无痛性甲状腺炎

无痛性甲状腺炎是一种自身免疫性甲状腺炎,表现为短暂、可逆的甲状腺滤泡破坏,局灶性淋巴细胞浸润。10％发生在产后,称之为产后甲状腺炎。甲状腺无疼痛及触痛为其特征。其典型的甲状腺功能变化类似于亚急性甲状腺炎。摄碘率、T3／T4比值及促甲状腺激素受体抗体（TRAb）有助于无痛性甲状腺炎与Graves病的鉴别。无痛性甲状腺炎在甲状腺毒症阶段为对症治疗,甲状腺功能减退（甲减）阶段视病情需要短期、小剂量补充甲状腺激素,而永久性甲减需终生替代治疗。甲状腺功能恢复正常后仍需继续随访。     

原发性甲状腺机能减退的甲状腺功能的恢复

大多数成人原发性甲减是由于慢性淋巴细胞性甲状腺炎。一般认为原发性甲减是永久性的并需要终生甲状腺激素替代治疗。但也确有一过性甲减发生。已有报告在分娩后(产后甲状腺炎)、服用锂、乙胺碘呋酮或服碘化物过多,亚急性甲状腺炎急性期后甲状腺功能恢复前,非进行型甲状腺炎,良性甲状腺疾病手术后以及甲亢~(131)I治疗后,发生一过性甲减。     

警惕医源性甲状腺功能减退症发病率增高的趋势

甲状腺功能减退症(甲减)是由不同原因引起甲状腺激素的缺乏或生物效应不足所致的慢性内分泌疾病临床综合征。其发病率约为2%~3%,近年来医源性甲减发病率明显增多。本文118例原发性甲减的原因有桥本甲状腺炎58例(49.15%),医源性甲减包括同位素治疗25例、甲状腺手术后15例、药物治疗10例(共占42.37%),产后甲状腺炎7例(8.03%),散发性克汀病3例(2.69%)。医源性甲减发病率增多的因素较多,可能与131I剂量过大、切除甲状腺组织较多、抗甲状腺药物剂量偏大等有关。其中因同位素及手术所致的甲减,均为破坏性的永久性甲减,需终身替代治疗,故尽量降低医源性甲减是内分泌科医师面临的当务之急。     

产后甲状腺炎6例临床报道

目的了解产后甲状腺炎的发病特点、诊断治疗预防,提高对产后甲状腺炎的认识。方法通过对既往收治的6例临床病例结合文献复习对产后甲状腺炎的发病特点、诊断治疗预后等资料进行回顾性分析。结果产后甲状腺炎,多发生在产后或流产后,其表现为暂时性或永久性甲状腺功能异常,无痛性甲状腺肿大。可自行缓解的甲亢或甲减。结论产后甲状腺炎是产后妇女常见的一种自身免疫性疾病,其本质是甲状腺自身免疫过程的急性阶段,其发病是神经-内分泌-免疫及环境、遗传等多种因素作用的结果。     

警惕医源性甲状腺功能减退症发病率增高的趋势

甲状腺功能减退症（甲减）是由不同原因引起甲状腺激素的缺乏或生物效应不足所致的慢性内分泌疾病临床综合征.其发病率约为2%～3%,近年来医源性甲减发病率明显增多.本文118例原发性甲减的原因有桥本甲状腺炎58例（49.15%）,医源性甲减包括同位素治疗25例、甲状腺手术后15例、药物治疗10例（共占42.37%）,产后甲状腺炎7例（8.03%）,散发性克汀病3例（2.69%）.医源性甲减发病率增多的因素较多,可能与131I剂量过大、切除甲状腺组织较多、抗甲状腺药物剂量偏大等有关.其中因同位素及手术所致的甲减,均为破坏性的永久性甲减,需终身替代治疗,故尽量降低医源性甲减是内分泌科医师面临的当务之急.     

亚急性甲状腺炎

亚急性甲状腺炎是以短暂疼痛的破坏性甲状腺组织损伤伴全身炎性反应为特征,是最常见的甲状腺疼痛疾病.放射性痛和转移性痛为其特征.甲状腺毒症阶段甲状腺激素升高和甲状腺摄碘率降低的双向分离现象是其重要特点.亚急性甲状腺炎在诊断困难时可依靠甲状腺针吸细胞学检查明确诊断.在甲状腺毒症阶段为对症治疗,甲状腺功能减退阶段视病情需要短期、小剂量补充甲状腺激素,而永久性甲状腺功能减退需终身替代治疗.甲状腺功能恢复正常后需继续随访.     

