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胺碘酮所致甲状腺毒症中的血清白细胞介素-6

Serum interleukin-6 in amiodarone-induced thyrotoxicosis.

作者信息

Bartalena L, Grasso L, Brogioni S, Aghini-Lombardi F, Braverman L E, Martino E

机构信息

Istituto di Endocrinologia, University of Pisa, Tirrenia-Pisa, Italy.

出版信息

J Clin Endocrinol Metab. 1994 Feb;78(2):423-7. doi: 10.1210/jcem.78.2.8106631.

DOI:10.1210/jcem.78.2.8106631
PMID:8106631
Abstract

Amiodarone, an iodine-rich cardiac drug, may induce thyrotoxicosis (AIT), which can occur in patients with preexisting thyroid abnormalities and in subjects with apparently normal thyroid glands. The pathogenesis of AIT is often due to iodine-induced excessive thyroid hormone synthesis, especially in patients with underlying thyroid disease. In some instances, however, AIT may be related to a destructive process due to amiodarone-induced thyroiditis, resulting in thyroid cell damage and thyroid hormone release into the circulation. Another thyroid inflammatory process, subacute thyroiditis, has been recently reported to be associated with markedly increased serum interleukin-6 (IL-6) levels. To investigate the significance of serum IL-6 levels in AIT, we evaluated in a cross-sectional study the following subjects: 27 AIT patients, 15 with no apparent thyroid abnormalities (AIT-) and 12 with nodular goiter and/or thyroid autoimmune disease (AIT+); 14 euthyroid patients receiving chronic amiodarone therapy; 10 patients with amiodarone-induced hypothyroidism; 56 patients with spontaneous hyperthyroidism due to Graves' disease (n = 35) or toxic adenoma/nodular goiter (n = 21); 20 subjects with nontoxic goiter; and 50 healthy controls. Serum free thyroid hormone concentrations did not differ in patients with amiodarone-induced or spontaneous hyperthyroidism. Mean (+/- SE) serum IL-6 values were as follows: AIT-, 573.5 +/- 78.7 fmol/L (range, 149.4-1145.1); AIT+, 152.7 +/- 46.3 fmol/L (range, < 25-505.6); euthyroid patients receiving chronic amiodarone therapy, 51.4 +/- 10.0 fmol/L (range, < 25-122.5); amiodarone-induced hypothyroidism, 43.8 +/- 8.4 fmol/L (range, < 25-84.3); Graves' disease, 108.2 +/- 18.2 fmol/L (range, < 25-250); toxic adenoma/nodular goiter, 97.6 +/- 10.3 fmol/L (range, < 25-168.9); nontoxic goiter, 47.3 +/- 7.1 fmol/L (range, < 25-106.6); and controls, 37.8 +/- 6.2 fmol/L (range, < 25-99.4). Serum IL-6 values in AIT- patients were markedly higher (P < 0.0001) than those in all other groups. Values in AIT+, although slightly higher, did not significantly differ from those in patients with spontaneous hyperthyroidism. AIT- patients had low 24-h thyroidal radioiodine uptake (RAIU), whereas AIT+ had inappropriately low normal to high (9-58%) RAIU values in the presence of excess iodine. The presence of markedly elevated serum IL-6 concentrations and low thyroidal RAIU values in patients with AIT without underlying thyroid disease suggests the presence of amiodarone-induced thyroiditis as the etiology of thyrotoxicosis. Treatment of 2 such patients with prednisone was associated with a dramatic reduction and prompt normalization of IL-6 and thyroid hormone values.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

胺碘酮是一种富含碘的心脏药物,可能诱发甲状腺毒症(胺碘酮所致甲状腺毒症,AIT),这在已有甲状腺异常的患者以及甲状腺看似正常的个体中均可能发生。AIT的发病机制通常是碘诱导甲状腺激素过度合成,尤其是在患有潜在甲状腺疾病的患者中。然而,在某些情况下,AIT可能与胺碘酮诱发的甲状腺炎导致的破坏性过程有关,从而导致甲状腺细胞损伤以及甲状腺激素释放进入循环。最近有报道称,另一种甲状腺炎症过程,即亚急性甲状腺炎,与血清白细胞介素-6(IL-6)水平显著升高有关。为了研究血清IL-6水平在AIT中的意义,我们在一项横断面研究中评估了以下受试者:27例AIT患者,其中15例无明显甲状腺异常(AIT-),12例有结节性甲状腺肿和/或甲状腺自身免疫性疾病(AIT+);14例接受慢性胺碘酮治疗的甲状腺功能正常患者;10例胺碘酮诱发的甲状腺功能减退患者;56例因格雷夫斯病(n = 35)或毒性腺瘤/结节性甲状腺肿(n = 21)导致的自发性甲状腺功能亢进患者;20例非毒性甲状腺肿患者;以及50例健康对照者。胺碘酮诱发的甲状腺功能亢进患者与自发性甲状腺功能亢进患者的血清游离甲状腺激素浓度无差异。平均(±标准误)血清IL-6值如下:AIT-为573.5±78.7 fmol/L(范围为149.4 - 1145.1);AIT+为152.7±46.3 fmol/L(范围为<25 - 505.6);接受慢性胺碘酮治疗的甲状腺功能正常患者为51.4±10.0 fmol/L(范围为<25 - 122.5);胺碘酮诱发的甲状腺功能减退患者为43.8±8.4 fmol/L(范围为<25 - 84.3);格雷夫斯病患者为108.2±18.2 fmol/L(范围为<25 - 250);毒性腺瘤/结节性甲状腺肿患者为97.6±10.3 fmol/L(范围为<25 - 168.9);非毒性甲状腺肿患者为47.3±7.1 fmol/L(范围为<25 - 106.6);对照者为37.8±6.2 fmol/L(范围为<25 - 99.4)。AIT-患者的血清IL-6值显著高于(P < 0.0001)所有其他组。AIT+患者的IL-6值虽然略高,但与自发性甲状腺功能亢进患者的值无显著差异。AIT-患者的24小时甲状腺放射性碘摄取(RAIU)较低,而AIT+患者在碘过量的情况下RAIU值却异常地处于低正常至高(9 - 58%)水平。在无潜在甲状腺疾病的AIT患者中,血清IL-6浓度显著升高且甲状腺RAIU值较低,这表明存在胺碘酮诱发的甲状腺炎作为甲状腺毒症的病因。对2例此类患者使用泼尼松治疗后,IL-6和甲状腺激素值显著降低并迅速恢复正常。(摘要截短至400字)

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