析对影响^131I治疗效果的因素进行分析。结果 Logistic回归分析显示,在实际给碘剂量一定的条件下（3～8 mCi）,病程、甲状腺质量、有无突眼、24 h摄碘率、甲状腺结节、甲状腺硬度是影响131 I治疗甲亢疗效的主要影响因素（F分别为3.984、5.234、5.171、4.314、4.156、5.612,P均〈0.05）。结论 131I治疗甲亢时,应对其影响因素进行综合分析,制定个体化治疗方案,以提高甲亢治愈率。     

分化型甲状腺癌^131Ⅰ清甲治疗患者淋巴细胞染色体畸变率的变化

目的 观察分化型甲状腺癌（DTC）患者术后^131Ⅰ清除剩余甲状腺（清甲）治疗后淋巴细胞染色体畸变率的变化。方法 20例分化型甲状腺癌术后行放射活度为3．7GBq的^131Ⅰ清甲治疗患者做为清甲组，分别于服^131Ⅰ治疗前1d及服^131Ⅰ治疗后1w采用外周血淋巴细胞培养及常规制片法检测染色体畸变率；以6例Graves病患者为甲亢治疗组，口服^131Ⅰ平均放射性活度为165MBq，6例服用安慰剂的正常自愿者为正常对照组，后两组均与清甲组同时服药或安慰剂并在相同时间用同样方法取外周血进行检测（以染色体畸变率〈2．5％，且“双着丝粒体＋着丝粒环”率〈0．05％为正常值）。结果 清甲组、甲亢治疗组及正常对照组在服^131Ⅰ或安慰剂前1d染色体畸变率均在正常水平。三组间差异无显著性（P〉0．05）；甲亢治疗组及正常对照组服^131Ⅰ或安慰剂后1w染色体畸变率及“双着丝粒体＋着丝粒环”率均无明显升高。两组间比较差异无显著性（P〉0．05）；清甲组服药后1w染色体畸变率及“双着丝粒体＋着丝粒环”率明显增高，与甲亢治疗组及正常对照组差异均有显著性（P〈0．05）。结论 DTC患者^131Ⅰ清甲治疗后短期内可引起染色体畸变率增高。     

~(131)Ⅰ治疗甲状腺功能亢进症的进展

近年来国内外发表了一些~(131)Ⅰ治疗甲状腺功能亢进症(甲亢)的临床指南.这些指南表明了~(131)Ⅰ治疗甲亢在5方面的进展,包括:(1)~(131)Ⅰ治疗亚临床甲亢;(2)~(131)Ⅰ治疗Graves甲亢合并甲状腺摄碘率升高的慢性淋巴细胞性甲状腺炎;(3)~(131)Ⅰ治疗儿童和青少年甲亢;(4)~(131)Ⅰ治疗Graves眼病;(5)~(131)Ⅰ治疗难治性重度甲亢.本文简要介绍并评价有关内容.     

(131)I and thyroid-associated ophthalmopathy

OBJECTIVE: Radioiodine ((131)I) used to obtain euthyroidism in thyrotoxic patients is suspected of having a worsening or provoking effect on thyroid-associated ophthalmopathy (TAO), an autoimmune disease closely related to Graves' disease. DESIGN: This review summarises the existing literature and describes risk factors influencing the course of TAO including thyroid function, cigarette smoking and treatment of Graves' hyperthyroidism (especially (131)I therapy). CONCLUSION: It is recommended that patients who may be at a greater risk of worsening ophthalmopathy are considered when choosing the modality of therapy of hyperthyroidism and also in deciding whether prophylactic systemic glucocorticoid treatment is indicated.     

Clinical and biochemical changes following 131I therapy for hyperthyroidism in patients not pretreated with antithyroid drugs