产后甲状腺炎

近十余年来国外不少学者注意到许多妇女产后可出现暂时性甲状腺功能改变,其特征为产后一过性、无痛性甲状腺肿大伴有可自发缓解的甲亢和/或甲减,~(131)Ⅰ摄取率减低,抗微粒体抗体(TMA)阳性。许多学者最初认为这种情况是Graves病或桥本甲状腺炎在产后的加重。但越来越多的证据表明产后出现的甲状腺功能改变主要是由于无痛性甲状腺炎所致,由于和产后关系密切,故又称“产后甲状腺炎,在产后妇女中的发病率为5.5～11.3％。其差别可能是由于观察病人的时间不同,以及诊断标准不同所致。由于产后甲状腺炎发病率高,故该病已越来越引起人们的重视。     

亚急性甲状腺炎

亚急性甲状腺炎是以短暂疼痛的破坏性甲状腺组织损伤伴全身炎性反应为特征,是最常见的甲状腺疼痛疾病。放射性痛和转移性痛为其特征。甲状腺毒症阶段甲状腺激素升高和甲状腺摄碘率降低的舣向分离现象是其重要特点。亚急性甲状腺炎在诊断困难时可依靠甲状腺针吸细胞学检查明确诊断：在甲状腺毒症阶段为对症治疗,甲状腺功能减退阶段视病情需要短期、小剂量补充甲状腺激素,而永久性甲状腺功能减退需终身替代治疗。甲状腺功能恢复正常后需继续随访.     

亚临床甲状腺功能减退症

亚临床甲状腺功能减退症(甲减)是一种业临床甲状腺疾病.诊断标准是血清促甲状腺激素(TSH)水平高于正常上限而游离T4水平尚在正常范围.目前全世界业临床甲减的平均患病率为4%～10%,主要发生在女性和老年人群.桥本甲状腺炎是最常见的病因.其卡要的临床危害包括引起血脂异常、导致动脉粥样硬化和,冠心病、影响认知功能,还可导致不孕和流产.治疗主要针对血清TSH10 mIU/L的患者,应用左旋-T4替代治疗.对于血清TSH 4～10 mIU/L,特别是甲状腺自身抗体阳性者需密切监测.此外,对妊娠期亚临床甲减患者的治疗要求控制TSH<2.5 mlU/L.     

甲减患者都需要补碘吗

甲状腺疾病与糖尿病两者之间有着比较密切的关系,一种情况下,糖尿病是在甲状腺疾病的基础上所继发,这种情况下患者往往先有较长时间的甲状腺疾病病史。另一种情况下是糖尿病和甲状腺疾病是两种并行的疾病。甲减是因为碘缺乏导致的疾病吗,甲状腺功能减退症(简称甲减)是由于甲状腺激素合成及分泌减少,或其生理效应不足所致机体代谢降低的一种疾病。按其发病部位分为原发性甲减或甲状腺性甲减、继发性甲减或垂体性甲减、三发性甲减或下丘脑性甲减、甲状腺激素不敏感综合征(组织对甲状腺激素抵抗)和消耗性甲减五类。     

Hypothyreose

An autoimmune thyroiditis represents the main reason of hypothyroidism, defined as a lack of thyroid hormone. This autoimmune process results in destruction of functioning thyroid follicles. While subclinical or latent hypothyroidism is defined on the basis of laboratory values (an elevation of TSH with normal peripheral hormone levels), the typical signs and symptoms are associated with hypothyroidism. In about 80% of cases antibodies against thyroid peroxidase can be measured, but only in about 40–50% of cases antibodies against thyroglobulin are detectable. If hypothyrodism has been diagnosed, substitution with levothyroxine should be initiated, with the therapeutic goal to decrease TSH level to the lower normal range. In cases of subclinical hypothyroidism, levothyroxine medication should be started in patients with a high TSH value, positive antibodies and/or the typical ultrasound of autoimmune thyroiditis. However, substitution with levothyroxine in any case of elevated TSH values should be avoided.     

Transition of thyroid autoantibodies by rituximab treatment for thyroid MALT lymphoma

Thyroid MALT lymphoma is an extremely rare malignancy believed to arise against a background of Hashimoto's thyroiditis. Rituximab is a monoclonal antibody directed against B cell specific antigen CD20. Recently, there have been reports that rituximab is effective for autoimmune thyroid diseases such as Graves' disease as well as for treatment of B cell malignant lymphoma. We present the changes in thyroid autoantibodies in Hashimoto's thyroiditis after rituximab administration for 3 cases of thyroid MALT lymphoma. Case 1 had been taking levothyroxine and was diagnosed with thyroid MALT lymphoma. She was treated with rituximab monotherapy, and her thyroid enlargement improved. Anti-thyroid peroxidase antibody (TPOAb) turned negative after rituximab monotherapy, and TSH levels decreased with the same levothyroxine dosage. Case 2 was diagnosed with recurrent thyroid MALT lymphoma after chemotherapy (CHOP). He suffered from leg sensory disturbance because of vincristine sulfate. The patient was treated with rituximab. TPOAb decreased, but did not turn negative. TSH levels were within normal range during the disease course, but TSH levels were low in comparison with before rituximab therapy. Case 3 was diagnosed with thyroid MALT lymphoma after radiation therapy on the neck for laryngeal cancer. Thyroid enlargement improved after rituximab monotherapy, and thyroid autoantibody levels decreased. TSH increased transiently after radiation therapy, but TSH decreased gradually without levothyroxine after rituximab monotherapy. We report 3 cases in which thyroid autoantibody levels in Hashimoto's thyroiditis decreased after rituximab monotherapy for thyroid MALT lymphoma, but it is controversial whether thyroid dysfunction due to Hashimoto's thyroiditis is restored.     

