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亚急性甲状腺炎早期甲状腺功能的改变。

Alteration of thyroid function in the early stage of subacute thyroiditis.

作者信息

Madeddu G, Langer M, Costanza C, Casu A R, Arras M L, Campus S

出版信息

Acta Endocrinol (Copenh). 1980 Dec;95(4):479-84. doi: 10.1530/acta.0.0950479.

Abstract

Measurement of serum triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyroxine-binding-globulin (TGB), antithyroglobulin antibodies (anti-hTg), thyroid 131I uptake and scanning was performed on 12 patients during the early phase of subacute thyroiditis. Serum thyrotropin (TSH) was measured during baseline conditions and following administration of synthetic thyrotropin-releasing-hormone (TRH). The stimulation with exogenous TSH was performed on 7 subjects. 131I uptake was depressed in all patients including those with solitary nodules. Free and total hormone concentrations were elevated in the three cases with diffuse gland involvement, whereas an increase of T3 alone was present in 3 patients with unilobar involvement. In the latter group and in the 2 patients with a nodular form T4, FT3 and FT4 levels were within normal limits. Interruption of the pituitary-thyroid feed-back mechanism with absence of thyrotropin response to TRH occurred in 11 patients, independent of whether thyroid hormone concentrations were elevated or normal. In one patient only with unilateral involvement, TSH responsiveness to TRH was normal while 131I uptake was not raised by exogenous TSH, indicating diffuse cellular damage. The normal values of FT3 and FT4 found in patients with normal T3 and T4 levels seem to exclude the possibility that the free hormones are responsible for the interrupted feed-back which represents the main cause of suppressed iodine uptake. However, it is possible that the pituitary-thyroid axis is responding to transient or light increases of free and total T3 and T4 still within their 'normal range'.

摘要

对12例亚急性甲状腺炎早期患者进行了血清三碘甲状腺原氨酸(T3)、甲状腺素(T4)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、甲状腺素结合球蛋白(TGB)、抗甲状腺球蛋白抗体(抗-hTg)、甲状腺131I摄取及扫描检查。在基线状态及给予合成促甲状腺激素释放激素(TRH)后测定血清促甲状腺激素(TSH)。对7名受试者进行了外源性TSH刺激试验。所有患者(包括有孤立结节的患者)的131I摄取均降低。3例弥漫性腺体受累患者的游离和总激素浓度升高,而3例单叶受累患者仅T3升高。在后一组以及2例结节型患者中,T4、FT3和FT4水平在正常范围内。11例患者出现垂体-甲状腺反馈机制中断,对TRH无促甲状腺激素反应,无论甲状腺激素浓度是升高还是正常。仅1例单侧受累患者,TSH对TRH的反应正常,而外源性TSH未使131I摄取增加,提示存在弥漫性细胞损伤。T3和T4水平正常的患者中FT3和FT4的正常值似乎排除了游离激素导致反馈中断的可能性,而反馈中断是碘摄取受抑制的主要原因。然而,垂体-甲状腺轴有可能仍在对游离和总T3及T4仍在其“正常范围”内的短暂或轻度升高做出反应。

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