BACKGROUND: Radioiodine therapy (131I) for the treatment of hyperthyroidism has been shown to be effective and safe. Despite the extensive experience with radioiodine therapy, the necessity for pretreatment with antithyroid drugs is controversial. Pretreatment is partly based on the concept that antithyroid drugs deplete the thyroidal hormonal stores, thereby reducing the risk of a radioiodine-induced aggravation of hyperthyroidism or thyroid storm. Few data are available on the frequency of clinically significant exacerbations of hyperthyroidism following 131I therapy without prior treatment with antithyroid drugs. The aim of the present study was to determine prospectively the early clinical and biochemical changes after 131I therapy in patients who were not pretreated with antithyroid drugs. METHODS: Patients with Graves' disease (n = 21), toxic multinodular goiter (n = 11) or toxic adenoma (n = 2) were studied before and after 131I therapy. Clinical and biochemical parameters of thyroid function were investigated before and 1, 2, 8, 11, 18 and 25 days after 131I treatment. Patients were given no antithyroid drugs prior to 131I therapy, all patients received beta-blocking agents for symptomatic relief. RESULTS: In 19 of 34 patients, a transient increase in thyroid hormone levels was observed, predominantly in the first week following 131I therapy. None of these patients experienced worsening of thyrotoxic symptoms. This transient increase in thyroid hormone levels was demonstrated in all patients with toxic multinodular goiter, whereas it was found in only six of 21 patients with Graves' disease. This difference could not readily be explained by differences in pretreatment thyroid hormone levels, administered dose or effectively absorbed dose of 131I. CONCLUSIONS: 131I treatment of hyperthyroidism without pretreatment with antithyroid drugs may cause a transient increase in thyroid hormone levels. Clinically significant exacerbations of hyperthyroidism were, however, not observed in our study population. Increased hormone levels following 131I therapy were more often seen in patients with toxic multinodular goiter than in patients with Graves' disease.     

Radioactive iodine for hyperthyroidism in children and adolescents: referral rate and response to treatment

Objectives Radioactive iodine (¹³¹I) therapy is increasingly viewed as a safe and effective treatment for paediatric and adolescent hyperthyroidism. Our objective was to estimate treatment response and its predictors and describe current referral practices for ¹³¹I therapy. Design Retrospective study. Patients One hundred and thirty‐one children 30 days–21 years old with laboratory evidence of hyperthyroidism, seen in an academic paediatric and adolescent endocrinology practice. Measurements Rate of referral, indications for ¹³¹I, predictors of poor treatment response. Results Thirty‐eight of 102 patients with persistent hyperthyroidism (37%) received ¹³¹I (160 μCi/g thyroid tissue/¹³¹I uptake), as did an additional 10 patients initially evaluated by adult thyroidologists. Primary indications were intolerance to (29%) or poor control on (19%) antithyroid drugs, patient preference (50%) and unknown (2%). Of 48 patients treated with ¹³¹I, 89% and 11% became hypothyroid after one and two ¹³¹I doses, respectively. The goal of ¹³¹I therapy was attainment of hypothyroidism. ‘Poor treatment response’ (seen in 27%) was defined as requirement for a second ¹³¹I dose or failure to achieve hypothyroidism after 6 months. Predictors of poor treatment response included: previous use of antithyroid drugs (37%vs. 0%, P = 0·02), ophthalmopathy (58%vs. 8%, P = 0·002), and an interval of ≥12 months from diagnosis to ¹³¹I (50%vs. 10%, P = 0·003). A very elevated free T4 tended to be more prevalent in those with poor response. Conclusions In children and adolescents with hyperthyroidism, high rates of success after ¹³¹I are achievable. Use of antithyroid drugs, pre‐existing eye disease and prolonged time to ¹³¹I may confer relative resistance to ¹³¹I.     

人工肝结合~(131)I治疗与内科常规治疗40例甲亢合并重症肝损害疗效的比较

目的:对人工肝结合131I治疗与内科常规治疗甲状腺功能亢进(甲亢)合并重症肝损害患者的临床疗效进行比较.方法:对近6年来我院40例甲亢合并重症肝损害患者的临床表现、实验室检查、治疗方式及预后进行回顾性分析,比较采用人工肝[方式有分子吸附再循环系统(molecula radsorbent recirculating system,MARS)、血浆置换]结合131I与内科常规治疗的疗效和预后.结果:人工肝组有25例患者,20例好转,5例病情恶化,内科常规治疗组共15例患者,6例好转,9例恶化,人工肝组好转率(80%)明显高于内科常规治疗组(40%),人工肝治疗能显著改善患者肝功能、甲状腺功能指标,缩短凝血酶原时间,提高治愈率.结论:甲亢合并重症肝损害病情复杂,治疗棘手,根据病情需要行人工肝治疗,在肝功能改善后行131I能明显改善预后,提高生存率,降低病死率.     