Riedel's thyroiditis presenting with hypothyroidism and hypoparathyroidism: dramatic response to glucocorticoid and thyroxine therapy

Riedel's thyroiditis is a rare fibro-inflammatory process originating in the thyroid gland with progressive extension and invasion of surrounding tissues. Patients frequently present with a stony hard thyroid mass suggestive of anaplastic carcinoma. We report a striking case of Riedel's thyroiditis associated with hypothyroidism, hypoparathyroidism and bilateral vocal cord paralysis. A dramatic response to high dose prednisone and levothyroxine therapy was seen, with recovery of parathyroid and vocal cord function. Our case suggests that early initiation of combination therapy may be important, particularly in the presence of severe disease.     

Thyrotoxic thyroiditis after radiotherapy for Hodgkin's disease

Exposure of the thyroid gland to ionizing radiation has been associated with a variety of abnormalities. Among these are tardive hypothyroidism and an increased risk of developing thyroid nodules and cancer. Although acute thyroiditis has been known to complicate radioactive iodine 131 therapy, it has rarely been associated with external beam irradiation. Thyrotoxic painless thyroiditis developed in two patients after mantle-field irradiation for Hodgkin's disease.     

Hypothyroidism and thyroiditis after therapy for Hodgkin's disease

During the follow-up of thyroid function of 151 patients with Hodgkin's disease in complete remission for at least 1 year, 26 cases of subclinical, 12 cases of manifest clinical hypothyroidism and 2 cases of hyperthyroidism (Graves-Basedow disease) were confirmed. Thyroid dysfunction was more frequent in patients who had undergone mantle or neck radiotherapy. Hypothyroidism was most often revealed from the 6th year on following radiotherapy. Thyroid autoantibody positivity was found to be more frequent in patients with thyroid dysfunction, and conversely, thyroid dysfunction was more frequent among the 28 patients with autoantibody positivity. Ultrasound examination and fine needle aspiration cytology of the thyroid confirmed thyroiditis in 96% of the patients with antibody positivity. No relationship was found between thyroiditis and the form of treatment for Hodgkin's disease. We have found that both neck irradiation and thyroiditis may play a role in the increased number of thyroid dysfunction in patients treated for Hodgkin's disease. Thyroiditis is not caused by neck radiotherapy but may be the result of immune regulation disorders in Hodgkin's disease. For substitution or isohormone therapy, levothyroxine is suggested for use. We suggest that examination of the thyroid should be performed at least once a year during the follow-up of Hodgkin's disease patients.     

Possible induction of Graves' disease and painless thyroiditis by gonadotropin-releasing hormone analogues.

Prolonged administration of gonadotropin-releasing hormone (GnRH) analogues induce a decrease in serum estrogen level, which may aggravate subclinical or mild autoimmune thyroid disease. Two patients developed Graves' thyrotoxicosis in association with an increase in anti-thyrotropin (TSH) receptor antibody activities at 4 months after initiation of buserelin acetate. GnRH analogue therapy was discontinued at the time of diagnosis but it took more than 2 years of methimazole therapy to obtain remission of Graves' disease. Another patient developed painless thyroiditis in association with an increase in antithyroid microsomal antibodies at 4 months after initiation of leuprolide acetate. These results indicate that GnRH analogues possibly induce clinical onset of Graves' thyrotoxicosis or destruction-induced thyrotoxicosis. Clinicians should be aware of this phenomenon. All patients who are to receive GnRH analogue therapy should be examined for antithyroid antibodies and family history of autoimmune thyroid disease, and should be followed accordingly.     

血尿碘及甲状腺功能测定对鉴别无痛性甲状腺炎的意义

目的　探讨血尿碘质量浓度及甲状腺功能在无痛性甲状腺炎患者与其他甲状腺毒症患者中的区别。方法　 2 0 0 2 - 0 1～ 0 4在第四军医大学西安医院住院初诊血甲状腺激素水平升高的患者 75例分为无痛性甲状腺炎组、亚急性甲状腺炎组、格雷夫斯病组 ,测量血清学及血、尿碘指标 ,观察各组与指标间的关系。结果　T3 、T4及血、尿碘与甲状腺毒症的种类有关。结论　无痛性甲状腺炎的发病并非少见 ,可通过临床表现、血尿碘和甲功测定等对此类疾病进行诊断和鉴别诊断。