Prevention of recurrent amiodarone-induced hyperthyroidism by iodine-131

Amioradone-induced hyperthyroidism is a common complication of amiodarone therapy. Although definitive interruption of amiodarone is recommended because of the risks of aggravation of the arrhythmias, some patients may require the reintroduction of amiodarone several months after normalisation of thyroid function. The authors undertook a retrospective study of the effects of preventive treatment of recurrences of amiodarone-induced hyperthyroidism with I131. The indication of amiodarone therapy was recurrent, symptomatic, paroxysmal atrial fibrillation in 13 cases and ventricular tachycardia in 5 cases (M = 14, average age 64 +/- 13 years). The underlying cardiac disease was dilated cardiomyopathy (N = 5), ischaemic heart disease (N = 3), hypertensive heart disease (N = 2), arrhythmogenic right ventricular dysplasia (N = 2) or valvular heart disease (N = 2). Two patients had idiopathic atrial fibrillation. An average dose of 576 +/- 184 MBq of I131 was administered 34 +/- 37 months after an episode of amiodarone-induced hyperthyroidism. Amiodarone was reintroduced in 16 of the 18 patients after a treatment-free period of 98 +/- 262 days. Transient post-radioiodine hyperthyroidism was observed in 3 cases (17%). Sixteen patients (89%) developed hypothyroidism requiring replacement therapy with L-thyroxine. There were no recurrences of amiodarone-induced hyperthyroidism. After 24 +/- 17 months follow-up, the arrhythmias were controlled in 13 of the 16 patients (81%) who underwent the whole treatment sequence. The authors conclude that preventive treatment with I131 is an effective alternative to prevent recurrence of amiodarone-induced hyperthyroidism in patients requiring reintroduction of amiodarone to control their arrhythmias.     

Radioactive iodine therapy in Graves' hyperthyroidism

Graves' disease is the most frequent cause of hyperthyroidism. Clinical thyrotoxicosis is directly caused by autoantibodies that activate the TSH receptor. The etiology is multifactorial, with genetic and nongenetic factors involved. Current treatment options are antithyroid drugs (ATD), radioiodine (131I) and surgery. Radioactive iodine is increasingly being used as definitive therapy, because it long has proven to be a safe, nonexpensive and effective treatment. Recent publications have discussed the use of 131I associated with ATD as well as the identification of predictors of treatment failure, which are discussed in this review. Antithyroid drugs are still the first choice therapy in patients with mild disease, small goiters, children, adolescents, and in pregnancy. Surgery is now rarely performed. It is indicated only in cases where ATD have not been effective and radioiodine is contraindicated or not acceptable by the patients.     

High dose of (131)I therapy for the treatment of hyperthyroidism caused by Graves' disease

Radioactive iodine ((131)I) has become the most widely used therapy for patients with hyperthyroidism caused by Graves' disease in the United States. There remains, however, significant variability among (131)I dosing regimens, and it is clear that most patients ultimately develop hypothyroidism after therapy. To avoid persistent hyperthyroidism, we adopted a high dose (131)I therapy protocol based on measurement of 24-h thyroid (123)I uptake designed to deliver 8 mCi (296 MBq) to the thyroid gland 24 h after (131)I administration. To evaluate the efficacy of this protocol, we reviewed our clinical experience over a 7-yr period. We treated 261 patients (219 women and 42 men) with hyperthyroidism caused by Graves' disease with (131)I [mean dose, 14.6 mCi (540 MBq)] between 1993 and 1999. Before treatment, 207 (79%) had received an antithyroid drug (109 propylthiouracil and 98 methimazole). We determined their thyroid status 1 yr after treatment in relation to age, pretreatment with an antithyroid drug, pretreatment thyroid size, and dose of (131)I retained in the thyroid 24 h after treatment. Among the 261 patients, 225 (86%) were euthyroid or hypothyroid 1 yr after treatment, and 36 patients (14%) had persistent hyperthyroidism and required a second treatment. The patients who had persistent hyperthyroidism were younger (P < 0.01), had larger thyroid glands (P < 0.01), higher pretreatment thyroid (123)I uptake values (P < 0.01), and higher serum T(4) concentrations (P < 0.01) and were more likely to have taken antithyroid medication before administration of (131)I (P = 0.01). Five of these patients developed transient hypothyroidism, followed by thyrotoxicosis. There was an asymptotic, inverse relationship between the retained dose of (131)I at 24 h and persistent hyperthyroidism, revealing a 5-10% failure rate despite delivery of up to 400 microCi (14.8 MBq)/g. A dose of (131)I that results in accumulation of 8 mCi (296 MBq) in the thyroid gland 24 h after administration is an effective treatment for the majority of patients with Graves' hyperthyroidism. Young patients with larger thyroid glands, higher serum T(4) concentrations, and higher 24-h thyroid (123)I uptake values, and those pretreated with antithyroid medication for greater than 4 months are at higher risk for treatment failure. A higher dose of (131)I may be advisable in such patients.     

Hyperthyroidism in children treated with long term medical therapy: twenty-five percent remission every two years

We use an antithyroid drug for the treatment of hyperthyroidism due to Graves' disease in children and adolescents for as long as the patients are willing to comply and/or tolerate the drug. In more than 60 patients treated since 1961, the remission rate was 25% in the first 2 yr. This report looks at these same patients again, followed for an additional 5 yr. Survival analysis methods applied to the follow-up data on 63 children confirm our original statistical findings and suggest a continuing remission rate of 25% every 2.1 +/- 0.4 (+/- SE) yr regardless of the duration of previous therapy. The median time to remission was 4.3 +/- 1.5 yr, and 75% of patients are predicted to be in remission in 10.9 +/- 2.3 yr. Of 36 patients who went into remission, defined by their being euthyroid for 1 yr after cessation of therapy, 1 relapsed, and 2 developed spontaneous hypothyroidism; the remainder are euthyroid 1-11.7 yr after therapy was discontinued. Of 14 who switched from medical therapy, 2 of 7 treated surgically and 4 of 7 treated with 131I are hypothyroid. Only 1 patient had a significant adverse reaction to both methimazole and propylthiouracil. While medical therapy may have some direct effect on the autoimmune response in hyperthyroidism, its role in affecting the time to ultimate remission is unknown. These data, however, describe the course of children so treated and allow us to present therapeutic options initially or during treatment based on statistically derived probabilities of outcome.     

The Birmingham pituitary database: auditing the outcome of the treatment of acromegaly

OBJECTIVE Graves' disease is recognized as an organ-specific autoimmune disorder caused by the presence of TSH receptor antibodies. The long-term effects of ¹³¹I treatment for Graves' disease on TSH receptor antibodies have not previously been studied. We have measured the TSH-binding Inhibitory immunoglobulin (TBII) Index and thyroid stimulating antibody (TSAb) activity in patients with Graves' disease following treatment with ¹³¹I. DESIGN A retrospective study. PATIENTS Two hundred and twenty-five patients with Graves' disease who were treated with ¹³¹I 1–13 years earlier were studied (1 year: 27 patients; 2–5 years: 42 patients; 6–9 years: 79 patients; 10–13 years: 77 patients). MEASUREMENTS The TBII index was measured as the percentage ¹²⁵I-TSH bound to pig thyroid membranes and TSAb activity as the amount of cAMP produced by cultured FRTL-5 cells. RESULTS TBII was detected in 78% of patients prior to ¹³¹I administration. Following ¹³¹I administration, the Incidence of positive TBII was 85% at the end of the first year decreasing to 40,19 and 17% at 2–5,6–9 and 10–13 years, respectively. The frequency of a positive TSAb was 74% at the end of the first year, and also decreased to 49, 27 and 29% at 2–5, 6–9 and 10–13 years, respectively. At more than 2 years after ¹³¹I therapy, the frequencies of hyperthyroidism In TBII and TSAb positive patients were 42% (19/45) and 30% (19/63), respectively, which were significantly higher than those In TBII and TSAb negative patients (8%: 12/153 and 8%:11/131, respectively). The frequency of hyperthyroidism after ¹³¹I treatment in patients with negative TBII before treatment (7%: 2/29) was significantly lower than that (29%: 30/102) In patients with positive TBII before treatment. CONCLUSIONS These results indicate that (1) the TBII Index and TSAb activity decreased over a period of more than 2 years after ¹³¹I therapy for Graves' disease, and (2) the TBII index before treatment may influence the long-term outcome of ¹³¹I therapy.